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Talk:Saturated fat/Archive 3

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Latest comment: 2 years ago by Tempes1 in topic Study

Saturated fats and cardiovascular health edit

Latest comment: 2 years ago58 comments8 people in discussion

In recent years there have been numerous studies and meta-studies [1][2][3][4][5] that cast serious doubt onto the notion that saturated fats contribute to cardiovascular disease. Some even point to saturated fats potentially having protective properties. Health authorities such as the WHO and AHA along with most governmental authorities are notoriously slow to stay up to date with the latest scientific findings. Therefore they should not be used as sole authorities on the topic. This article does not do a sufficient job at representing modern scientific literature on the topic and is heavily biased towards decades-old studies, most of which have been discredited either due to flawed methodologies or corruption. Tempes1 (talk) 17:36, 26 June 2021 (UTC)Reply

Only the first two sources are scholarly, and they're ancient, and so nothing to do with "recent years". Alexbrn (talk) 17:41, 26 June 2021 (UTC)Reply
Also a matter of WP:UNDUE that chronic saturated fat consumption is not a risk factor for cardiovascular disease - comments above by Tempes1 are out of synch with the majority scientific view which has held for decades. Undue weight: "articles should not give minority views or aspects as much of or as detailed a description as more widely held views or widely supported aspects. Generally, the views of tiny minorities should not be included at all." The article's 2020 Cochrane review and the AHA advisory panel are the state of science showing the convincing causal effect of chronic saturated fat consumption and cardiovascular diseases. Until we see something compelling to the contrary, the article is accurate as stated. Zefr (talk) 17:58, 26 June 2021 (UTC)Reply
All of those studies were published within the past decade, and all of them are published in reputable scientific journals. The point stands that there is a changing scientific consensus. The majority of scholarly studies on the topic in the past decade do not support the consensus among health authorities that saturated fats contribute to cardiovascular health. This article makes no mention of this shifting consensus (which is no longer a minority view according to modern scientific literature). This is problematic. Skimming through the archive, I can see that this has been a long-standing issue and that this article appears to have gate keepers actively suppressing this information. I have no interest in debating the issue or engaging in edit wars. I am simply stating facts. Have a nice day. Tempes1 (talk) 18:11, 26 June 2021 (UTC)Reply
Please do not archive this discussion, as there may be others who want to contribute to the discussion. Considering how long-standing this issue is and how controversial it seems to be, there should be an ongoing dialog. Tempes1 (talk) 18:19, 26 June 2021 (UTC)Reply

Zefr (talk) 19:19, 26 June 2021 (UTC)Reply

Tempes1 you only linked to two studies (a meta-analysis of epidemiology published in 2010, and a systematic review from 2014). The 2014 review by Rajiv Chowdhury and colleagues is a favourite of those in the low-carb community but it was deeply flawed. This is because the health effect of a macronutrient (in this case saturated fat, known as SFA) that delivers most of the daily calories cannot be studied in isolation in a meta-analysis but depends on what it is replaced with. They also lumped together lots of different studies with entirely different methods. Calories from saturated fat were replaced with low-quality carbohydrates which are clearly bad for cardiovascular disease. If the comparison nutrient is refined carbohydrates then SFA will not appear the be associated with an increased risk of heart disease. Have you read the follow up commentary in the same journal? "The meta-analysis of dietary fatty acids and risk of coronary heart disease by Chowdhury et al. (1) contains multiple errors and omissions, and the conclusions are seriously misleading". The authors of the meta-analysis also admitted they made "numerical errors" [6], [7]. Psychologist Guy (talk) 19:25, 26 June 2021 (UTC)Reply
I linked to 7 peer reviewed studies and meta-analyses, which respectively cite many more studies. As I said earlier, this is not the place to be debating nutrition. I am not a qualified nutritional scientist and neither are you. We are merely here to relay relevant information in an unbiased and objective manner. It seems quite clear that this is no longer considered a fringe view in the scientific and health communities. For observers, here is a more organized, non-exhaustive list of modern studies, meta-analyses and reviews concluding that saturated fats are unlikely to contribute to CV disease.
Meta-analyses:
Studies:
Reviews:
Tempes1 (talk) 22:53, 26 June 2021 (UTC)Reply

Tempes1 it is pretty much universally agreed (minus a few denialists) that LDL is strongly related to CVD risk. It is also agreed that saturated fat raises LDL as many clinical trials have demonstrated this. There is no dispute here even one of your reviews confesses this as do two of the meta-analysis you cited. However, the second "review" you list is not a review, it is an editorial piece by a known low-carb high-fat fad diet proponent, Aseem Malhotra. This guy is always in the news in the UK because he writes controversial things. He likes to be a contrarian. He makes the ill-founded claim that "LDL cholesterol is not associated with cardiovascular disease and is inversely associated with all-cause mortality". That is crazy statement. What is his source? Uffe Ravnskov. The editorial is a joke and not worth discussing.

The other review you listed was funded by Nina Teicholz's "Nutrition Coalition" and you can scroll down to the bottom of the article in small print and see that every author of the article was funded by the dairy or beef industry (you were complaining about the sugar industry but you have no problem with this?). It is not a neutral review but it actually contradicts the Aseem Malhotra editorial you cite. The review admits that saturated fat (SFA) does increase LDL "Although SFAs increase low-density lipoprotein (LDL) cholesterol, in most individuals, this is not due to increasing levels of small, dense LDL particles, but rather larger LDL particles, which are much less strongly related to CVD risk". You need to be an extreme denialist to claim that LDL cholesterol is not associated with cardiovascular disease and the authors of this review do not actually claim that but they are left with a problem because they want to promote saturated fat foods but they have to admit it raises LDL, so they come up with the solution that this is irrelevant because only the particle size matters. This is irresponsible because quantity rather than the size of the LDL particle is also associated with risk of CHD.

The review funded by Teicholz claims that only the LDL particle size is important and that although saturated fat raises LDL it only increases the larger LDL particles which are not a problem. The review actually admits "it is evident that LDL particles play a causal role in the development of CVD and that, in general, there is a relationship between lowering of LDL cholesterol and CVD benefit". This is in contradiction to Malhotra and Ravnskov. You have not read the reviews you have cited.

When you eat a diet high in saturated fat it raises the LDL so it defeats any CVD benefit. We already have an article on Saturated fat and cardiovascular disease and I have raised concerns about that review on the talk-page. LDL number, rather than the density, is also strongly related to CVD risk. It's irresponsible to tell people to eat a diet high in saturated fat because it will significantly raise LDL. The authors knows this but they downplay its importance. We don't know enough about large LDL particle size. We know that small and medium LDL particles are positively associated with all cardiovascular disease and stroke (there are literally loads of papers confirming this) but we do not know enough about large LDL particles and CVD risk, are you claiming otherwise? This study actually looked at particle size after a high-fat meal was eaten (full-fat dairy) and it found that "Large VLDL particles and chylomicrons demonstrated the largest increase in concentration" [8]. So yes it's true there is evidence that foods high in saturated fat increase large LDL particles but if you look in the literature there are not many clinical trials that have measured particle size in relation to diet.

We know that LDL is strongly related to CVD risk so it is unsafe to tell people to eat a diet that greatly increases the LDL. To claim that large LDL particles are less of a risk is irresponsible because as stated the number rather than the density of particles is also a risk factor for cardiovascular disease. The authors of the paper are sponsored by full fat dairy and the beef industry so they have to say what they do so people consume their foods but it is irresponsible at the end of the day. Much more research on LDL particle size needs to be done but as it stands the scientific consensus is clear, foods high in saturated fat are a risk factor for heart disease because they raise LDL. Nobody is saying they should not be eaten at all but they should be reduced in the total diet or eaten in moderation. The links above by Zefr confirm this. Psychologist Guy (talk) 22:38, 27 June 2021 (UTC)Reply

@Tempes1: Hey Tempes, I would be vary of whoever is providing you with this information as they are either intentionally misleading you, or are uninformed and uneducated on the topic. Since they presented such a large error I would also be vary of their other recommendations. Make sure to have high levels of scrutiny for their advice to prevent this. In this instance (saturated fat), there is a flaw with the presented methodology (prospective cohorts).

People genetically start out with different cholesterol levels. So if me and you eat the same amount of saturated fat, say 20% of caloric intake, we will still have different cholesterol scores. If my score is worse than yours then there is a higher probability that I will suffer from more related illnesses.

How could it be possible to correlate any positive/negative cardiovascular effects if we both eat the same amount of saturated fat while I suffer more? what if we now include more groups, people that eat a little bit more saturated fat and have a lower score, and people that eat a little bit less saturated fat and have a higher score? Since that is the case, over a wide enough population, any negative or positive correlations cancel out even when there is cause and effect.

The only correlation I could find would be that high cholesterol level = worse health outcomes and that low cholesterol = better health outcomes independent of saturated fat intake. I could not determine whether saturated fat caused your score because the general population eats similar amounts of saturated fat, yet has different cholesterol levels. This is shown mathematically here: https://pubmed.ncbi.nlm.nih.gov/313701/ - If you cannot access the full study, simply search for SciHub or SciHub proxy and enter the DOI. It allows bypassing of paywalls, and no researchers are hurt in the process as they do not receive compensation when their article is purchased (researchers moreso enjoy when their research is read).

"It is well known that serum cholesterol level will differ from individual to individual on a diet held constant"

"If the intrinsic (baseline) level were known for each individual then it could be utilized to adjust the serum cholesterol level."

"The results given here imply that the zero correlations found by various cross-sectional observational studies (prospective cohorts) actually do not negate the evidence that diet has an effect on serum cholesterol. In statistical parlance, a cross-sectional study has near zero power for detecting such a relationship. It is expected that correlations near zero would arise between diet and serum cholesterol whether they are related or not. Thus cross-sectional observation of this relationship seems to be inappropriate."

"If the investigator (scientist) knows a person's customary dietary intake this will not tell the investigator the level of serum cholesterol of the person, even though, if that person modifies his diet to reduce his intake of dietary lipids, his serum cholesterol will go down from its present level. After dietary modification in a total population there will still be considerable differences between people in terms of their serum cholesterol levels and, therefore, in terms of their risk levels."

"Since diet and serum cholesterol have a zero correlation cross-sectionally, a study of the relationship between diet and coronary heart disease incidence will suffer from the same difficulties as the study of diet and serum cholesterol. A corollary of the mathematical model here presented is that a correlation close to zero would likely be observed between diet and coronary heart disease incidence."

"For another disease in which diet is a cause agent, a prospective incidence study following a cross-sectional assessment of diet would presumably be valuable." (but not in this instance, because of randomness, aka varying levels of baseline cholesterol despite a similar diet)

"An appropriate design for demonstrating or refuting diet and coronary heart disease incidence is a dietary change experiment" (such as those referenced above by "Psychologist Guy" and "Zefr" which are randomized controlled trials).

To editors: Would it be possible to include an explanation of this in the article to prevent people from becoming mislead because of the inability of prospective cohorts to study the relationship? RBut (talk) 20:31, 28 June 2021 (UTC)Reply

Thanks for the informed responses, particularly about the 2020 Nutrition Coalition review. I had thought it was a better source than I now suspect and see it was also added to Wikipedia on June 18th as a supposed criticism of the Seven Countries Study. Tdr26 (talk) 04:30, 3 July 2021 (UTC)Reply

Tempes1 has a point. And this is indeed by no means a minority view anymore. However I can understand the resistance by people here since nutritional guidelines and big organizations have not updated any recommendations about saturated fat intake. Tempes already provided quite a few references. Here is just a small addition:

And I realize the following is not a reliable source, but just for people who are interested to dig deeper into the actual science, the possibly best scientific presentation of this topic can be found here. It also includes some arguments why despite growing evidence against the nutritional guidelines regarding saturated fats, we still have many scientists and organizations holding on to this. Also related is this discussion here.

In summary big organizations and guidelines currently hold on to this outdated view, so the best thing Wikipedia can do at this time is to at least present some of the counter-arguments. I think it's long overdue to add those. Gorgos19 (talk) 15:42, 4 July 2021 (UTC)Reply

He says quoting old, weak sources. Got anything decent & recent? Alexbrn (talk) 15:44, 4 July 2021 (UTC)Reply
5 and 6 years is not old. And even if it were old, that would only be a bad thing if in the meantime new evidence came out suggesting something else. The sad part is that the whole evidence for saturated fats causing CVD is based on seriously flawed science. I recommend watching my linked presentations. As it stands today we have some weak evidence for saturated fats causing CVD and some weak evidence for saturated fats even helping in it, in particular with regards to all cause mortality. A quick Google Scholar search for relatively new studies confirms what I assumed: While you immediately find the same old reasoning for reducing saturated fats based on flawed epidemiology, you can also easily find counter points. Gorgos19 (talk) 16:03, 4 July 2021 (UTC)Reply
WP:MEDRS suggests a 5 year cut off for an actively researched area like this. When there are high-quality publications why scrape around for old studies (while banging on about "outdated views") or iffy stuff like in PLOS ONE? pmid:32827219 looks recent and at the top-of-tree quality wise. What does it say? Let's make sure we have recent, quality evidence and be sure to avoid some of the quackery and faddism around fat eh? Alexbrn (talk) 16:23, 4 July 2021 (UTC)Reply
You're calling peer reviewed science published in reputable journals quackery and faddism? You've discredited yourself as a neutral participant in this conversation. You are not in a position to question peer reviewed science as a wikipedia editor, much less accuse these reputable scientists of being quacks. As for the study you cited, the results are ambiguous, as it states that reduction in saturated fats has no effect on all-cause mortality or cardiovascular mortality. We can logically deduce that this means one of two things: A. Increasing cardiovascular events does not in of itself increase all-cause or cardiovascular mortality rates (probably impossible) or B. Null results. Unfortunately the authors do not expound on this obvious contradiction in conclusions, and I'm in no position to critique their methodology. Either way, that study does not provide sufficient evidence to discount all other recent studies that do not agree with it, and in a way it even agrees with them. Tempes1 (talk) 18:03, 4 July 2021 (UTC)Reply
Gorgos, randomized controlled trials reduce bias, while meta-analyses of cohorts can increase bias - I hope you realise that. In regard to butter there have not been many randomized controlled trials before 2015. The "is butter back review" was based on 9 cohort studies which admitted "No RCTs were identified". However since that butter review was published we now have several RCTs published in the medical literature on butter consumption. No surprise that it raised LDL-C and total blood cholesterol. Here is a link to two of those [9] and [10], the latter link is the best RCT published on the subject to date. Butter is usually between 63% and 70% saturated fat. The study found that the butter was 66% saturated fatty acids, nearly half of that was palmitic acid. Coconut oil has been shown to significantly increase HDL-C (this is because of the lauric acid it contains which is also present in human breast milk). According to all the evidence from the medical literature and recommendations from health organizations - palmitic acid raises LDL levels more than any other saturated fatty acid so this is the one to watch out for and cut down on. This is common knowledge so it is ridiculous to recommend to eat butter in high amounts when it has been proven to raise LDL-C and the total blood cholesterol. The guidelines are not "flawed" about this. There will very likely be a meta-analysis or review of RCTs in the future of butter consumption but until then I don't think we should be citing a 2015 review of 9 cohorts. Psychologist Guy (talk) 17:14, 4 July 2021 (UTC)Reply
@Psychologist Guy Nobody is questioning if it raises LDL-C, that is not the question we are discussing and is a good illustration for the confusion in the scientific discussions. Saturated fats also increase HDL-C and thus the very important LDL:HDL and TG:HDL ratio which are much better predictors for CVD than LDL alone. @talk:Alexbrn Here is a great response to your reference (responded study here also interesting, relevant and not old).
This is a very recent analysis only one year old. @talk:Alexbrn your reference is even included in there. I just quote the abstract:

'The recommendation to limit dietary saturated fatty acid (SFA) intake has persisted despite mounting evidence to the contrary. Most recent meta-analyses of randomized trials and observational studies found no beneficial effects of reducing SFA intake on cardiovascular disease (CVD) and total mortality, and instead found protective effects against stroke. Although SFAs increase low-density lipoprotein (LDL) cholesterol, in most individuals, this is not due to increasing levels of small, dense LDL particles, but rather larger LDL particles, which are much less strongly related to CVD risk. It is also apparent that the health effects of foods cannot be predicted by their content in any nutrient group without considering the overall macronutrient distribution. Whole-fat dairy, unprocessed meat, and dark chocolate are SFA-rich foods with a complex matrix that are not associated with increased risk of CVD. The totality of available evidence does not support further limiting the intake of such foods.'

Gorgos19 (talk) 18:29, 4 July 2021 (UTC)Reply
I intentionally did not read it but picked it as an example of a high-quality source of the type we should be using. So long as we use such sources, representing them faithfully with WP:NPOV, then our job is done. Alexbrn (talk) 18:35, 4 July 2021 (UTC)Reply
I am not aware of any long-term evidence that foods high in saturated fat raise HDL. Only coconut oil has been shown to increase HDL-C but it also has been shown to raise LDL-C but the rise in HDL-C is because it contains lauric acid but not enough research has been done on this, no other saturated fat foods contains lauric acid. In every RCT to date butter (and other dairy), red meat and other SFA foods increase LDL-C, this is because they all contain a significant palmitic acid. You have admitted that SFA-rich foods raise LDL-C which increases the total cholesterol level. The position you arguing is cholesterol denialism, i.e. LDL has no relevance to cardiovascular disease. That's why it's key proponents like the meta-analysis you cite above claim that its only the particle size that is important. We have already discussed why that view is not taken seriously in the medical community. The idea that larger LDL particles are not a concern is false, the authors of the said paper do not mention that quantity rather than the size of the LDL particle is also associated with risk of CHD. The meta-analysis you are quoting is funded by the dairy and beef industry and was hosted by Nina Teicholz, see my first reply on this talk-page. You can also see the Saturated fat and cardiovascular disease article and its history. There has been a consensus to remove that paper from Wikipedia. Psychologist Guy (talk) 18:52, 4 July 2021 (UTC)Reply
Here you go, see conclusion. But I can see that due to the history of the last decades, it will take a while even for Wikipedia to adapt. In the meantime, there is strong evidence that the effect of saturated fats in the absence of carbohydrates does not cause CVD which might be worth mentioning in the article. (just leaving this info here if someone wants to take the effort to add this) Gorgos19 (talk) 20:21, 4 July 2021 (UTC)Reply
To be clear I was referring to the Cochrane review, not something else! Alexbrn (talk) 18:57, 4 July 2021 (UTC)Reply
The Cochrane review you posted concluded that reduction in saturated fats did not reduce all-cause or cardiovascular mortality. Is that conclusion represented faithfully in this article? Tempes1 (talk) 19:06, 4 July 2021 (UTC)Reply
The conclusion says "reducing saturated fat intake for at least two years causes a potentially important reduction in combined cardiovascular events". So anything aligned with that is going to be more or less faithful. Alexbrn (talk) 19:09, 4 July 2021 (UTC)Reply
It also says: "We found little or no effect of reducing saturated fat on all-cause mortality (RR 0.96; 95% CI 0.90 to 1.03; 11 trials, 55,858 participants) or cardiovascular mortality (RR 0.95; 95% CI 0.80 to 1.12, 10 trials, 53,421 participants), both with GRADE moderate-quality evidence." Tempes1 (talk) 19:13, 4 July 2021 (UTC)Reply
Not in the conclusion I'm reading. Trying to pick stuff out of the results to arrive at something other than the author's conclusion is a kind of WP:CHERRYPICKING and WP:OR. Best not do that. Alexbrn (talk) 19:20, 4 July 2021 (UTC)Reply
I believe the entire study is relevant, not just the tiny paragraph in the end that skips over many of the relevant findings. You're the one cherry picking here; I want all findings to be represented here, not just the ones that support a particular narrative, as seems to be the case with you. Can you explain why you believe the findings on mortality should be ignored? The author would not have mentioned those findings if they were of no relevance. Do you believe that when people are doing research on health issues such as heart attacks and strokes, they're not generally concerned with how it relates to mortality? Tempes1 (talk) 21:37, 4 July 2021 (UTC)Reply

@Gorgos19 and Tempes1: The AHA have already confronted your references and arguments: https://www.ahajournals.org/doi/10.1161/CIR.0000000000000510

"In the past few years, meta-analyses of observational studies and randomized clinical trials have come to discordant conclusions about the relationship between dietary saturated fat and risk of CVD.9,10,12,15–17 This has created confusion among patients, their physicians, and the public. In this article, we analyze and discuss the methodology and interpretation of results reported by these researchers and the reasons for the divergent findings."

They listed several reasons for why previous meta analysis (which you have quoted) are flawed:

"Meta-analyses of prospective observational studies aiming to determine the effects on CVD of saturated fat that did not take into consideration the replacement macronutrient have mistakenly concluded that there was no significant effect of saturated fat intake on CVD risk."

"The reason for the 2-year minimum duration is that changes in polyunsaturated fatty acids very slowly equilibrate with tissue fatty acid levels; it takes ≈2 years to achieve 60% to 70% of the full effect.20,30 Trials of serum cholesterol–lowering agents show that a reduction in coronary heart disease (CHD) incidence occurs with a lag of 1 to 2 years. These systematic reviews9,10,16 together found and analyzed 6 additional trials7,23,32–35 that replaced saturated with polyunsaturated fat but did not have ≥1 of these characteristics crucial to testing the hypothesis."

They have even addressed specific trials you have quoted. Which you can find if you open up the study.

And if you look above, I cited mathematical evidence that prospective cohorts are unable to study the relationship due to randomness of baseline ldl levels... aka people eating the same amount of saturated fat will have different ldl levels. You cannot correlate something that has too much randomness. Only expertiments can study such a relationship, which there are, which the AHA cited. But there are also experiments that were not designed properly, which the AHA explained why they were not able to study the relationship. RBut (talk) 21:51, 4 July 2021 (UTC)Reply

I'm well aware of the AHA's stance on the issue. I am not advocating that we ignore what they're saying. I'm advocating that readers of this article are given both sides of the debate, not just the side that the gatekeepers of this article agree with. We have already proven in this discussion that it is no longer considered a fringe view within the scientific community. Tempes1 (talk) 22:54, 4 July 2021 (UTC)Reply
Tempes1 - mortality is an entirely different topic. Mortality, chronic disease and time-scale is complex but we shouldn't expect a significant effect on mortality from these types of trials for two years testing reduction in one type of food on patients who have had chronic diseases for decades.
We have full access to the review [11] and we can see the 15 RCTs they used. It is really not a surprise that the reduction of saturated fat had little or no effect on mortality because most of the people in the trials had CVD, cancer or other pre-existing health problems. I think you are forgetting this. The median trial time was just over two years (Some were a bit longer) which is considered long-term for this type of study so this is why these trials were included in the review. However, in regard to chronic diseases that develop over decades this is a short-term time-scale! Also when you look individually at some of the trials they were only using small reductions of saturated fat in the diet - what I am getting at here is not all the trials had people significantly reduce their saturated fat consumption it was different for each.
I am sure you can find some flaws with this review and you obviously dispute it but can you show a specific macronutrient from an RCT that can significantly reduce all-cause mortality in cancer and CVD patients in 2 years? I don't think so, yet you seem to be expecting that in the results from these trials.
Six RCTs included only people at high risk of cardiovascular disease, four at moderate risk, and four at low risk (three with raised cancer risk or cancer diagnosis, one with no specific health risks), while one trial included participants at low and high CVD risk. Two of the trials were based on "men with angina referred for angiography", and two other trials were based on "men with angina or following MI" etc. Many of the men in these trials had already had heart attacks yet when you check the results from the trials there was a reduction in cardiovascular events in people who had reduced SFA compared with those on higher SFA but little effect on the risk of dying. A key result from this review was "The greater the decrease in saturated fat, and the more serum total cholesterol is reduced, the greater the protection from cardiovascular events." That is not compatible with the type of cholesterol denialism you are endorsing. The findings are in accord to public health agencies and support the scientific consensus to reduce total saturated fat intake from the diet. Psychologist Guy (talk) 22:11, 4 July 2021 (UTC)Reply
Mortality is not a different topic. CV disease and mortality go hand-in-hand. If CV disease didn't increase one's risk of death, it would not be nearly as big of an issue as it is. If the lack association with mortality was not relevant for the given study they would not have mentioned it. They did mention it, hence it is relevant. And once again, you are not in a position to question peer reviewed science. Your armchair critiques are unnecessary and unhelpful. We need to represent the science in a fair and balanced manner, regardless of our personal beliefs. It doesn't matter if we think we know better. Tempes1 (talk) 22:48, 4 July 2021 (UTC)Reply
But if the views you present have been refuted, what is the point of representing them as if they are credible? Peer review does not mean tertiary source. You have no tertiary source in support of your position not because tertiary sources are slow, but because the position is inaccurate. Tertiary sources have addressed your position as I have pointed out. They explained why it is inaccurate. They have covered the exact studies you have referenced. This is not just a personal view because "we know better". RBut (talk) 23:08, 4 July 2021 (UTC)Reply
You're claiming that the 2017 AHA review that you linked above refutes the 2020 Cochrane review that we're currently discussing (or other reviews and meta-studies occurring after the AHA review)? As far as tertiary sources go, there are plenty that support the view that saturated fats are not inherently unhealthy. However I've been around long enough to know that no matter how many tertiary sources I list, those with an agenda will always find some excuse for why those sources are not valid, as has already been done with the many academic sources I've cited. Let's put that theory to the test though. Why is this time article, which is a top result in google, an invalid tertiary source? Mainstream, but maybe not scientific enough? Here's another more recent one by examine. On point with the science, but perhaps not mainstream enough? Other top results in google taking recent science into account: Healthline, medicalnewstoday.com, harvard.edu. Tempes1 (talk) 00:49, 5 July 2021 (UTC)Reply
I also want to make it known that at least two of the people involved in this discussion who are against proper representation of the debate are vegans. Conflicts of interest abound. Tempes1 (talk) 01:15, 5 July 2021 (UTC)Reply

Examine and time are not tertiary sources when it comes to research... Official agencies and institutions are.

Here is the conclusion of the Cochrane review:

"The findings of this updated review suggest that reducing saturated fat intake for at least two years causes a potentially important reduction in combined cardiovascular events. Replacing the energy from saturated fat with polyunsaturated fat or carbohydrate appear to be useful strategies, while effects of replacement with monounsaturated fat are unclear. The reduction in combined cardiovascular events resulting from reducing saturated fat did not alter by study duration, sex or baseline level of cardiovascular risk, but greater reduction in saturated fat caused greater reductions in cardiovascular events."

And if you further go down to the "plain language summary":

"Key results"

"We found 15 studies with over 56,000 participants. The evidence is current to October 2019. The review found that cutting down on saturated fat led to a 17% reduction in the risk of cardiovascular disease (including heart disease and strokes), but had little effect on the risk of dying. The review found that health benefits arose from replacing saturated fats with polyunsaturated fat or starchy foods. The greater the decrease in saturated fat, and the more serum total cholesterol is reduced, the greater the protection from cardiovascular events. People who are currently healthy appear to benefit as much as those at increased risk of heart disease or stroke (people with high blood pressure, high serum cholesterol or diabetes, for example), and people who have already had heart disease or stroke. There was no difference in effect between men and women."

"This means that, if 56 people without cardiovascular disease, or 53 people who already have cardiovascular disease, reduce their saturated fat for around 4 years, then one person will avoid a cardiovascular event (heart attack or stroke) they would otherwise have experienced."

"Quality of the evidence"

"There is a large body of evidence assessing effects of reducing saturated fat for at least two years. These studies provide moderate‐quality evidence that reducing saturated fat reduces our risk of cardiovascular disease."

It is evident the Cochrane review is not in support of your position.

And no need for red herrings. Stick to your arguments. RBut (talk) 01:32, 5 July 2021 (UTC)Reply

Government agencies are not tertiary sources when it comes to research either. You seem to have no problem citing them. You also failed to address why Harvard is not a valid tertiary source. I'm not sure why you're quoting the Cochrane review, I've already read it, and you're making redundant points that have already been debated. Tempes1 (talk) 01:40, 5 July 2021 (UTC)Reply
I was addressing your last comment: "You're claiming that the 2017 AHA review that you linked above refutes the 2020 Cochrane review that we're currently discussing"
How did you come to the conclusion that the Harvard article supports your position? RBut (talk) 01:46, 5 July 2021 (UTC)Reply
Tempes1 you have to be insane to think that a single dietary control can reduce all cause mortality in a few years for patients with chronic diseases who have had those diseases for decades. There is not any medical evidence nor do any health agencies or organizations around the world claim reduction of saturated fat for a few years can reduce all cause mortality so you are not being fair when you expect results to suggest otherwise. The results from the study are not "anomalies", they fit the scientific consensus. I have read through the 15 RCTs individually. In a nutshell we cannot reduce all-cause mortality by dietary methods alone in a small time-scale of 2 or 3 years for those with chronic diseases. I don't think you have thought this subject through.
If you are questioning the results then what macronutrient do you expect to reduce all-cause mortality in CVD and cancer patients in a period of 2-3 years? There is no such food. No such study ever done has shown otherwise. All-cause mortality is the death rate from all causes of death. How can limiting the ratio of a single macronutrient do that in two years? Do you expect miracles in that small time-scale from chronic diseases that people have had for decades? There is no evidence that any macronutrient can reduce all-cause mortality in such a short time-scale yet from your comments you seem to be suggesting otherwise but the results do show us that reducing saturated fat can decrease the risk of CVD. So you are going against the mainstream scientific evidence.
The Cochrane review contradicts what you have claimed, as the overall result was that "reduction in saturated fat caused greater reductions in cardiovascular events". That has been scientifically demonstrated yet you deny it. I am well aware that CVD increases one's risk of death, it is a serious problem. I am saying we should not expect a strong association when it comes to diet because you just can't put a group of ill CVD or cancer patients on a diet and expect within two or 3 years to reduce all-cause mortality or CVD mortality but you seem to expecting this from the review. Mortality and diet does not work like this but yes they are studied as important outcomes. The results showed us that reducing saturated fat for two years reduces cardiovascular events but not mortality. We can prevent heart disease by dietary methods over many years but there is no reliable evidence all-cause mortality can be reversed by diet in a 2 or 3 year time frame. The bottom line is that you are disputing the results from the study not me. I am not disputing the results, I am explaining what they are. The results support the scientific consensus that a reduction of saturated fat can reduce risk of CVD events. We do not need to pretend on the article there is a "controversy" about this. The position you are promoting is called cholesterol denialism, it is a type of denialism. It isn't suitable for Wikipedia which is a mainstream encyclopedia when it comes to medical science. And no, time, examine.com and healthline are not reliable sources and neither is Nina Teicholz. You have cited these sources multiple times. There is no chance they will end up on the article. Psychologist Guy (talk) 01:48, 5 July 2021 (UTC)Reply
It's clear to me that no progress can presently be made, as some parties are not arguing in good faith. I'm adding an NPOV tag to the article until this issue can be resolved, perhaps with the help of neutral experts on the topic who aren't pushing an agenda. Tempes1 (talk) 01:55, 5 July 2021 (UTC)Reply
You have ignored my response. How did you come to the conclusion that the Harvard article supports your position? RBut (talk) 01:57, 5 July 2021 (UTC)Reply
I didn't say that it supports my position. I said that it takes recent science into account. Specifically, it mentions the existence of recent studies disputing long-standing perceptions of saturated fats raising the risk of CVD, it says that reducing saturated fats may be conditionally beneficial, and it acknowledges that "saturated fat may not be as harmful as once thought". Tempes1 (talk) 02:06, 5 July 2021 (UTC)Reply
It is not recent science. That weblink was written in 2014 and cited a meta-analysis of prospective cohort studies from 2010. You wrote below that recent correlation meta-analyses are weak and unreliable yet you are happy to refer to older ones if they support your position. Psychologist Guy (talk) 19:31, 6 July 2021 (UTC)Reply

break edit

The point is it doesn't matter what the article says so long as it is reflecting the recent, high-quality literature. Use WP:MEDASSESS to help. I'm glad we at least now seem to be discussing that rather than old or fringe studies, or Youtube videos. If different quality sources say different things then WP:YESPOV is your friend. Alexbrn (talk) 06:59, 5 July 2021 (UTC)Reply

Recent reviews (of cohort or observational studies) published in the last 4 years on saturated fat and cancer or CVD:

  • 2021 review [12] "Diets high in saturated fat were associated with higher mortality from all-causes, CVD, and cancer, whereas diets high in polyunsaturated fat were associated with lower mortality from all-causes, CVD, and cancer. Diets high in trans-fat were associated with higher mortality from all-causes and CVD. Diets high in monounsaturated fat were associated with lower all-cause mortality."
  • 2019 review [13] "The pooled results indicated that dietary consumption of total fat and saturated fat were not associated with three major types of skin cancer. High consumption of monounsaturated fat was significantly associated with a decreased risk of BCC (RR: 0.90, 95% CI: 0.85–0.96) and high level of polyunsaturated fat intake was potentially positively associated with SCC (RR: 1.19, 95% CI: 1.06–1.33)."
  • 2018 review [14] "This meta-analysis provides significant evidence of positive association between higher saturated fat intake and AD and dementia risk."
  • 2017 review [15] "Reducing saturated fat and replacing it with carbohydrate will not lower CHD events or CVD mortality although it will reduce total mortality. Replacing saturated fat with PUFA, MUFA or high-quality carbohydrate will lower CHD events".
  • 2017 review [16] "These meta-analyses have shown that saturated fat intake negatively impacts upon breast cancer survival."
  • 2017 review [17] "Findings from this large, international cohort consortium suggest that modifying dietary fat intake (ie, replacing saturated fat with polyunsaturated fat) may reduce lung cancer risk, particularly among smokers and for squamous cell and small cell carcinoma."

Currently there are 1997 (!), 2001 and 2003 meta-analyses or reviews being cited on the article in the "Association with diseases" section, these are massively outdated. Why are we citing stuff from 1997? The entire section needs updating with modern high-quality sourcing. It is clear from the evidence that a diet high in saturated fat is significantly associated with mortality, CVD, various cancers including prostate (but not skin cancer), dementia and Alzheimer's disease whilst polyunsaturated fat is not. Psychologist Guy (talk) 12:51, 6 July 2021 (UTC)Reply

It is clear that you are not looking at this from a neutral point of view and have closed your eyes to all of the information posted thus far that does not conform to your predetermined beliefs. The studies that you just posted are either of very low quality (e.g. uncontrolled correlation studies), or are on niche topics that are not relevant to the discussion as it pertains to an average healthy individual (e.g. effects on cancer victims/survivors, or otherwise already chronically ill people). That information maybe be relevant to the article and may be worthy of including, but it is not part of this discussion, and at this point it feels like you're trying to hide and obfuscate relevant information in a sea of irrelevant rants and links. No one here has ever denied the correlation between high saturated fat intake and various health problems. The issue at hand is whether or not it's a causal relationship, and what conditions surround those correlations. This is precisely what the recent studies that you've been dismissing out of hand have been trying to figure out. The fact that you don't understand these nuances after writing so many big paragraphs and linking to all these papers is disheartening. Tempes1 (talk) 16:19, 6 July 2021 (UTC)Reply
The comments about "neutrality" or predetermined beliefs are stupid because anyone can see what your agenda is. Unfortunately you are not being honest, these recent studies they are not "low-quality" and I am linking to them because it is clear the entire section of the article needs updating. Why do we need content from 1997 on the article? Is that reliable to you?
Most of the studies you have linked to are old or older prospective cohort studies, so when the results of said studies suit you you are happy to cite them but when I cite recent meta-analysis or reviews of prospective cohorts or observational studies published in the last 4 years you suddenly say they are not reliable? That is a double-standard. I am not convinced you have actually read through the studies you have cited. You have been citing old meta-analysis of cohort studies when it suits you like this one you linked to multiple times [18] and this in your first post on this talk-page [19] linking to a cohort from Japan from nearly 12 years ago? But you dismiss a recent systematic review from 2021? [20] The other 3 links you cited included correlation studies. You have been citing "uncontrolled" epidemiology all a long. You are now trying to dismiss studies because they were not done on "average healthy individual". That is a ridiculous statement because most of the studies you have cited yourself were not done on average healthy individuals. You are obviously not reading any of the studies, not even the ones you have cited yourself.
You have basically dug yourself a hole you cannot get out of here. You have been citing old meta-analysis of cohort studies from the very beginning of this talk-page but now you say they are not reliable and are "very low quality". I think its obvious who has the "predetermined beliefs". You are not interested in improving this article, so this is obviously a waste of time. Psychologist Guy (talk) 17:35, 6 July 2021 (UTC)Reply
@Psychologist Guy Your accusations to user Tempes1 don't hold up in my opinion. I unfortunately won't have the time to commit to further discussion here, but just a bit of searching in Google Scholar will literally find you endless studies (incl recent ones) questioning the causality and significance of saturated fats itself. You don't seem to really understand the issue at hand and also the reason why this has been questioned by so many. Gorgos19 (talk) 16:27, 7 July 2021 (UTC)Reply
The scientific consensus is clear on this topic and the position you are arguing is WP:Fringe. Telling people to go on Google scholar is not the way this works, you did this earlier by telling people to go to YouTube. We have to follow WP:MEDRS for WP:Biomedical information on Wikipedia which means the best type of evidence is meta-analyses or systematic reviews, not individual studies which are primary. But I looked in 2020 and 2021 for studies on saturated fat there are not "endless" studies of scientists questioning causality of saturated fat consumption - there are some editorials which would not be reliable per MEDRS. The best evidence to date on this subject is the Cochrane review of RCTs which concluded that reducing saturated fat for at least two years "causes a potentially important reduction in combined cardiovascular events". That is causation not correlation. In your first post you linked to a butter cohort meta-analysis and in your second and third post on this talk-page you linked to a review that included observational studies and another that included prospective cohorts. So you have also been citing correlation studies like Tempes1 has. Psychologist Guy (talk) 18:37, 7 July 2021 (UTC)Reply
Even the Cochrane study is questioning the importance of reduction of saturated fats in general. This is not properly reflected in the article. And it's a general discussion in the scientific community that it matters a lot about the context. Saturated fats in the absence of carbohydrates don't seem to be a problem, while replacing saturated fats with carbohydrates or polyunsaturated fats does in fact seem to be problematic. I realize this alone won't convince you, but I hope someone in the future will take the time to update the article appropriately. Gorgos19 (talk) 19:25, 7 July 2021 (UTC)Reply
If you have a meta-analysis or review and you think it is reliable then you should update the article. I agree the article needs updating, if you add reliable sources I would support your edits. "Saturated fats in the absence of carbohydrates don't seem to be a problem", unfortunately this is a carnivore diet claim that is found on social media but not supported by any reliable evidence from the medical literature and is potentially fatal advice in the long-term. This sort of unfounded dangerous claim will not find its way onto the article. We rely on WP:MEDRS. Unless any different users weigh in on this or have any other suggestions to improve the article, I will not further comment here. Psychologist Guy (talk) 20:07, 7 July 2021 (UTC)Reply
Just going to leave this here: https://openheart.bmj.com/content/1/1/e000032. Gorgos19 (talk) 09:16, 8 July 2021 (UTC)Reply
User:Psychologist Guy I would also add that in my opinion the read on MEDRS is being interpreted a bit too stringently in cases like this where the wording does not warrant and as long as a study meets basic criteria it is not precluded from use, and the guidelines read more as preferences for selecting the highest quality information first to be presented with weight not to checkmate any opposing idea so that it cannot be at all. Reading the MEDRS policy word for word, I get the feeling that the core guiding principle is not spreading health misinformation based on overly weak evidence or prematurely and based on the arguments I have read so far, that is not going to be in question as long as the claims are tempered to the evidence representing them. Per your own argument the landscape is rather tumultuous and the existing consensus does seem to be changing albeit slowly. In addition, Per the current active discussion on Reliable Sources regarding Roman et. al its not up to editors to interpret and manipulate the conclusions of a study for any reason or to checkmate the emerging ideas in any way, and in this case that translates to report that there is a non-zero number of credible studies that say in no overly dramatic verbiage that the saturated fat CVD link is in question if not outright disputing it. That is then backed up by medical advice publications like Healthline and WebMD as I pointed out to you in the FT noticeboard. FrederickZoltair (talk) 14:02, 8 July 2021 (UTC)Reply

Gorgos19 that is an opinion piece, and James DinNicolantonio is clearly not a reliable source for medical claims. He's even co-written a book with Joseph Mercola. I am disappointed that you have fallen victim to quackery like this. Psychologist Guy (talk) 19:32, 8 July 2021 (UTC)Reply

FrederickZoltair, there are experienced editors familiar with MEDRS like Alexbrn or MjolnirPants who have been on Wikipedia a long time, they have told you why you are wrong over at the FT noticeboard. You keep citing or referring to WebMD etc which are not reliable sources for medical claims per the rules of this website which sets the bar a lot higher when it comes to biomedical content than other websites which is why we need reviews on this topic otherwise every article would be destroyed with minority opinions from primary sources. You have not given any high-quality references and your claim about the consensus shifting is clearly false. I direct you to the top of this talk page, Zefr's comment Undue weight: "articles should not give minority views or aspects as much of or as detailed a description as more widely held views or widely supported aspects. Generally, the views of tiny minorities should not be included at all." The article's 2020 Cochrane review and the AHA advisory panel are the state of science showing the convincing causal effect of chronic saturated fat consumption and cardiovascular diseases." You are presenting a minority opinion so we do not need to set up a false-balance and I looked over your posts at the FT noticeboard but you did not list any reliable sources. I think we can end this discussion and just agree to disagree. Psychologist Guy (talk) 19:32, 8 July 2021 (UTC)Reply
Appeals to authority are fallacious arguments at best and while I disagree with the more conspiratorial minded claims Tempes1 has made I do not agree that this is a minority view. The entire crux of this reasoning lies with a very staunch interpretation of MEDRS that I disagree with as you and the others on FT are taking the policy to mean it excludes all but the highest quality evidence when it reads that in order of weight the highest quality evidence is preferred while you also simultaneously differentiate between low-medium, medium, and high quality sources based on nothing but your own opinions of science in general, which is being challenged here by at least three editors. The policy is not a difference engine that only picks the largest and well known studies, nor does it say Wikipedia is a scientific meritocracy that enables anyone (even experienced editors) to decide what is and is not science. The simple fact is there is nothing in the policy that forbids the use of most of the studies being cited here. For gods sake you all act like simply mentioning an opposing viewpoint is encouraging misinformation when its obvious this has not been a fringe theory for at least several years, but as they say when all you have is a hammer....FrederickZoltair (talk) 20:32, 8 July 2021 (UTC)Reply
In addition, MEDRS literally directs editors to go to pubmed via WP:MEDSEARCH and start searching from there. Additional studies to consider: Controversies and discrepancies in the effect of dietary fat and cholesterol on cardiovascular risk and Faith in Fat: A Multisite Examination of University Students’ Perceptions of Fat in the Diet, Dairy Fats and Cardiovascular Disease: Do We Really Need to Be Concerned?, A healthy approach to dietary fats: understanding the science and taking action to reduce consumer confusion, Dietary Fats and Chronic Noncommunicable Diseases , Fat, Sugar, Whole Grains and Heart Disease: 50 Years of Confusion , Efficacy of dietary odd-chain saturated fatty acid pentadecanoic acid parallels broad associated health benefits in humans: could it be essential? (This one is heavy and I may be mis-interpreting its results)FrederickZoltair
All of those are primary sources, mostly editorials or opinion pieces and two of them were published by MDPI. You have been told why we do not use primary sources. I see that two editors have told you already why MDPI is unreliable for biomedical content on Wikipedia at the FT noticeboard. Did you read MEDRS? I am bolding this so it is made clear "Ideal sources for biomedical information include: review articles (especially systematic reviews) published in reputable medical journals; academic and professional books written by experts in the relevant fields and from respected publishers; and guidelines or position statements from national or international expert bodies. Primary sources should generally not be used for medical content – as such sources often include unreliable or preliminary information, for example early lab results which don't hold in later clinical trials." So why are you pasting in random low-quality opinion pieces which are primary sources? You have not cited any reviews.
Also, you may have not read some of the papers you just cited in full. For example this paper [21] is not disputing the consensus on saturated fat. The paper points out a true fact, yes health organizations (at least in America) in the past did get the guidelines wrong for advising a total low-fat diet (restriction on all fatty acids). We didn't know enough about the different kinds of fat back then. Science corrects itself. Yes the consensus can change if the evidence is strong, there is no conspiracy to suppress evidence. The paper is recommending a relatively high-UFA diet (a diet high in unsaturated fat, in accord with the Mediterranean diet). This is completely mainstream nutritional advice that public health agencies and organizations around the world now support i.e. getting more monounsaturated and polyunsaturated fats into the diet whilst reducing saturated fat to prevent CVD. The paper concludes that unsaturated fats have a protective role that "decreases risk factors as well as morbidity and mortality related to CVD." In short this paper does not support what you think it does but it is a primary source as is everything else you linked to so will not be used on Wikipedia. Hopefully you now understand the difference between a primary and secondary source and please do not link to any more of those. Psychologist Guy (talk) 21:44, 8 July 2021 (UTC)Reply
It only took literally most of a days worth of back of forth with three different editors to actually get a straight answer rather than a dismissal, and this is still kind of a dismissal. I did not realize they were primary, and as I indicated above I did not understand them all fully. Now that I know what to look for, I can so thank you. FrederickZoltair (talk) 22:12, 8 July 2021 (UTC)Reply
User:Psychologist Guy. Please examine these. They are all reviews or meta-analyses, and are recent and many of them challenge many claims in the current article. This list has grown rather long, and I have been reading all night. I obviously dont expect a response to all or even most. I will continue reading and parsing and attempt to eliminate the lower quality or off-topic ones. Thanks.

https://pubmed.ncbi.nlm.nih.gov/31841151/ - "The AHA stance regarding the strength of the evidence for the recommendation to limit SFAs for heart disease prevention may be overstated and in need of reevaluation."

https://pubmed.ncbi.nlm.nih.gov/32562735/ - "The recommendation to limit dietary saturated fatty acid (SFA) intake has persisted despite mounting evidence to the contrary. "

https://pubmed.ncbi.nlm.nih.gov/26586275/ - "This paper reviews the evidence linking saturated fats and sugars to CHD, and concludes that the latter is more of a problem than the former. Dietary guidelines should shift focus away from reducing saturated fat, and from replacing saturated fat with carbohydrates, specifically when these carbohydrates are refined."

https://pubmed.ncbi.nlm.nih.gov/25764080/ - "However, some evidence suggests that consumption of saturated fat does not increase that risk."

https://pubmed.ncbi.nlm.nih.gov/25979502/ - "Dietary fats have a major impact on human health. A growing body of evidence suggests that inflammatory status should be included as one of the characteristics for which dietary fats are evaluated relative to their impact on human health. At this time, it is uncertain how dietary fats might affect inflammatory status, but current evidence suggests that the gut microbiome is important in this regard ........... In light of the lack of consensus regarding which biomarker is best for monitoring inflammatory status, it is recommended that as many inflammation biomarkers be measured as feasible and that studies be appropriately powered in recognition of the highly variable nature of these biomarkers."
https://pubmed.ncbi.nlm.nih.gov/26268692/ - " Conclusions: Saturated fats are not associated with all cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes, but the evidence is heterogeneous with methodological limitations. Trans fats are associated with all cause mortality, total CHD, and CHD mortality, probably because of higher levels of intake of industrial trans fats than ruminant trans fats. Dietary guidelines must carefully consider the health effects of recommendations for alternative macronutrients to replace trans fats and saturated fats."

https://pubmed.ncbi.nlm.nih.gov/31434641/ - "This is the most extensive systematic review of trials to date to assess effects of polyunsaturated fats on newly diagnosed diabetes and glucose metabolism, including previously unpublished data following contact with authors. Evidence suggests that increasing omega-3, omega-6, or total PUFA has little or no effect on prevention and treatment of type 2 diabetes mellitus. " our entry claims "Many review articles also recommend a diet low in saturated fat and argue it will lower risks of cardiovascular diseases,[7] diabetes, or death.[8]"

https://pubmed.ncbi.nlm.nih.gov/31791641/ - "Conclusion: This meta-analysis further demonstrated that a higher consumption of dietary SFA is associated with a lower risk of stroke, and every 10 g/day increase in SFA intake is associated with a 6% relative risk reduction in the rate of stroke. Further research is needed to explore the influence of specific SFA types and different macronutrient replacement models of SFA on the stroke risk." Our entry currently number 28 is a broken link.

https://pubmed.ncbi.nlm.nih.gov/31377181/ - " Conclusions: The effects of dietary SFAs on MetS will be influenced by other specific nutrients. Replacement of SFA by MUFA and PUFA has been associated with a decrease in MetS. Dietary recommendations should emphasize on different qualities of fat intake, not only to reduce total fat intake, to obtain health benefits in adults. "
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5496233/ - "Short-term fish oil supplementation is associated with increasing the insulin sensitivity among those people with metabolic disorders."

https://pubmed.ncbi.nlm.nih.gov/32238384/ - "Moderate certainty evidence shows that most macronutrient diets, over six months, result in modest weight loss and substantial improvements in cardiovascular risk factors, particularly blood pressure. At 12 months the effects on weight reduction and improvements in cardiovascular risk factors largely disappear. "

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6414510/ - "Despite the relatively large number of studies included in this review, there is still some uncertainty regarding the effects of a Mediterranean‐style diet on clinical endpoints and CVD risk factors for both primary and secondary prevention. The quality of evidence for the modest benefits on CVD risk factors in primary prevention is low or moderate, with a small number of studies reporting minimal harms. There is a paucity of evidence for secondary prevention. The ongoing studies may provide more certainty in the future."

https://pubmed.ncbi.nlm.nih.gov/27355649/ - "This systematic review and meta-analysis suggests relatively small or neutral overall associations of butter with mortality, CVD, and diabetes. These findings do not support a need for major emphasis in dietary guidelines on either increasing or decreasing butter consumption, in comparison to other better established dietary priorities; while also highlighting the need for additional investigation of health and metabolic effects of butter and dairy fat."

https://pubmed.ncbi.nlm.nih.gov/32020162/ - "In prospective cohort studies, higher Lineoleic Acid intake, assessed by dietary surveys or biomarkers, was associated with a modestly lower risk of mortality from all causes, CVD, and cancer. These data support the potential long-term benefits of PUFA intake in lowering the risk of CVD and premature death."
https://pubmed.ncbi.nlm.nih.gov/33283417/ - Conclusions: "VLCHF and LF diets with moderate energy restriction demonstrate similar weight loss and improvements to BP to 3 months. However, adherence is likely poor without intensive support from health professionals. Dietary SFA should be monitored to ensure recommended intakes, but longer-term studies with high adherence are required to confirm the level of CVD-risk and potential harms."

https://pubmed.ncbi.nlm.nih.gov/26979840/ - "This meta-analysis reveals that higher SFA intake is inversely associated with risk of stroke morbidity and mortality with race, sex, and BMI as key factors influencing this risk. There seems to be a threshold of SFA intake for inverse relation of SFA intake with stroke. However, the stroke-reducing or -increasing effects for specific subtypes and specific food sources of SFA can be concealed. Functions of specific subtypes of SFA (e.g. lignoceric acid) and specific food sources of SFA (i.e. plant vs. animal) in relation to stroke need to be clarified in further studies."
Yes its MDPI but its a recent review. - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5793267/ - "It is now clear that the role of SFA in the causation of CHD has been much exaggerated. Until the 1980s the weight of evidence indicated that a high intake of SFA causes a raised TC which may then lead to CHD. But evidence that has steadily accumulated since around 1990 demonstrates that SFA plays a relatively minor role in CHD. The findings from many cohort studies have provided strong evidence that SFA has a much weaker association with risk of CHD than do several other dietary factors including trans fats (which increase risk), as well as fish, and fruit and vegetables (which reduce risk). The belief that a reduced intake of SFA is the key dietary change for the prevention of CHD led millions of people to increase their intake of carbohydrates, most of which were refined. But this dietary change has a negligible effect on the ratio of TC to HDL-cholesterol and, in consequence, has no impact on risk of CHD. A reduced intake of SFA combined with an increased intake of PUFA may reduce the risk of CHD, but even that assertion has been questioned."
Current issues with the article:
(This is a list, not a complaint and if I receive no feedback I will begin making changes slowly).

- The original cochrane review is one of the only accepted newer sources currently used in the entry and primarily used for the majority reinforce of the links between saturated fat and cvd. If it is leaned on so heavily, it should include commentary about its methodology that points out any potential issues like is currently qualified in the article for the cancer references as well as the studies own comments regarding its own conclusions. I will try to locate a reliable source that does this rationally.
- references 24 cites a guidelines article from 2007. The new guidelines are here and haven't changed much except that they say "The same has not been clearly shown for replacement with carbohydrates and monounsaturatedfatty acids (MUFAs). . Obviously clinical guidelines from 2016 do not supersede meta-analyses re-reviews from 2020 but its interesting as it challenges the claim of replacing saturated fat with carbohydrate for two years leading to reduction in cvd risk claim.
- Reference 25 cites a book that is just about 11 years old. I downloaded a pdf version and found the actual claim is not quite so simply reinforced. It lists a chart of causes that include saturated fat, and another chart with breakdowns by percentage of which saturated fat is simply one of the causes and that data set is from 1981. Additionally it seems to be arguing for a causal framework of thinking rather than directly citing evidence proving a cause via other studies. Second opinon would be appreciated in any case. See page 537 (and the amusing comic) and the conclusion on 547.
- Reference 28 leads to a dead link. Their new recommendations about risk factors are: "Addressing just one risk factor, such as exercising more, will help, but in order to significantly reduce your risk of CVD, it’s important to look at your lifestyle as a whole. If you are already living with CVD, staying healthy and active can help you live longer and reduce the chances of it getting worse." and "Your total fat intake should not exceed 30% of your total energy intake, and you should avoid industrial trans fats. Limit your consumption of free sugars to less than 10% (ideally 5%) of your total energy intake and reduce your salt intake to less than 5g a day. Adults should consume at least five portions (400 grams) of fresh fruit and vegetables every day." and "low levels of saturated and trans fats, low levels of salt, low levels of sugar, plenty of whole foods, plenty of fruit and vegetables". and "According to the World Health Organization, as many as 80% of all heart attacks and strokes are preventable. The majority of deaths due to CVD are precipitated by risk factors such as high blood pressure, high cholesterol, obesity, or diabetes, which can, to a large extent, be prevented or controlled through the consumption of a healthy diet, regular exercise and avoiding tobacco. Keeping an eye on your blood pressure, cholesterol levels and blood sugar levels is also very important.Eat a healthy and balanced diet: Eating a healthy, balanced diet is crucial to maintaining a healthy heart and circulation system. A healthy diet should include a wide variety of unprocessed and fresh foods, including plenty of fruit and vegetables (at least five portions every day), whole grains, nuts and foods low in saturated fats, sugars and salt. Be wary of processed foods, which often contain high levels of salt, and drink lots of water!" There is no pronounced claim I can see that links saturated fat to CVD so the entry need to have this line qualified.
- Reference 34 is from 2011 and is 404. Cant find good link. Remove.
- Reference 35 is from 2003 and 404. I found the good link but its too old imo (the who website its on is a version of it from 2003 and not current). remove.
- Reference 36 is old irish.ie guidelines on cholesterol from 2011 that specifically recommended against saturated fat. The new guidelines are here and makes no mention of the lipid hypothesis or saturated fat (except to say monounsaturated fat lowers cholesterol) and suggests a Mediterranean diet but also specifically highlights healthy lifestyle in addition to it and not the diet alone and also recommends ::::: avoiding trans fats.
- Reference 37 is the old dietary guidelines for americans. This should not be used as a reference for the lipid hypothesis as while the research is strong that ldl causes cvd, the link between saturated fat and ldl is the question.
- Reference 38 is a book from 2007. Remove.
- References 34-38 are not proper citations for a claim that is in contention. Recommend removing the entire line.
- Under Dyslipidemia, reference 28 comes up again but is a dead link.
- Reference 39 is from 1997 and needs to be removed.
- Reference 42 - Same as above in reference 25 but a different chapter and page. Shortly after mentioning this study it says "It is a reasonable argument that ultimately these fac-tors should be considered together, and not separately,in part because of shared underlying determinants andalso because of multiple benefits of their ameliorationon a population level. This logic supports the conceptof “absolute risk,” a measure of estimated probabil-ity that an individual will experience a coronary––or,more broadly, cardiovascular––event within a definedperiod. The blood lipid profile may contribute one ormore components to such a calculation, dependingon the model used. The product is a risk estimate thatguides policy for resource allocation, or treatment de-cisions for individuals, on the basis of the aggregaterisk from multiple factors. A transition toward this ap-proach is in progress, but conventional single-factorguidelines and practices remain and are the focus of thediscussion that follows."
- Reference 43 - Same book as above in reference 25 but a different chapter and page. The entry currently says "absence of an adverse blood lipid profile, the other known risk factors have only a weak atherogenic effect" - yet the actual text after that sentence is: "However, evidence was noted earlier that risk of coronary events continues to be reduced with reduction in LDL-cholesterol from levels well be-low those conventionally thought to confer increased risk. Perhaps atherogenesis is stimulated when factors are present to increase oxidation of LDL or produce other adverse molecular changes, even at relatively low concentrations of LDL-cholesterol. This under-standing supports rethinking assumptions in risk es-timation and target-setting for treatment based onparticular levels of blood lipids." So kind of the opposite of what is implied by our entry now unless I am misunderstanding (and I may be so second opinions are welcome).
- Reference 44 says in its abstract (I cannot acces the full review) - "In conclusion, while beneficial effects on atherosclerotic risk are mainly ascribed to cis-unsaturated fatty acids, it remains debateable whether trans and saturated fatty acids in the diet have to be replaced by cis-unsaturated fatty acids or by carbohydrates. To answer this question adequately more validated methods are needed that reflect in vivo lipid peroxidation, inflammation and haemostasis. " Which is different than what the entry says when citing it.
- Reference 50 is too old. There is an MDPI review [[22]] from 2019 that says "In order to reduce the cervical cancer risk, we may need to promote the long-term consumption of antioxidants, such as vitamins A, C, D and E, carotenoids, vegetables and fruits, and avoid cigarette smoking. To reduce the endometrial cancer risk, we should take care to avoid continuously consuming fat, energy sugar and acrylamide. To reduce the ovarian cancer risk, we should take care to avoid the long-term consumption of pro-inflammatory foods, including saturated fat, carbohydrates, animal proteins and acrylamide. The present study reviewed the relationship between the dietary and nutrient intake and the gynecologic cancer risk. Most papers were epidemiological studies and clinical trials. There were few experimental studies. Thus, the mechanisms through which diet and nutrition influence the development of gynecologic cancers are not clearly understood. Further research using in vitro and in vivo approaches is needed to clarify these mechanisms." which is far from singling out saturated fat. The entry should be changed.
- Bone section needs to be changed entirely as reference 54 is far too old and newer research (MDPI review) like this from 2019 says: "Some studies, however, demonstrated that a high-fat diet contributes to achieving peak bone mass, along with microstructure, at a younger age. Contrary to these results, others have shown that a high-fructose diet consumption leads to stronger bones with a superior microarchitecture than those with the intake of a high-glucose diet and, at the same time, research indicated that a high-fat diet usually deteriorates cancellous bone parameters, and that the incorporation of fructose into a high-fat diet did not aggravate bone mass loss. High-fat/high-sucrose diets have shown both beneficial and detrimental influences on bone metabolism. Combined, these studies showed that nutrition exerts different effects on bone health. Thus, a better understanding of the regulation between dietary nutrition and bone health might provide a basis for the development of strategies to improve bone health by modifying nutritional components."
- Reference 55 is a link to a Wikipedia article and should be removed or re-linked to the WHO dietary guidelines page linked in an earlier reference.
- Under dietary recommendations the sources look recent and decent, but the qualifying paragraph is from a 2003 source and should just be removed. The research I cited above and the newer guidelines also cited above definitely call this association into question. In fact keep the guidelines and recent sources, but remove all the exposition based on studies that are 15+ years old.
- Reference 71 is a good example of that and is also extremely old from 2004. The entry says is "no lower safe limit of specific saturated fatty acid intakes has been identified" from the abstract, yet the study itself in its conclusion says "At this time, research on how specific saturated fatty acids contribute to CAD and on the role each specific saturated fatty acid plays in other health outcomes is not sufficient to make global recommendations for all persons to remove saturated fats from their diet." This is a problematic reference.
FrederickZoltair (talk) 00:12, 10 July 2021 (UTC)Reply

Saturated fats and cardiovascular health take 2 edit

Latest comment: 2 years ago20 comments4 people in discussion

I know how impossible it is to edit this page without getting autao reverted without any comments, so I will not try, I will try to discuss first, so. One of the things that I often get reverted for is that I don't use new enough sources, so I would like to propose a revert of this statement.

"The relationships are accepted as causal."

today it has 2 references, one from 2007 which states as we write in the article and one book which is from 2011 (I dont have access, but Im sure it says something simmilar), i.e. to old for MEDRS 5 years?? The first source is "European guidelines on cardiovascular disease prevention in clinical practice: executive summary" from 2007, if we instead read the newest (that I cant find) version of that same report [23] from 2016 (almost passing the 5 year rule, but at least much closer) it no longer states anything (that I can find) about causal relationship, so I suggest that we take away that sentence totally. Agree/disagree? @Tempest1 @Alexbrn , anyone else? --Stefan-S talk 14:30, 25 July 2021 (UTC)Reply

Whilst those sources are old, we can just cite the 2017 review from the American Heart Association presidential advisory which notes "Taking into consideration the totality of the scientific evidence, satisfying rigorous criteria for causality, we conclude strongly that lowering intake of saturated fat and replacing it with unsaturated fats, especially polyunsaturated fats, will lower the incidence of CVD and "Taking into consideration the totality of evidence, LDL cholesterol links saturated fat and its replacement macronutrients to CVD by very strong scientific evidence that satisfies rigorous criteria for causality. Three independent guidelines committees rated this evidence as Level A, Strong." [24] Psychologist Guy (talk) 17:09, 25 July 2021 (UTC)Reply
So you say that since the European guideline have changed, and now does not say causal, we need to find another one that does? Maybe since the this is a source in form of a 'national' guideline and it has changed, we could acknowledge that? So maybe there actually is reason to write something about the slow change in opinion, even on the highest level? --Stefan-S talk 23:35, 25 July 2021 (UTC)Reply
The 2016 European Guidelines says "Elevated levels of plasma LDL-C are causal to atherosclerosis" and "Reduction of LDL-C decreases CV events". There is hardly any mention of saturated fat, although it does say "Saturated fatty acid intake should be reduced to a maximum of 10% of energy intake by replacing it with polyunsaturated fatty acids". I don't see any change of opinion here. All guidelines are telling people to restrict saturated fat and eat more polyunsaturated fatty acids. There are a lot of risk factors for CVD (hypertension, high blood cholesterol, smoking, diabetes, uric acid, obesity, chronic kidney disease, physical inactivity, dyslipidaemia etc). What is this obsession trying to prove the guidelines wrong about saturated fat? It seems new users show up to this talk-page every few months and say the same thing but never question the other risk factors. Psychologist Guy (talk) 00:51, 26 July 2021 (UTC)Reply
So the source does not say saturated fat is causal to CV anymore, they say high LDL is causal to CV event, and you should lower Saturated fat. If you use that source to say that they say Saturated Fat is causal to CV that is OR in my book. I'm not a new user, I have edited wikipedia for 14 years longer than you! What I am, is tired of fighting on talk pages, but do a edit or try now and then. The obsession is to try to get the truth out there, as have been stated in this thread part 1, there is very little good science that actually proves that Saturated fat is bad (Im not saying there are not lots of science saying it, just good science). We all should know what fake 'news' is, we should all know what. If you have followed the low carb 'movement' for the last 5+ years, you should know that there is a awful lot of things the looks bad in the traditional nutrition science. Please read up on [25], Tim Noakes, Gary Fettke all whom have been 'prosecuted' for proposing low carb/high fat diet. In all cases, they where accused of not providing the truth, all the cases in Sweden, South Africa and Australia they where fully exonerated by state investigations, and if you read more about Tim Noakes and Gary Fettke there are accusations of how the dietists associations in each country played a very dirty game and in Australia there is proof? that they where paid by the food industry and asked by them to go after Gary. Just read about the scientific quotes that we use in wikipedia that classify low carb and keto as a 'fad diet', when it is the first diet 'invented' in last century, so how can it be fad??? OR? maybe, but since it is listed in a peer reviewed scientific paper we say that. To me that does not make sense, it is using wikipedia rules to push a POW.
The whole problem is that it is very hard to prove causality, and most papers that states causality dont follow the strict 2-4? times higher effect that is needed for epidemiological studies, what some scientists that don't work is university lab with funding from big food and farma believe is that carbs is causing CVD. And that hypertension, high blood cholesterol, diabetes, uric acid, obesity, chronic kidney disease, dyslipidemia etc are all effects of to much carbs, not risk factors for CVD, so it is reversed. So Im not arguing about obesity, high blood pressure, they are part of the package, but I do not think that high blood pressure is caused by saturated fat, same as lots of saturated fat dont give you 'high' cholesterol, or obesity or most of the other 'risk factors' on you list. I'm not expecting to rewrite this whole page, since there is a good chunk of 'high quality' science that still states this, but what I would like is to acknowledge that there are differing points of views and they are also of high quality, and we should give that more weight. Just my 2 cents, sorry for the rambling. --Stefan-S talk 03:25, 26 July 2021 (UTC)Reply
Another take on this is that we have a issue with our evidence pyramid, where we have Clinical guidelines that is built on observational studies, and real RCT that disproves, the effects of the observational studies, but probably due to the influence of big food and farma (which I acknowledge) that we cant prove is not reported on the clinical guidelines. So the pyramid don't work. But again, I'm not expecting you to see the light :-), I'm only hoping that we can give a little bit more space for a opposing view. --Stefan-S talk 03:32, 26 July 2021 (UTC)Reply
WP:NOTAFORUM. Wikipedia only exists to reflect accepted knowledge (not Truth™). I'd no more use Noakes as a source for dietary science as I would for COVID-19 or vaccination.[26] We need to improve the sourcing in this article, not descent into a vortex of pseudoscience. Alexbrn (talk) 06:33, 26 July 2021 (UTC)Reply
Thanks Alex for your comment, but I don't think you answered anything I talked about? I did not ask to use Tim as a source, even though I did not know that people you think are pseudoscientists, are not allowed? I though you wanted us to follow MEDRS? It does not say that. A scientists that dares to admit that he is wrong sometimes, is not a bad scientists, rather the other way around, in my opinion. This is typical on how you think, some sources are pseudoscience and therefore should not be used no matter what. Accepted knowledge changes, and it is time to start to write that. --Stefan-S talk 23:46, 26 July 2021 (UTC)Reply
Not really sure what you're on about but yes, we should use the WP:BESTSOURCES and obviously avoid pseudoscientific nonsense and/or the weird pronouncements of "diet gurus". I already mentioned the Cochrane SR above as something that is usable. You've mentioned no sources? Alexbrn (talk) 02:40, 27 July 2021 (UTC)Reply

Stefan you have not given any reliable references indicating the guidelines have changed. There is good evidence that reducing saturated fat intake reduces the risk of CVD and CHD events. We are after high-quality sources but you have not listed any. One of the best sources to date I have seen on this topic is the SACN report on saturated fat published in 2019. The report looked at 47 systematic reviews and meta-analyses and concluded that:

  • higher saturated fat consumption is linked to raised blood cholesterol
  • higher intakes of saturated fat are associated with increased risk of heart disease
  • saturated fats should be swapped with unsaturated fats
  • there is no need to change current advice that saturated fat should not exceed around 11% of food energy [27]. This is the sort of high-quality reference that we are after to improve this article. This was a review of 47 systematic reviews and meta-analyses, the most detailed I have seen on this topic to date. The report is over 400 pages long [28]. There is not any reliable evidence going the other way. We do not need to present a false balance and giving equal weight to minority fringe views. Psychologist Guy (talk) 00:50, 27 July 2021 (UTC)Reply
Thanks, good link (but very long). So the one of the best source you can find says The effect of saturated fat on health has been hotly debated in recent years .... and the relationship between saturated fat and cardiovascular disease (CVD) has been called into question, which to me says exactly what I am trying to say, there are more and more debate and I think we should give some room for that debate. As I have stated above, I'm not saying we should say that saturated fat is good, since the way our MEDRS is written that is against the rules, but I do think we should give more room for the alternative view, and your source clearly states that that view exists. I will try to do a more thorough review of your source later, but it will take hours so cant do it right now, but my quick evaluation was that in many cases they had a few meta studies that they checked, majority is associational studies, so they are already acknowledged by our evidence pyramid to be not so strong, then many of them had no effect as result, and a minority of them had some 'positive' effect of reduced saturated fat, and this was used to prove the that saturated fat was still bad and put in a country clinical guideline, i.e. elevating low quality evidence to a very high level. But all if this is OR, I know, but I will try to do to show you the point. --Stefan-S talk 23:50, 27 July 2021 (UTC)Reply
OK, I tried to read the paper, and make conclusion (which of course is WP:OR is that is don't have strong evidence. Let me explain what I interpret (please correct me if I'm wrong) that it says.
I only checked the first 2 and what I think most important topic they cover, CVD Deaths and CVD Events. For CVD deaths the paper says, no effect, reduction of saturated fat have no effect on either cardiovascular or total mortality, this was one RCT meta analysis and I think 3 observational meta analysis! Ponder that for a while.
Secondly for CVD events, I think that translates to heart attack? They had one RCT meta analysis, it stated 17%, 7% or 8% relative risk reduction of a reduction in Saturated fat. They also had 3 what they called prospective cohorts studies, i.e. observational studies. All of them reported no effect. I will accept to ignore this, since observational studies needs a very high risk to be considered proving causal effect, but I'm pretty sure they will use observational studies in some of the other topics further into the report and call them causal and adequate. But never mind. So this was enough for them to say that there was adequate evidence for that saturated fat are causal on CVD events!?
OK, lets accept that, I mean 17% sounds quite big right, that should mean that if everyone reduced their fat intake we would get 17% less cardiovascular events right? I will accept that as quite convincing in a good RCT! Well, no, it is not that simple, from the source (Hooper et al (2015) ) we can find that they say, "The number needed to treat for an additional beneficial outcome (NNTB) was 56 in primary prevention trials, so 56 people need to reduce their saturated fat intake for ~four years for one person to avoid experiencing a CVD event", as a absolute risk that is about 1.8% per 4 year (if my math is correct?), i.e. if everyone reduced their saturated fat intake as per the RCT we would get about 0.45% less Cardiovascular events per year and no change in deaths or mortality. So again I will do some WP:OR and say, no big deal, I'm surprised that we can use such sources. But then we don't try write the truth, only what is stated in 'reliable' sources and they say that...... So I know that I will either get slammed or ignored for this comment, but my point is, with 0.45% absolute risk, in the best source you can find, and that same source states that this topic is hotly debated, I think there is room to "fairly represent all significant viewpoints that have been published by reliable sources", and your source states hotly debated, which means that it should be a significant viewpoint. ~~~~ --Stefan-S talk 13:10, 29 July 2021 (UTC)Reply
Stefan it is not up to us to question the results of reliable sources on talk-pages, you can do your own research off this website. I and several other users have also been guilty of writing original research, writing hundreds of words questioning studies etc on this talk-page it doesn't lead anywhere. We all do it, but this talk-page is not a forum it is about how we can improve the article. In regard to the report the conclusion's support the mainstream consensus "There was adequate evidence from RCTs that reducing intake of saturated fats reduced the risk of CVD events" and "There was adequate evidence from RCTs that substituting saturated fats with PUFA reduced the risk of CVD events". High quality references have shown that reducing saturated fat in the diet reduces the risk of CVD events and that is what the article reflects. Psychologist Guy (talk) 23:02, 3 August 2021 (UTC)Reply
Not even that far above this section I posted like a dozen reliable medical sources within 5 years that question the CVD saturated fat link.FrederickZoltair (talk) 23:50, 10 August 2021 (UTC)Reply
No you didn't sadly. Most of what you cited was off-topic, old or from unreliable journals. Do you have a reliable source from 2020 or 2021? Psychologist Guy (talk) 00:34, 11 August 2021 (UTC)Reply
I most certainly did, please actually read what I am talking about instead of assuming. Its at the end of the Break section. FrederickZoltair (talk) 00:53, 11 August 2021 (UTC)Reply
Yeah I have been through it, nothing you cited was reliable or on topic. This is about PUFA ratios [29] on type 2 diabetes not relevant to this article and doesn't mention saturated fat. This [30] is about fish oil supplementation. How is that relevant to this article? This meta-analysis you cited [31] is about dietary macronutrient patterns on different fad diets. It is not relevant to this article. This [32] is on the Mediterranean diet, it is not relevant to this article and suggests on-going research is needed. This [33] is about linoleic acid a polyunsaturated fatty acid. What has this got to do with saturated fat? This was on topic, but it was out of date [34]. And this [35] does not support your case it supports the scientific consensus and concludes that "SFAs promote and n-3 PUFAS reduce inflammation". So you believe SFA foods cause inflammation! That paper actually concludes that saturated fat foods cause inflammation. In another line it even said "Not surprisingly, those subjects consuming extra SFAs from butter showed elevations in plasma markers of inflammation." I don't know what sort of Google search or Google scholar search you did but you have not read any of these papers. I don't need to click through the rest. You have not cited anything reliable or on-topic you appear to be just citing random material. This is not going to improve the article. Psychologist Guy (talk) 01:24, 11 August 2021 (UTC)Reply
Unlike you I am not "looking" for certain evidence to justify my preconceptions, I am looking for any and all evidence relevant to the subject to make the entry better and I find these constant bad faith assumptions a real debbie downer. For your information, I followed the MEDRS guide and searched for recent reviews and meta analyses within the past 5 years that deal with SFA and its subtypes in regards to CVD on Pubmed with no help from you mind you, nor your caustic dismissal of me last month for having the gall to question "senior editors". What is this, like the umpteenth time you have called someone a teicholz apologist/quack/not as good at science as you? What is it senior editors are always saying? There is no cabal, and its usually got more to do with you than it does with the editor you are accusing. FrederickZoltair (talk) 15:51, 12 August 2021 (UTC)Reply
Again, no apology for your bad edits or behavior here. You have been citing off-topic material on this talk-page and repeatedly citing irrelevant links. You have not been following MEDRS, you went on Google scholar or pubmed and typed in fat or saturated fat and pasted in anything you could find. You didn't even read those papers because most of them were not on topic. Please read WP:COMPETENCE, this is the last time I reply to you. Psychologist Guy (talk) 19:38, 12 August 2021 (UTC)Reply
THIS IS A TALK PAGE, there is no such thing as "bad edits" merely discussion within the confines of Wikipedia policy and growth as editors. Name me one place in the entirety of my edit history where I fully made bad faith edits or got into a revert war with anyone (aside from my unfortunate hypersensitivity toward Alexbrn which I apologized for and that was not even an insult merely a little conspiratorial!)? You insult me directly, tell me the work I have done so far is pointless/not valid, accuse me of sock puppetry, continuously bully everyone and anyone who disagrees with you, make arguments to authority, directly tell me I lack scientific competence and furthermore what I do and do not understand in addition to discounting my own experiences and somehow promoting your own as more valid (when did Wikipedia become a scientific meritocracy!?), and finally wrap it all under this smarmy self righteous condescension about how you've been studying the topic for over twenty years and thus your opinions are more valid? Literally Wikipedia policy is written around not promoting original research or primary sources regardless of how much of an expert you are or are not. I hope you are true to your word. FrederickZoltair (talk) 23:59, 12 August 2021 (UTC)Reply

Saturated fat and the brain edit

Latest comment: 2 years ago14 comments2 people in discussion

On this article there is no mention of saturated fat and its role in the brain or its relationship to neurological diseases. There is strong evidence that a high intake of saturated fat increases cognitive decline (alzheimer's disease, dementia) and the risk of neurological diseases [36], [37], [38]. There is an unrelated discussion to this at the Omega-3 fatty acid talk page [39]. The human brain is roughly 60% fat but it is unclear how much of this is saturated fat. It has been shown that omega-3 docosahexaenoic acid (DHA) is very important for brain function. How much saturated fat is in the brain? A section about saturated fat and its relationship to the brain should be added to this article. Psychologist Guy (talk)

I disagree. Association is about as far from direct evidence as you can get of anything except that an association exists. Also your third study is from 2014 and we are in 2021 so it breaks the five year rule. FrederickZoltair (talk) 23:16, 10 August 2021 (UTC)Reply
Epidemiology does have its limitations but it's impossible to have evidence-based medicine without epidemiology. Most of the studies in clinical nutritional research are epidemiological because they are easier to do, last longer and can sample large general populations [40]. Whilst it is true that RCTS are considered the highest level of evidence to infer causality they can have drawbacks like expense, the fact they are not widely applicable and trial participants typically don't represent the population as a whole [41], this is why there are more observational studies than RCTS. This is why we need all available methodologies which make up the evidence based pyramid [42] that we get our data from. We can't just throw out all of epidemiology. Above you cited 20 or so studies and they were nearly all epidemiological, for example a review paper of observational studies from 2015 you cited claimed "Saturated fats are not associated with all cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes, but the evidence is heterogeneous with methodological limitations." [43], you listed about 10 or so more of these. You don't even read what you cite. The very papers you cite are making associations and have admitted limitations. This is a complex field that takes decades to study amongst changing populations, we are not going to receive "direct evidence" from a single study. Psychologist Guy (talk) 01:00, 11 August 2021 (UTC)Reply
Your reply really cuts down to the root of my primary complaint with the entry as it is. I find it laughable that none of the recent reviews I posted are "on topic" with regards to questioning the saturated fat cvd link even though per MEDRS they are valid, but you post 3 vague studies citing a vague association and we should add that asap with its own section? You see no issue with this? I don't feel like fighting with you or even responding to your ridiculous not in good faith claims about me or my arguments or really engaging in a debate with you regarding anything and furthermore do not appreciate your condescension. Meet the standard of MEDRS with your claim or it doesn't go in, simple as that in my opinion. Furthermore, your studies themselves paint the association as just that and not a cause for good reason, because the data does not support it. The difference is I am calling merely for representation of a direct claim ("There is no robust evidence that current population-wide arbitrary upper limits on saturated fat consumption in the United States will prevent CVD or reduce mortality.") whereas you are now claiming an entire category of debilitating degenerative diseases are concretely caused by saturated fat yet no health authority study directly certifies or even mimics the claims. FrederickZoltair (talk) 01:44, 11 August 2021 (UTC)Reply
There have been 3 other low-carb/keto/carnivore diet advocates citing that same paper on this very talk-page you guys are like a broken record. The paper was funded by the dairy and beef industry and was hosted by Nina Teicholz's workshop. Teicholz is a low-carb quack who tells people not to eat fruits or vegetables but load up on full fat dairy and red meat. Crazy. There is no point in citing industry funded research, I think even you would admit the conflict of interest and biases prevalent in that study. Are the dairy industry going to suddenly turn round and tell people not to consume foods high in saturated fat? I don't think so!
As for saturated fat consumption and dementia it is accepted by all governmental and public health agencies/organizations and health charities around the world that a diet high in saturated fat increases the risk of cognitive decline and dementia. There is no conspiracy. For example Dementia Australia tell people to "avoid foods high in saturated fat" and eat more polyunsaturated fats [44], the NHS tells people to lower their saturated fat consumption to prevent dementia [45] and Age Scotland that have a pdf document on diet and dementia say "You should try to eat fewer foods that are high in saturated fat such as processed meats, butter and cheese. Instead eat foods containing unsaturated fat such as oily fish, nuts, seeds and avocados." That was just a quick search but you can find any authority on dementia and they will tell you the same. This is the scientific consensus based on good findings from evidence-based medicine but you continue to argue against it by citing quackery. It is a waste of time to continue this. Psychologist Guy (talk) 13:18, 11 August 2021 (UTC)Reply

Also, I know you will "cry MDPI" but since I am not advocating for this to be included in the article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6720297/ - "The perspective of the use of KD in various diseases has been growing recently. Abnormal glucose metabolism uptake, diminished mitochondrial-associated brain energy metabolism, changes in neurotransmitter release, and increased inflammatory response are the key pathophysiological metabolic alterations observed in AD. Furthermore, KD may modulate a broad array of metabolic and signaling changes underlying the pathophysiology of neurodegenerative disorders. Based on the limited animal studies and clinical trials, KD has beneficial effects for enhancing mitochondrial function and cellular metabolism. It is associated with improved cognitive performance in elderly adults with AD. The improvement of the cognitive outcomes depends on the level and duration of ketosis. The best results of KD treatment are expected in early presymptomatic stages of AD. However, it requires a practical diagnostic approach." FrederickZoltair (talk) 02:20, 11 August 2021 (UTC)Reply

WP:NOTFORUM. You are using this talk-page just to dump irrelevant or off-topic links. MDPI is an unreliable junk science journal, we don't cite it on Wikipedia but the double standard has been noted, you are happy to cite research that makes associations if it suits your bias but if it doesn't you say "associations" are not direct evidence. This article is not about the ketogenic diet. Nothing you have cited on this talk-page is on topic or reliable so I think we can end this discussion. Psychologist Guy (talk) 13:18, 11 August 2021 (UTC)Reply
So lets review, you feel it necessary to dump information onto this article, its talk page, and me about epidemiology and alzheimers using a shaky at best set of studies (one of which is also too old per MEDRS), but when anyone else does it, all of a sudden we are quoting WPNOTFORUM and talking about how science and epidemiology works? Not to mention assuming someone just doesn't understand a thing and hence that is why you disagree with them is a conservative talking point tactic btw and its rude as hell and you do it often. Not to mention a ketogenic diet is defined (even on Wikipedias entry for it) as being high in saturated fat and low in carbohydrate so its kind of relevant to the claim that there is a solid link between saturated fat and degenerative diseases when RECENT research is fricking ongoing directly claiming the opposite and not only claiming the opposite but showing it in their results and urging for more research!? Furthermore this study as I said when I posted it is not for the entry (even though claiming an entire journal is junk science is ridiculous and furthermore untrue even according to the entry you linked for MDPI), it was for you to try to force you to acknowledge that the jig is up and the narrative you have subscribed to for god knows how long (and is the primary narrative of this entry) is either wrong, or requires re-examining per the growing body of evidence I keep linking to in various forms. As much as you dance around it, my collection of studies above is recent and are meta analyses and per MEDRS are valid regardless of your personal feelings about them (or willingness to nitpick every detail which is strangely absent from the studies you agree with). So I ask again, do you honestly not see the issue with inferring this association is valid and not even acknowledging the growing body of evidence that suggests the presupposition that saturated fats role in health is changing? And I am the one with the problem he says....killing me smalls. Oh and I forgot to add, I am not a keto/low carb/carnivore/whathaveyou advocate as you keep trying to associate me with which is also again just another disingenuous debate tactic. At least were I to call you a vegan advocate (which I haven't done), I can look at your edit history and confirm it rather than just launching vague accusations in your general direction (as well as not calling your reading comprehension into question which to this comment I still have not done per good faith). It does not take a super science genius to realize the basic polices regarding point of view and weight are not being adhered to here. And also, MDPI posted a response to Wikipedia's entry here. and in addition the MDPI entry page talk page is currently on fire with debate regarding the reliability of MDPI in general and it is far from settled. FrederickZoltair (talk) 18:56, 11 August 2021 (UTC)Reply
What I listed is obviously a reliable source [46] as was the other review only the other was out of date, not sure why you would say all of those are "shaky". As for off-topic material I have explained this here, you have been using this talk-page to dump off-topic material. Why for example were you quoting studies on fish oil or PUFAS? What does that have to do with saturated fat? I went through all the studies you pasted in and many of them were not on this topic this is not an attack on you personally it is a fact. Go and read through the studies you cited, most of them are not on saturated fat and disease.
MDPI is not a reliable source for anything medical because we have better higher quality sources that are available. If you would like others to weigh in on this then start a post over at another board such as the WikiProject Medicine but they would tell you the same. The Ketogenic diet is used to treat epileptic patients so if it works to stop seizures in theory it may improve other neurological disorders but there is lack of research on this currently, none of the research is long-term, this may change in a decade. As far as I know there are no high-quality reviews showing ketogenic diets have successfully been used to treat dementia patients long-term. If that changes in 5 or 10 years then let us know with a reliable source but for now the MDPI paper is not good quality and cannot be used on Wikipedia. If you disagree then you can go to another board and ask for a third opinion. Psychologist Guy (talk) 21:06, 11 August 2021 (UTC)Reply
For the third time I am not advocating for MDPI on wikipedia or even in this entry (even though your obvious bias against it is plain as day and unjustified in my opinion as it is a common and large journal even per our own Wikipedia entry but that is not relevant to this discussion). Are you even reading my words or just making up the straw-man before you even start writing? I am not advocating for keto/low carb or their inclusion here. I am merely pointing out that the saturated fat CVD link has been called into question by recent reliable scientific evidence and our entry does not even acknowledge it. Full stop. For example, this was published last week., and this was published in Feb 2020 and This was published in 2019. How can you with a straight face say that no reliable evidence exists that questions said link? In support of your Alzheimer's claim you submit a review that says the evidence of association is strong, but an association is an ASSOCIATION and not a cause. The claim can be defined as shaky when used to make a direct claim like "this means that saturated fat causes alzheimers", and if you went into any scientific institution and said "See these reviews prove X without a doubt and that settles all debate" then you will be laughed at and I think you know that. However when a study that hints at questioning the saturated fat cvd link you crawl through it with a magnifying glass which again is not your role as an editor. If you take issue with studies that are published and not retracted or found to be questionable by other reliable sources,then contact the publisher or authors, but its not your prerogative to hinder its inclusion for any reason. Oh and also. - "Krauss: While it is generally felt that dietary saturated fat is harmful, this really does not reflect how we should be thinking about saturated fat and health. The amount of saturated fat that we consume in our diet has a relatively small effect on the saturated fat in our body compared with the amount that is produced from carbohydrates.". Dr. Ronald_Krauss. Not trying to get a primary Q/A (even though its from the NIH) in the entry but this is getting silly. Not to mention this. Again not trying to include non MEDRS sources but this shatters the idea that the consensus is united and these ideas are fringe. FrederickZoltair (talk) 16:56, 12 August 2021 (UTC)Reply
This talk-page is not a forum, you are just doing random Googling and citing any crap you can find. Its hard to tell if you are trolling or are just incompetent. Two of the review papers you just linked to are actually reliable and I wouldn't object to citing some of this content but these reviews are of association studies. You are happy to cite meta-analyses of epidemiological studies if the result supports your bias but if a result from a meta-analysis says saturated fat is bad for health you get angry and say you are only interested in causality, not associations? It is impossible to take you seriously and I have seen no evidence that you actually read any of the papers you cite because two of the papers you cited are making associations and yes this is how clinical medicine often works. But why are you citing reviews of observational cohort studies if you only want "direct evidence"? Do you know what a cohort study is? Do you know what prospective and retrospective means? Do you know what the strengths and weaknesses of randomized controlled trial are? You need to go back to school and learn a few things. You shouldn't be discussing this topic because you lack the basic knowledge about how medical studies are done.
Here is what one of the meta-analyses you just linked to says "This current meta-analysis of cohort studies suggested that total fat, SFA, MUFA, and PUFA intake were not associated with the risk of cardiovascular disease. However, we found that higher TFA intake is associated with greater risk of CVDs in a dose-response fashion." [47], yet you have dismissed meta-analyses of cohorts on this very talk-page as being "shaky" and "unreliable" because they can only make associations and do not give "direct" evidence. Yet you are citing pure epidemiology that is making associations. Psychologist Guy (talk) 19:20, 12 August 2021 (UTC)Reply
As for cognitive decline, I never said saturated fat causes Alzheimer's or dementia you are misquoting me on purpose. It is likely but from all the cohort studies the evidence says that saturated fat increases the risk. We do not know the mechanism there is a lack of randomized controlled trials but we have meta-analyses of numerous epidemiological studies. Every meta-analysis to date published on saturated fat and dementia has concluded the same thing. Once consistent results are obtained it is reasonable to infer causality but as we still need more research on this topic we suspend making that judgement so I never said it causes dementia but yes, this is likely. There is a useful link about that here "The judgement as to whether an observed statistical association represents a cause-effect relationship between exposure and disease requires inferences far beyond the data from a single study and involves consideration of criteria that include the magnitude of the association, the consistency of findings from other studies and biologic credibility." [48], we have the consistency of other findings, and I also recommend you read this link [49]. Unfortunately, you are not competent to be discussing this topic this explains why above you were citing studies on PUFAS and fish oil, you probably didn't even know what PUFAS means. I have been researching these topic for 20 years and I have only scratched the surface. I have given you two links there so you can learn about causation and epidemiology as you need to learn the basics because you contradict yourself repeatedly on this topic. You have done some Google searching and spammed in some quackery, it does not make you an expert on this topic. Based on what I have seen you have no constructive edits on this website and your account is very likely to be a sock-puppet. If you continue to use this talk-page to dump off-topic or fringe material I will report your account at the admin board. Psychologist Guy (talk) 19:21, 12 August 2021 (UTC)Reply
Oh please. I love how you accuse everyone else of being ignorant and pedantic and the minute you do not overpower someone with the tediousness and condescension of your attitude alone you start citing policy and claims of sock-puppetry. Curiously you leave out the second half of my writings under the break section in which I spent about six hours going through every citation in the article and listing dead/broken links or deceptive statements using old and no longer MEDRS qualifying resources. Your accusation of sock puppetry has no evidence and if you disagree I encourage you to have an admin run a check against me and my IP address. In addition, your comments are in blatant violation of good faith and in general the spirit of Wikipedia. I was nothing but polite to you when we first started these discussions and you should note that you were the first to be unnecessarily rude and anything but helpful to a new editor like myself while doubling down on your opinions. I admittedly made some mistakes interpreting some of the research and standards of MEDRS but that is normal for a learning experience on a new platform as a new user. My only crime is being a long time lurker and prior donator to the Wikipedia project as a whole without ever contributing until recently where I created two noticeboards regarding the weinstein article which resulted in consensus based changes that in my opinion make the article better. You'll notice I have not been active recently due to having a professional life that keeps be busy from time to time. Furthermore I find your profiling of my behavior ridiculous. Not making edits on controversial and hotly debated entries first is not a failure and had you done the same, this article would be of much higher quality than it is now. FrederickZoltair (talk) 20:06, 12 August 2021 (UTC)Reply
All irrelevant. You have repeatedly argued against cohort (epidemiological) meta-analyses or reviews that make associations as 'shaky' useless and unreliable but all of the links you have been citing yourself are epidemiological meta-analyses or reviews that make associations - so you are happy to cite these association studies when it suits you but you complain at other editors for citing them if those studies come to a different conclusion. When you are told this and asked about your contradictory behavior, you do not reply. WP:GF only can go on for so long which I respected for a while but your recent behavior has gone beyond this. It is clear this discussion needs to be closed. Psychologist Guy (talk) 21:00, 12 August 2021 (UTC)Reply
Its almost like I am following MEDRS! I have given your insults and awful attitude enough of my time. Make your own project medicine post, or wait until more editors volunteer, and get consensus for the change you want to make or keep it to yourself until the article has been brought up to a medicine article standard per MEDRS. You can use my non-valid contributions above where I combed over every citation for working links and to confirm they backed up what was claimed in the entry if it helps. FrederickZoltair (talk) 21:44, 12 August 2021 (UTC)Reply

Post on Wikipedia project medicine regarding saturated fat and shifting consensus. edit

Latest comment: 2 years ago1 comment1 person in discussion

https://en.wikipedia.org/wiki/Wikipedia_talk:WikiProject_Medicine#Saturated_Fat,_shifting_consensus,_Cardiovascular_disease_(CVD)_,_and_general_health. Please contribute so we can improve this entry. Thank you FrederickZoltair (talk) 22:18, 12 August 2021 (UTC)Reply

Saturated fat and the brain edit

Latest comment: 2 years ago14 comments2 people in discussion

On this article there is no mention of saturated fat and its role in the brain or its relationship to neurological diseases. There is strong evidence that a high intake of saturated fat increases cognitive decline (alzheimer's disease, dementia) and the risk of neurological diseases [50], [51], [52]. There is an unrelated discussion to this at the Omega-3 fatty acid talk page [53]. The human brain is roughly 60% fat but it is unclear how much of this is saturated fat. It has been shown that omega-3 docosahexaenoic acid (DHA) is very important for brain function. How much saturated fat is in the brain? A section about saturated fat and its relationship to the brain should be added to this article. Psychologist Guy (talk)

I disagree. Association is about as far from direct evidence as you can get of anything except that an association exists. Also your third study is from 2014 and we are in 2021 so it breaks the five year rule. FrederickZoltair (talk) 23:16, 10 August 2021 (UTC)Reply
Epidemiology does have its limitations but it's impossible to have evidence-based medicine without epidemiology. Most of the studies in clinical nutritional research are epidemiological because they are easier to do, last longer and can sample large general populations [54]. Whilst it is true that RCTS are considered the highest level of evidence to infer causality they can have drawbacks like expense, the fact they are not widely applicable and trial participants typically don't represent the population as a whole [55], this is why there are more observational studies than RCTS. This is why we need all available methodologies which make up the evidence based pyramid [56] that we get our data from. We can't just throw out all of epidemiology. Above you cited 20 or so studies and they were nearly all epidemiological, for example a review paper of observational studies from 2015 you cited claimed "Saturated fats are not associated with all cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes, but the evidence is heterogeneous with methodological limitations." [57], you listed about 10 or so more of these. You don't even read what you cite. The very papers you cite are making associations and have admitted limitations. This is a complex field that takes decades to study amongst changing populations, we are not going to receive "direct evidence" from a single study. Psychologist Guy (talk) 01:00, 11 August 2021 (UTC)Reply
Your reply really cuts down to the root of my primary complaint with the entry as it is. I find it laughable that none of the recent reviews I posted are "on topic" with regards to questioning the saturated fat cvd link even though per MEDRS they are valid, but you post 3 vague studies citing a vague association and we should add that asap with its own section? You see no issue with this? I don't feel like fighting with you or even responding to your ridiculous not in good faith claims about me or my arguments or really engaging in a debate with you regarding anything and furthermore do not appreciate your condescension. Meet the standard of MEDRS with your claim or it doesn't go in, simple as that in my opinion. Furthermore, your studies themselves paint the association as just that and not a cause for good reason, because the data does not support it. The difference is I am calling merely for representation of a direct claim ("There is no robust evidence that current population-wide arbitrary upper limits on saturated fat consumption in the United States will prevent CVD or reduce mortality.") whereas you are now claiming an entire category of debilitating degenerative diseases are concretely caused by saturated fat yet no health authority study directly certifies or even mimics the claims. FrederickZoltair (talk) 01:44, 11 August 2021 (UTC)Reply
There have been 3 other low-carb/keto/carnivore diet advocates citing that same paper on this very talk-page you guys are like a broken record. The paper was funded by the dairy and beef industry and was hosted by Nina Teicholz's workshop. Teicholz is a low-carb quack who tells people not to eat fruits or vegetables but load up on full fat dairy and red meat. Crazy. There is no point in citing industry funded research, I think even you would admit the conflict of interest and biases prevalent in that study. Are the dairy industry going to suddenly turn round and tell people not to consume foods high in saturated fat? I don't think so!
As for saturated fat consumption and dementia it is accepted by all governmental and public health agencies/organizations and health charities around the world that a diet high in saturated fat increases the risk of cognitive decline and dementia. There is no conspiracy. For example Dementia Australia tell people to "avoid foods high in saturated fat" and eat more polyunsaturated fats [58], the NHS tells people to lower their saturated fat consumption to prevent dementia [59] and Age Scotland that have a pdf document on diet and dementia say "You should try to eat fewer foods that are high in saturated fat such as processed meats, butter and cheese. Instead eat foods containing unsaturated fat such as oily fish, nuts, seeds and avocados." That was just a quick search but you can find any authority on dementia and they will tell you the same. This is the scientific consensus based on good findings from evidence-based medicine but you continue to argue against it by citing quackery. It is a waste of time to continue this. Psychologist Guy (talk) 13:18, 11 August 2021 (UTC)Reply

Also, I know you will "cry MDPI" but since I am not advocating for this to be included in the article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6720297/ - "The perspective of the use of KD in various diseases has been growing recently. Abnormal glucose metabolism uptake, diminished mitochondrial-associated brain energy metabolism, changes in neurotransmitter release, and increased inflammatory response are the key pathophysiological metabolic alterations observed in AD. Furthermore, KD may modulate a broad array of metabolic and signaling changes underlying the pathophysiology of neurodegenerative disorders. Based on the limited animal studies and clinical trials, KD has beneficial effects for enhancing mitochondrial function and cellular metabolism. It is associated with improved cognitive performance in elderly adults with AD. The improvement of the cognitive outcomes depends on the level and duration of ketosis. The best results of KD treatment are expected in early presymptomatic stages of AD. However, it requires a practical diagnostic approach." FrederickZoltair (talk) 02:20, 11 August 2021 (UTC)Reply

WP:NOTFORUM. You are using this talk-page just to dump irrelevant or off-topic links. MDPI is an unreliable junk science journal, we don't cite it on Wikipedia but the double standard has been noted, you are happy to cite research that makes associations if it suits your bias but if it doesn't you say "associations" are not direct evidence. This article is not about the ketogenic diet. Nothing you have cited on this talk-page is on topic or reliable so I think we can end this discussion. Psychologist Guy (talk) 13:18, 11 August 2021 (UTC)Reply
So lets review, you feel it necessary to dump information onto this article, its talk page, and me about epidemiology and alzheimers using a shaky at best set of studies (one of which is also too old per MEDRS), but when anyone else does it, all of a sudden we are quoting WPNOTFORUM and talking about how science and epidemiology works? Not to mention assuming someone just doesn't understand a thing and hence that is why you disagree with them is a conservative talking point tactic btw and its rude as hell and you do it often. Not to mention a ketogenic diet is defined (even on Wikipedias entry for it) as being high in saturated fat and low in carbohydrate so its kind of relevant to the claim that there is a solid link between saturated fat and degenerative diseases when RECENT research is fricking ongoing directly claiming the opposite and not only claiming the opposite but showing it in their results and urging for more research!? Furthermore this study as I said when I posted it is not for the entry (even though claiming an entire journal is junk science is ridiculous and furthermore untrue even according to the entry you linked for MDPI), it was for you to try to force you to acknowledge that the jig is up and the narrative you have subscribed to for god knows how long (and is the primary narrative of this entry) is either wrong, or requires re-examining per the growing body of evidence I keep linking to in various forms. As much as you dance around it, my collection of studies above is recent and are meta analyses and per MEDRS are valid regardless of your personal feelings about them (or willingness to nitpick every detail which is strangely absent from the studies you agree with). So I ask again, do you honestly not see the issue with inferring this association is valid and not even acknowledging the growing body of evidence that suggests the presupposition that saturated fats role in health is changing? And I am the one with the problem he says....killing me smalls. Oh and I forgot to add, I am not a keto/low carb/carnivore/whathaveyou advocate as you keep trying to associate me with which is also again just another disingenuous debate tactic. At least were I to call you a vegan advocate (which I haven't done), I can look at your edit history and confirm it rather than just launching vague accusations in your general direction (as well as not calling your reading comprehension into question which to this comment I still have not done per good faith). It does not take a super science genius to realize the basic polices regarding point of view and weight are not being adhered to here. And also, MDPI posted a response to Wikipedia's entry here. and in addition the MDPI entry page talk page is currently on fire with debate regarding the reliability of MDPI in general and it is far from settled. FrederickZoltair (talk) 18:56, 11 August 2021 (UTC)Reply
What I listed is obviously a reliable source [60] as was the other review only the other was out of date, not sure why you would say all of those are "shaky". As for off-topic material I have explained this here, you have been using this talk-page to dump off-topic material. Why for example were you quoting studies on fish oil or PUFAS? What does that have to do with saturated fat? I went through all the studies you pasted in and many of them were not on this topic this is not an attack on you personally it is a fact. Go and read through the studies you cited, most of them are not on saturated fat and disease.
MDPI is not a reliable source for anything medical because we have better higher quality sources that are available. If you would like others to weigh in on this then start a post over at another board such as the WikiProject Medicine but they would tell you the same. The Ketogenic diet is used to treat epileptic patients so if it works to stop seizures in theory it may improve other neurological disorders but there is lack of research on this currently, none of the research is long-term, this may change in a decade. As far as I know there are no high-quality reviews showing ketogenic diets have successfully been used to treat dementia patients long-term. If that changes in 5 or 10 years then let us know with a reliable source but for now the MDPI paper is not good quality and cannot be used on Wikipedia. If you disagree then you can go to another board and ask for a third opinion. Psychologist Guy (talk) 21:06, 11 August 2021 (UTC)Reply
For the third time I am not advocating for MDPI on wikipedia or even in this entry (even though your obvious bias against it is plain as day and unjustified in my opinion as it is a common and large journal even per our own Wikipedia entry but that is not relevant to this discussion). Are you even reading my words or just making up the straw-man before you even start writing? I am not advocating for keto/low carb or their inclusion here. I am merely pointing out that the saturated fat CVD link has been called into question by recent reliable scientific evidence and our entry does not even acknowledge it. Full stop. For example, this was published last week., and this was published in Feb 2020 and This was published in 2019. How can you with a straight face say that no reliable evidence exists that questions said link? In support of your Alzheimer's claim you submit a review that says the evidence of association is strong, but an association is an ASSOCIATION and not a cause. The claim can be defined as shaky when used to make a direct claim like "this means that saturated fat causes alzheimers", and if you went into any scientific institution and said "See these reviews prove X without a doubt and that settles all debate" then you will be laughed at and I think you know that. However when a study that hints at questioning the saturated fat cvd link you crawl through it with a magnifying glass which again is not your role as an editor. If you take issue with studies that are published and not retracted or found to be questionable by other reliable sources,then contact the publisher or authors, but its not your prerogative to hinder its inclusion for any reason. Oh and also. - "Krauss: While it is generally felt that dietary saturated fat is harmful, this really does not reflect how we should be thinking about saturated fat and health. The amount of saturated fat that we consume in our diet has a relatively small effect on the saturated fat in our body compared with the amount that is produced from carbohydrates.". Dr. Ronald_Krauss. Not trying to get a primary Q/A (even though its from the NIH) in the entry but this is getting silly. Not to mention this. Again not trying to include non MEDRS sources but this shatters the idea that the consensus is united and these ideas are fringe. FrederickZoltair (talk) 16:56, 12 August 2021 (UTC)Reply
This talk-page is not a forum, you are just doing random Googling and citing any crap you can find. Its hard to tell if you are trolling or are just incompetent. Two of the review papers you just linked to are actually reliable and I wouldn't object to citing some of this content but these reviews are of association studies. You are happy to cite meta-analyses of epidemiological studies if the result supports your bias but if a result from a meta-analysis says saturated fat is bad for health you get angry and say you are only interested in causality, not associations? It is impossible to take you seriously and I have seen no evidence that you actually read any of the papers you cite because two of the papers you cited are making associations and yes this is how clinical medicine often works. But why are you citing reviews of observational cohort studies if you only want "direct evidence"? Do you know what a cohort study is? Do you know what prospective and retrospective means? Do you know what the strengths and weaknesses of randomized controlled trial are? You need to go back to school and learn a few things. You shouldn't be discussing this topic because you lack the basic knowledge about how medical studies are done.
Here is what one of the meta-analyses you just linked to says "This current meta-analysis of cohort studies suggested that total fat, SFA, MUFA, and PUFA intake were not associated with the risk of cardiovascular disease. However, we found that higher TFA intake is associated with greater risk of CVDs in a dose-response fashion." [61], yet you have dismissed meta-analyses of cohorts on this very talk-page as being "shaky" and "unreliable" because they can only make associations and do not give "direct" evidence. Yet you are citing pure epidemiology that is making associations. Psychologist Guy (talk) 19:20, 12 August 2021 (UTC)Reply
As for cognitive decline, I never said saturated fat causes Alzheimer's or dementia you are misquoting me on purpose. It is likely but from all the cohort studies the evidence says that saturated fat increases the risk. We do not know the mechanism there is a lack of randomized controlled trials but we have meta-analyses of numerous epidemiological studies. Every meta-analysis to date published on saturated fat and dementia has concluded the same thing. Once consistent results are obtained it is reasonable to infer causality but as we still need more research on this topic we suspend making that judgement so I never said it causes dementia but yes, this is likely. There is a useful link about that here "The judgement as to whether an observed statistical association represents a cause-effect relationship between exposure and disease requires inferences far beyond the data from a single study and involves consideration of criteria that include the magnitude of the association, the consistency of findings from other studies and biologic credibility." [62], we have the consistency of other findings, and I also recommend you read this link [63]. Unfortunately, you are not competent to be discussing this topic this explains why above you were citing studies on PUFAS and fish oil, you probably didn't even know what PUFAS means. I have been researching these topic for 20 years and I have only scratched the surface. I have given you two links there so you can learn about causation and epidemiology as you need to learn the basics because you contradict yourself repeatedly on this topic. You have done some Google searching and spammed in some quackery, it does not make you an expert on this topic. Based on what I have seen you have no constructive edits on this website and your account is very likely to be a sock-puppet. If you continue to use this talk-page to dump off-topic or fringe material I will report your account at the admin board. Psychologist Guy (talk) 19:21, 12 August 2021 (UTC)Reply
Oh please. I love how you accuse everyone else of being ignorant and pedantic and the minute you do not overpower someone with the tediousness and condescension of your attitude alone you start citing policy and claims of sock-puppetry. Curiously you leave out the second half of my writings under the break section in which I spent about six hours going through every citation in the article and listing dead/broken links or deceptive statements using old and no longer MEDRS qualifying resources. Your accusation of sock puppetry has no evidence and if you disagree I encourage you to have an admin run a check against me and my IP address. In addition, your comments are in blatant violation of good faith and in general the spirit of Wikipedia. I was nothing but polite to you when we first started these discussions and you should note that you were the first to be unnecessarily rude and anything but helpful to a new editor like myself while doubling down on your opinions. I admittedly made some mistakes interpreting some of the research and standards of MEDRS but that is normal for a learning experience on a new platform as a new user. My only crime is being a long time lurker and prior donator to the Wikipedia project as a whole without ever contributing until recently where I created two noticeboards regarding the weinstein article which resulted in consensus based changes that in my opinion make the article better. You'll notice I have not been active recently due to having a professional life that keeps be busy from time to time. Furthermore I find your profiling of my behavior ridiculous. Not making edits on controversial and hotly debated entries first is not a failure and had you done the same, this article would be of much higher quality than it is now. FrederickZoltair (talk) 20:06, 12 August 2021 (UTC)Reply
All irrelevant. You have repeatedly argued against cohort (epidemiological) meta-analyses or reviews that make associations as 'shaky' useless and unreliable but all of the links you have been citing yourself are epidemiological meta-analyses or reviews that make associations - so you are happy to cite these association studies when it suits you but you complain at other editors for citing them if those studies come to a different conclusion. When you are told this and asked about your contradictory behavior, you do not reply. WP:GF only can go on for so long which I respected for a while but your recent behavior has gone beyond this. It is clear this discussion needs to be closed. Psychologist Guy (talk) 21:00, 12 August 2021 (UTC)Reply
Its almost like I am following MEDRS! I have given your insults and awful attitude enough of my time. Make your own project medicine post, or wait until more editors volunteer, and get consensus for the change you want to make or keep it to yourself until the article has been brought up to a medicine article standard per MEDRS. You can use my non-valid contributions above where I combed over every citation for working links and to confirm they backed up what was claimed in the entry if it helps. FrederickZoltair (talk) 21:44, 12 August 2021 (UTC)Reply

Post on Wikipedia project medicine regarding saturated fat and shifting consensus. edit

Latest comment: 2 years ago1 comment1 person in discussion

https://en.wikipedia.org/wiki/Wikipedia_talk:WikiProject_Medicine#Saturated_Fat,_shifting_consensus,_Cardiovascular_disease_(CVD)_,_and_general_health. Please contribute so we can improve this entry. Thank you FrederickZoltair (talk) 22:18, 12 August 2021 (UTC)Reply

Saturated fats and cardiovascular health take 2 edit

Latest comment: 2 years ago22 comments5 people in discussion

I know how impossible it is to edit this page without getting autao reverted without any comments, so I will not try, I will try to discuss first, so. One of the things that I often get reverted for is that I don't use new enough sources, so I would like to propose a revert of this statement.

"The relationships are accepted as causal."

today it has 2 references, one from 2007 which states as we write in the article and one book which is from 2011 (I dont have access, but Im sure it says something simmilar), i.e. to old for MEDRS 5 years?? The first source is "European guidelines on cardiovascular disease prevention in clinical practice: executive summary" from 2007, if we instead read the newest (that I cant find) version of that same report [64] from 2016 (almost passing the 5 year rule, but at least much closer) it no longer states anything (that I can find) about causal relationship, so I suggest that we take away that sentence totally. Agree/disagree? @Tempest1 @Alexbrn , anyone else? --Stefan-S talk 14:30, 25 July 2021 (UTC)Reply

Whilst those sources are old, we can just cite the 2017 review from the American Heart Association presidential advisory which notes "Taking into consideration the totality of the scientific evidence, satisfying rigorous criteria for causality, we conclude strongly that lowering intake of saturated fat and replacing it with unsaturated fats, especially polyunsaturated fats, will lower the incidence of CVD and "Taking into consideration the totality of evidence, LDL cholesterol links saturated fat and its replacement macronutrients to CVD by very strong scientific evidence that satisfies rigorous criteria for causality. Three independent guidelines committees rated this evidence as Level A, Strong." [65] Psychologist Guy (talk) 17:09, 25 July 2021 (UTC)Reply
So you say that since the European guideline have changed, and now does not say causal, we need to find another one that does? Maybe since the this is a source in form of a 'national' guideline and it has changed, we could acknowledge that? So maybe there actually is reason to write something about the slow change in opinion, even on the highest level? --Stefan-S talk 23:35, 25 July 2021 (UTC)Reply
The 2016 European Guidelines says "Elevated levels of plasma LDL-C are causal to atherosclerosis" and "Reduction of LDL-C decreases CV events". There is hardly any mention of saturated fat, although it does say "Saturated fatty acid intake should be reduced to a maximum of 10% of energy intake by replacing it with polyunsaturated fatty acids". I don't see any change of opinion here. All guidelines are telling people to restrict saturated fat and eat more polyunsaturated fatty acids. There are a lot of risk factors for CVD (hypertension, high blood cholesterol, smoking, diabetes, uric acid, obesity, chronic kidney disease, physical inactivity, dyslipidaemia etc). What is this obsession trying to prove the guidelines wrong about saturated fat? It seems new users show up to this talk-page every few months and say the same thing but never question the other risk factors. Psychologist Guy (talk) 00:51, 26 July 2021 (UTC)Reply
So the source does not say saturated fat is causal to CV anymore, they say high LDL is causal to CV event, and you should lower Saturated fat. If you use that source to say that they say Saturated Fat is causal to CV that is OR in my book. I'm not a new user, I have edited wikipedia for 14 years longer than you! What I am, is tired of fighting on talk pages, but do a edit or try now and then. The obsession is to try to get the truth out there, as have been stated in this thread part 1, there is very little good science that actually proves that Saturated fat is bad (Im not saying there are not lots of science saying it, just good science). We all should know what fake 'news' is, we should all know what. If you have followed the low carb 'movement' for the last 5+ years, you should know that there is a awful lot of things the looks bad in the traditional nutrition science. Please read up on [66], Tim Noakes, Gary Fettke all whom have been 'prosecuted' for proposing low carb/high fat diet. In all cases, they where accused of not providing the truth, all the cases in Sweden, South Africa and Australia they where fully exonerated by state investigations, and if you read more about Tim Noakes and Gary Fettke there are accusations of how the dietists associations in each country played a very dirty game and in Australia there is proof? that they where paid by the food industry and asked by them to go after Gary. Just read about the scientific quotes that we use in wikipedia that classify low carb and keto as a 'fad diet', when it is the first diet 'invented' in last century, so how can it be fad??? OR? maybe, but since it is listed in a peer reviewed scientific paper we say that. To me that does not make sense, it is using wikipedia rules to push a POW.
The whole problem is that it is very hard to prove causality, and most papers that states causality dont follow the strict 2-4? times higher effect that is needed for epidemiological studies, what some scientists that don't work is university lab with funding from big food and farma believe is that carbs is causing CVD. And that hypertension, high blood cholesterol, diabetes, uric acid, obesity, chronic kidney disease, dyslipidemia etc are all effects of to much carbs, not risk factors for CVD, so it is reversed. So Im not arguing about obesity, high blood pressure, they are part of the package, but I do not think that high blood pressure is caused by saturated fat, same as lots of saturated fat dont give you 'high' cholesterol, or obesity or most of the other 'risk factors' on you list. I'm not expecting to rewrite this whole page, since there is a good chunk of 'high quality' science that still states this, but what I would like is to acknowledge that there are differing points of views and they are also of high quality, and we should give that more weight. Just my 2 cents, sorry for the rambling. --Stefan-S talk 03:25, 26 July 2021 (UTC)Reply
Another take on this is that we have a issue with our evidence pyramid, where we have Clinical guidelines that is built on observational studies, and real RCT that disproves, the effects of the observational studies, but probably due to the influence of big food and farma (which I acknowledge) that we cant prove is not reported on the clinical guidelines. So the pyramid don't work. But again, I'm not expecting you to see the light :-), I'm only hoping that we can give a little bit more space for a opposing view. --Stefan-S talk 03:32, 26 July 2021 (UTC)Reply
WP:NOTAFORUM. Wikipedia only exists to reflect accepted knowledge (not Truth™). I'd no more use Noakes as a source for dietary science as I would for COVID-19 or vaccination.[67] We need to improve the sourcing in this article, not descent into a vortex of pseudoscience. Alexbrn (talk) 06:33, 26 July 2021 (UTC)Reply
Thanks Alex for your comment, but I don't think you answered anything I talked about? I did not ask to use Tim as a source, even though I did not know that people you think are pseudoscientists, are not allowed? I though you wanted us to follow MEDRS? It does not say that. A scientists that dares to admit that he is wrong sometimes, is not a bad scientists, rather the other way around, in my opinion. This is typical on how you think, some sources are pseudoscience and therefore should not be used no matter what. Accepted knowledge changes, and it is time to start to write that. --Stefan-S talk 23:46, 26 July 2021 (UTC)Reply
Not really sure what you're on about but yes, we should use the WP:BESTSOURCES and obviously avoid pseudoscientific nonsense and/or the weird pronouncements of "diet gurus". I already mentioned the Cochrane SR above as something that is usable. You've mentioned no sources? Alexbrn (talk) 02:40, 27 July 2021 (UTC)Reply

Stefan you have not given any reliable references indicating the guidelines have changed. There is good evidence that reducing saturated fat intake reduces the risk of CVD and CHD events. We are after high-quality sources but you have not listed any. One of the best sources to date I have seen on this topic is the SACN report on saturated fat published in 2019. The report looked at 47 systematic reviews and meta-analyses and concluded that:

  • higher saturated fat consumption is linked to raised blood cholesterol
  • higher intakes of saturated fat are associated with increased risk of heart disease
  • saturated fats should be swapped with unsaturated fats
  • there is no need to change current advice that saturated fat should not exceed around 11% of food energy [68]. This is the sort of high-quality reference that we are after to improve this article. This was a review of 47 systematic reviews and meta-analyses, the most detailed I have seen on this topic to date. The report is over 400 pages long [69]. There is not any reliable evidence going the other way. We do not need to present a false balance and giving equal weight to minority fringe views. Psychologist Guy (talk) 00:50, 27 July 2021 (UTC)Reply
Thanks, good link (but very long). So the one of the best source you can find says The effect of saturated fat on health has been hotly debated in recent years .... and the relationship between saturated fat and cardiovascular disease (CVD) has been called into question, which to me says exactly what I am trying to say, there are more and more debate and I think we should give some room for that debate. As I have stated above, I'm not saying we should say that saturated fat is good, since the way our MEDRS is written that is against the rules, but I do think we should give more room for the alternative view, and your source clearly states that that view exists. I will try to do a more thorough review of your source later, but it will take hours so cant do it right now, but my quick evaluation was that in many cases they had a few meta studies that they checked, majority is associational studies, so they are already acknowledged by our evidence pyramid to be not so strong, then many of them had no effect as result, and a minority of them had some 'positive' effect of reduced saturated fat, and this was used to prove the that saturated fat was still bad and put in a country clinical guideline, i.e. elevating low quality evidence to a very high level. But all if this is OR, I know, but I will try to do to show you the point. --Stefan-S talk 23:50, 27 July 2021 (UTC)Reply
OK, I tried to read the paper, and make conclusion (which of course is WP:OR is that is don't have strong evidence. Let me explain what I interpret (please correct me if I'm wrong) that it says.
I only checked the first 2 and what I think most important topic they cover, CVD Deaths and CVD Events. For CVD deaths the paper says, no effect, reduction of saturated fat have no effect on either cardiovascular or total mortality, this was one RCT meta analysis and I think 3 observational meta analysis! Ponder that for a while.
Secondly for CVD events, I think that translates to heart attack? They had one RCT meta analysis, it stated 17%, 7% or 8% relative risk reduction of a reduction in Saturated fat. They also had 3 what they called prospective cohorts studies, i.e. observational studies. All of them reported no effect. I will accept to ignore this, since observational studies needs a very high risk to be considered proving causal effect, but I'm pretty sure they will use observational studies in some of the other topics further into the report and call them causal and adequate. But never mind. So this was enough for them to say that there was adequate evidence for that saturated fat are causal on CVD events!?
OK, lets accept that, I mean 17% sounds quite big right, that should mean that if everyone reduced their fat intake we would get 17% less cardiovascular events right? I will accept that as quite convincing in a good RCT! Well, no, it is not that simple, from the source (Hooper et al (2015) ) we can find that they say, "The number needed to treat for an additional beneficial outcome (NNTB) was 56 in primary prevention trials, so 56 people need to reduce their saturated fat intake for ~four years for one person to avoid experiencing a CVD event", as a absolute risk that is about 1.8% per 4 year (if my math is correct?), i.e. if everyone reduced their saturated fat intake as per the RCT we would get about 0.45% less Cardiovascular events per year and no change in deaths or mortality. So again I will do some WP:OR and say, no big deal, I'm surprised that we can use such sources. But then we don't try write the truth, only what is stated in 'reliable' sources and they say that...... So I know that I will either get slammed or ignored for this comment, but my point is, with 0.45% absolute risk, in the best source you can find, and that same source states that this topic is hotly debated, I think there is room to "fairly represent all significant viewpoints that have been published by reliable sources", and your source states hotly debated, which means that it should be a significant viewpoint. ~~~~ --Stefan-S talk 13:10, 29 July 2021 (UTC)Reply
Stefan it is not up to us to question the results of reliable sources on talk-pages, you can do your own research off this website. I and several other users have also been guilty of writing original research, writing hundreds of words questioning studies etc on this talk-page it doesn't lead anywhere. We all do it, but this talk-page is not a forum it is about how we can improve the article. In regard to the report the conclusion's support the mainstream consensus "There was adequate evidence from RCTs that reducing intake of saturated fats reduced the risk of CVD events" and "There was adequate evidence from RCTs that substituting saturated fats with PUFA reduced the risk of CVD events". High quality references have shown that reducing saturated fat in the diet reduces the risk of CVD events and that is what the article reflects. Psychologist Guy (talk) 23:02, 3 August 2021 (UTC)Reply
Not even that far above this section I posted like a dozen reliable medical sources within 5 years that question the CVD saturated fat link.FrederickZoltair (talk) 23:50, 10 August 2021 (UTC)Reply
No you didn't sadly. Most of what you cited was off-topic, old or from unreliable journals. Do you have a reliable source from 2020 or 2021? Psychologist Guy (talk) 00:34, 11 August 2021 (UTC)Reply
I most certainly did, please actually read what I am talking about instead of assuming. Its at the end of the Break section. FrederickZoltair (talk) 00:53, 11 August 2021 (UTC)Reply
Yeah I have been through it, nothing you cited was reliable or on topic. This is about PUFA ratios [70] on type 2 diabetes not relevant to this article and doesn't mention saturated fat. This [71] is about fish oil supplementation. How is that relevant to this article? This meta-analysis you cited [72] is about dietary macronutrient patterns on different fad diets. It is not relevant to this article. This [73] is on the Mediterranean diet, it is not relevant to this article and suggests on-going research is needed. This [74] is about linoleic acid a polyunsaturated fatty acid. What has this got to do with saturated fat? This was on topic, but it was out of date [75]. And this [76] does not support your case it supports the scientific consensus and concludes that "SFAs promote and n-3 PUFAS reduce inflammation". So you believe SFA foods cause inflammation! That paper actually concludes that saturated fat foods cause inflammation. In another line it even said "Not surprisingly, those subjects consuming extra SFAs from butter showed elevations in plasma markers of inflammation." I don't know what sort of Google search or Google scholar search you did but you have not read any of these papers. I don't need to click through the rest. You have not cited anything reliable or on-topic you appear to be just citing random material. This is not going to improve the article. Psychologist Guy (talk) 01:24, 11 August 2021 (UTC)Reply
Unlike you I am not "looking" for certain evidence to justify my preconceptions, I am looking for any and all evidence relevant to the subject to make the entry better and I find these constant bad faith assumptions a real debbie downer. For your information, I followed the MEDRS guide and searched for recent reviews and meta analyses within the past 5 years that deal with SFA and its subtypes in regards to CVD on Pubmed with no help from you mind you, nor your caustic dismissal of me last month for having the gall to question "senior editors". What is this, like the umpteenth time you have called someone a teicholz apologist/quack/not as good at science as you? What is it senior editors are always saying? There is no cabal, and its usually got more to do with you than it does with the editor you are accusing. FrederickZoltair (talk) 15:51, 12 August 2021 (UTC)Reply
Again, no apology for your bad edits or behavior here. You have been citing off-topic material on this talk-page and repeatedly citing irrelevant links. You have not been following MEDRS, you went on Google scholar or pubmed and typed in fat or saturated fat and pasted in anything you could find. You didn't even read those papers because most of them were not on topic. Please read WP:COMPETENCE, this is the last time I reply to you. Psychologist Guy (talk) 19:38, 12 August 2021 (UTC)Reply
THIS IS A TALK PAGE, there is no such thing as "bad edits" merely discussion within the confines of Wikipedia policy and growth as editors. Name me one place in the entirety of my edit history where I fully made bad faith edits or got into a revert war with anyone (aside from my unfortunate hypersensitivity toward Alexbrn which I apologized for and that was not even an insult merely a little conspiratorial!)? You insult me directly, tell me the work I have done so far is pointless/not valid, accuse me of sock puppetry, continuously bully everyone and anyone who disagrees with you, make arguments to authority, directly tell me I lack scientific competence and furthermore what I do and do not understand in addition to discounting my own experiences and somehow promoting your own as more valid (when did Wikipedia become a scientific meritocracy!?), and finally wrap it all under this smarmy self righteous condescension about how you've been studying the topic for over twenty years and thus your opinions are more valid? Literally Wikipedia policy is written around not promoting original research or primary sources regardless of how much of an expert you are or are not. I hope you are true to your word. FrederickZoltair (talk) 23:59, 12 August 2021 (UTC)Reply
Why is this discussion being archived when it hasn't been resolved? Please leave the discussions up, so that new editors don't repeat the same circular arguments. Tempes1 (talk) 14:45, 26 October 2021 (UTC)Reply
By policy we can archive finished conversations over 90 days old so the other content should be archived, we even have a bot for this now, I archived old material from July so that is by policy within the rules, it is well over 90 days old. In one of your first comments on this page you said you didn't want any of your material archived, it seems you want to put your arguments on here for some kind of advertising, sorry but this is not how Wikipedia works. Off-site, someone has been spamming this Wikipedia talk-page on various low-carb and carnivore diet forums asking for other people to join the discussion. That is an advertisement for meat-puppetry. The last comment in this current section discussion was by FrederickZoltair on 12 August 2021. I agree with you as it has not been 90 days for this section but FrederickZoltair is an obvious throwaway account with no Wikipedia edits outside of this talk-page and there was no consensus from their suggestions so its clear the discussion was finished. Psychologist Guy (talk) 15:17, 26 October 2021 (UTC)Reply

Study edit

Latest comment: 2 years ago3 comments3 people in discussion

This new study https://academic.oup.com/ajcn/advance-article/doi/10.1093/ajcn/nqab287/6369072 is quite impressive. They had quite a large group of participants and provided food for them over a rather long time period. In concludes 'A low-carbohydrate diet, high in saturated fat, improved insulin-resistant dyslipoproteinemia and lipoprotein(a), without adverse effect on LDL cholesterol. Carbohydrate restriction might lower CVD risk independently of body weight, a possibility that warrants study in major multicentered trials powered on hard outcomes.' Gorgos19 (talk) 09:29, 24 October 2021 (UTC)Reply

This is indeed a high quality study and I think it merits mention in this article Tempes1 (talk) 00:46, 27 October 2021 (UTC)Reply
No, that is a single feeding trial for 140 days on a biased sample of subjects. It is not evidence for anything and one of its authors is a well known low-carb crank. But this has already been explained to you many times before. WP:MEDRS applies "Ideal sources for biomedical information include: review articles (especially systematic reviews) published in reputable medical journals; academic and professional books written by experts in the relevant fields and from respected publishers; and guidelines or position statements from national or international expert bodies. Primary sources should generally not be used for medical content – as such sources often include unreliable or preliminary information, for example early lab results which don't hold in later clinical trials." We need high quality sources for this article like a review of many clinical trials, not a single feeding trial. Psychologist Guy (talk) 11:46, 24 October 2021 (UTC)Reply
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