Talk:Saturated fat

NPOV dispute - Research showing no link between saturated fat and CV risk is missing from this article

This paper was published September, 2022. It unfortunately does not fit popular opinion despite utilizing scientific rigor. I assume that's the reason for its exclusion. https://academic.oup.com/eurjpc/article-abstract/29/18/2312/6691821

It came to the same conclusion this meta-analysis did in 2014: https://www.acpjournals.org/doi/10.7326/M13-1788?articleid=1846638

Which came to the same conclusion this meta-analysis did in 2010: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824152/

(The point is to illustrate that this has been an ongoing debate for at least 12 years.)

Apparently the science is not so clear cut on the relationship between saturated fat and CV risk, but that's not the impression someone reading this article would get. Are we going to present all the scientific data, or are we taking sides? Agenda or no? 2600:4040:5012:7500:3000:9EF2:F8B5:125A (talk) 13:29, 26 March 2023 (UTC)

2014 is old, but the more recent paper might be worth mentioning. Or is it just an outlier? We cite WHO stuff which is more recent. Bon courage (talk) 13:56, 26 March 2023 (UTC)

The best sources on this are the World Health Organization (2023) [1], American Heart Association [2] (2017), UK Scientific Advisory Committee on Nutrition (2019), [3] and Cochrane review (2020) [4]. In total they have looked at hundreds of studies. The scientific consensus is clear on this, high saturated fat intake does increase CVD risk. Psychologist Guy (talk) 16:15, 26 March 2023 (UTC)

We have about 60 years research on this, it has been known for a long time since the research of D. Mark Hegsted and colleagues that palmitic acid increases LDL-c and total cholesterol. The debate has continued in recent years about specific saturated fatty acids on CVD risk. Long-chain saturated fatty acids increase CVD risk (palmitic and myristic acid for example) but stearic acid a medium-chain saturated fatty acid is neutral or may lower LDL. It's probably worth mentioning this on the article at some point. The World Health Organization have discussed it. Psychologist Guy (talk) 16:38, 26 March 2023 (UTC)

Yeah, Cochrane is a always a great source. Let’s see what it actually said:

“ We found little or no effect of reducing saturated fat on all‐cause mortality (RR 0.96; 95% CI 0.90 to 1.03; 11 trials, 55,858 participants) or cardiovascular mortality (RR 0.95; 95% CI 0.80 to 1.12, 10 trials, 53,421 participants), both with GRADE moderate‐quality evidence.

There was little or no effect of reducing saturated fats on non‐fatal myocardial infarction (RR 0.97, 95% CI 0.87 to 1.07) or CHD mortality (RR 0.97, 95% CI 0.82 to 1.16, both low‐quality evidence), but effects on total (fatal or non‐fatal) myocardial infarction, stroke and CHD events (fatal or non‐fatal) were all unclear as the evidence was of very low quality. There was little or no effect on cancer mortality, cancer diagnoses, diabetes diagnosis, HDL cholesterol, serum triglycerides or blood pressure, and small reductions in weight, serum total cholesterol, LDL cholesterol and BMI. There was no evidence of harmful effects of reducing saturated fat intakes.” Antisoapbox (talk) 21:41, 9 June 2023 (UTC)

Hopefully you have read that review, rather than just the abstract. Firstly, the trials in most cases were only two years long and they were on "participants at varying levels of risk of cardiovascular disease, men and women, with mean ages from 46 to 66 years". But you deliberately left out "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" and "In this review, saturated fat reduction had little or no effect on all‐cause or cardiovascular mortality but did appear to reduce the risk of cardiovascular events by 17%". The conclusion is that reduction of saturated fat reduced risk of cardiovascular events in the participants that had or were at risk of cardiovascular disease by 17%. If you have any Cochrane reviews telling us the opposite that increased saturated fat consumption reduces cardiovascular events, let us know but no such finding has ever been published because saturated fat clearly increases CVD risk and yes it takes decades, not two years but those trials have shown us reducing CVD for around two years can reduce CVD events. Psychologist Guy (talk) 23:48, 9 June 2023 (UTC)

Here is a major study: [5]. The conclusion is: "In this cohort, substituting omega 6 linoleic acid for saturated fat did not provide the intended benefits, but increased all cause morality, cardiovascular death, and death from coronary heart disease." A recent meta-analysis -- included in the provided link -- addresses more recently raised concerns, and reaffirms the original result. Therefore exclusion of this result is an NPOV issue.

With every food investigated in nutrition there will always be an outlier study. There is no point in cherry picking 1 study or meta-analysis when every other meta-analysis and review says the opposite as you are ignoring consensus. The study you are quoting is from 2013. We since have many recent reviews published between 2014 and 2023 which conclude linoleic acid consumption lowers risk of CVD and mortality [6], [7], [8], [9]. Psychologist Guy (talk) 21:40, 6 June 2023 (UTC)

It is undeniable that the wikipedia article on saturated fat violates NPOV.

"Available evidence from adequately controlled randomised controlled trials suggest replacing SFA with mostly n-6 PUFA is unlikely to reduce CHD events, CHD mortality or total mortality. The suggestion of benefits reported in earlier meta-analyses is due to the inclusion of inadequately controlled trials. These findings have implications for current dietary recommendations.".

Source: doi.org/10.1186/s12937-017-0254-5 sbelknap (talk) 20:59, 9 September 2023 (UTC)

You already cited that paper before on the red meat talk-page. It's a bit silly to be talking about CHD mortality or total mortality from randomized controlled trials that are around a year and a half long. There is no long-term clinical data. Of course there will be no signifcant effect here. Total mortality is not something that can be studied within a year from a couple of short-term trials. The best evidence that we have for this are epidemiological studies that look at decades of data and show consistent results. Psychologist Guy (talk) 20:53, 10 September 2023 (UTC)

You have misstated the findings of the Hamley meta-analysis. Perhaps you have not read it. Is this one behind a paywall for you?

If you have access to the article, look at Figure 6.

Poor-quality RCTs show that switching satfat → PUFA *reduces* CHD mortality while the high-quality RCTs show switching satfat → PUFA *does not reduce* CHD mortality.

I propose that the findings of Hamley be included in this wikipedia article on Saturated Fat. sbelknap (talk) 22:21, 10 September 2023 (UTC)

Most controlled trials will not give us good results for CHD mortality or total mortality because nearly all of the controlled trials are short-term. Hopefully you realise this. We need long-term data, that is why we rely on epidemiological studies here.

Many of these short-term trials that the author you cite mentions are between 1 and 2 years. In a human lifetime that is a short time. It will not give us significant data about mortality. The paper you are talking about by Steven Hamley is online in full [10]. The review he is criticizing is the Hooper review [11]. The Hooper review reported that there was little or no effect of reducing saturated fat on all‐cause mortality or cardiovascular mortality. The reduction was in cardiovascular events. It is not our purpose here to be doing original research like Steven Hamley has been doing. The Hooper review is a high-quality source and is cited on the article. There is no reason to cite a weak source like Steven Hamley. If like Hamley you believe certain controlled trials are "inadequate" that is up to you, but this type of original research will not be put onto the article. It is not up to us to question reliable reviews here, we just report what they say. The Hooper review is cited on the article. Psychologist Guy (talk) 00:22, 11 September 2023 (UTC)

I've published two meta-analyses. I'm familiar with how this is done.

Hamley's meta-analysis is a separate analysis and is not a commentary on the Hooper review. He does critique prior meta-analyses, including Hooper. This is a routine part of a meta-analysis & systematic review. Hamley does a more comprehensive analysis than Hooper, as he studies how different types of studies compare.

In the methods section of Steven Hamley's meta-analysis, he states, "I followed the PRISMA (www.prisma-statement.org) guidelines [52] throughout the design, implementation, analysis, and reporting of this meta-analysis."

Hamley does follow the PRISMA guidelines. Hooper does not follow the PRISMA guidelines. For these and other reasons, the Hamley review is of higher quality than the Hooper review.

This article could be improved by including the points made by Hamley. sbelknap (talk) 04:02, 11 September 2023 (UTC)

Ramsen and Hamley both deal with the question whether SFA should be replaced primarily with omega 6. Ramsen concludes that

"RCT that substituted mixed n-3/n-6 PUFA in place of TFA and SFA reduced CHD risk. By contrast, n-6 specific PUFA interventions tended to increase CHD risk.".

Hamley concludes that

"By contrast, n-6 specific PUFA interventions tended to increase CHD risk."

Both authors are looking for the best way to replace SFA and conclude that a replacement with primarily omega 6 does not reduce risk. Based on these two studies it seems that replacing SFA with a mix of omega 3 and omega 6 is the best strategy to reduce CVD risk. CarlFromVienna (talk) 09:26, 11 September 2023 (UTC)

You are correct that Hamley & Ramsen have different conclusions. Thanks for sharing your original research. As you know, editors are not to cite their own original research for content in wikipedia articles. Neither Hamley nor Ramsen draw the conclusion you state, that "replacing SFA with a mix of omega 3 and omega 6 is the best strategy to reduce CVD risk."

The way ahead with this article is to cite Hamley's findings. sbelknap (talk) 11:40, 11 September 2023 (UTC)

Hamley seems to be using some subjective criteria about what he classifies as a "adequately controlled trial" and the ones which are "inadequate" in his view. The adequate trials all seem to support his POV. For example this 1965 trial that used corn oil [12] was using high-dose corn oil in supplement form. The conclusion of this trial is that there was no benefit. This is not surprising. The subjects were consuming corn oil capsules, not a healthy diet. This is in contrast to another trial he cited that involved a plasma-cholesterol-lowering diet that included soybean oil, fish and vegetables [13], the conclusion was "the cholesterol-lowering diet reduced the incidence of total CHD". Yet Hamley excludes this trial as "inadequate". Why would we cite an article by Hamley that does original research?

I would agree that replacing SFA with a mix of omega 3 and omega 6 is a good strategy to reduce CVD risk. The scientific consensus is telling people to consume a mixture of n-3/n-6 PUFA in place of SFA. The idea to include just n-6 or "mostly" n-6 is not the consensus view. Hamley seems to be misrepresenting scientific consensus. The consensus view is very clear, we do not need to add one opinion piece from Hamley challenging it. See WP:Fringe. Psychologist Guy (talk) 11:58, 11 September 2023 (UTC)

Here, you misstate Hamley's methods, describing his criterion for "adequately-controlled" as being subjective. You also mischaracterize Hamley's article as "an opinion piece." Hamley is conducting and reporting meta-research and review in his article. If one follows his process, one obtains the same meta-research result. Perhaps you are unfamiliar with PRISMA. The failure of the Cochrane group to distinguish RCT quality is a deviation from PRISMA, which perhaps accounts for why the Cochrane meta-analysis does not claim adherence to PRISMA.

In the methods section, Hamley describes the criterion he used:

"Clinical trials were identified from earlier meta-analyses. Relevant trials were categorised as ‘adequately controlled’ or ‘inadequately controlled’ depending on whether there were substantial dietary or non-dietary differences between the experimental and control groups that were not related to SFA or mostly n-6 PUFA intake, then were subject to different subgroup analyses."

Hamley excludes the Oslo Diet Heart study because of a dietary difference between the experimental and control groups that was unrelated to SFA or (mostly) ω-6 PUFA intake—trans fatty acids: that is, in the Oslo Diet Heart study, "only the experimental group (the high n-6 PUFA group) received advice to avoid major sources of industrial trans fatty acids (TFA), such as common/hard margarines, shortenings and/or hydrogenated oils." This info is presented by Leren et al in the primary source. There is nothing subjective or original about Hamley's exclusion of the Oslo Diet Heart study. In fact, this critique of the Oslo Diet Heart study is well-known.

These objections to inclusion of Hamley's meta-analysis in this wikipedia article on saturated fat are without merit. Hamley is more careful in his meta-analysis than other authors, he adheres to PRISMA & he reaches conclusions that are important and relevant here. Hamley's work is a high-quality secondary source. Inclusion of Hamley's work would improve this article. sbelknap (talk) 12:26, 11 September 2023 (UTC)

The title of this discussion is „no link between SFA and CVD“. Both studies you brought up do not deal with this question but with the question if SFA should be replaced with primarily omega 6. That is a different discussion. Do you have any study that actually deals with the question at hand and supports that there is no link between SFA and CVD? If not this discussion can be closed. CarlFromVienna (talk) 15:30, 11 September 2023 (UTC)

"Saturated fat and cardiovascular disease" listed at Redirects for discussion

The redirect Saturated fat and cardiovascular disease has been listed at redirects for discussion to determine whether its use and function meets the redirect guidelines. Readers of this page are welcome to comment on this redirect at Wikipedia:Redirects for discussion/Log/2023 August 28 § Saturated fat and cardiovascular disease until a consensus is reached. Mdewman6 (talk) 22:54, 28 August 2023 (UTC)

"Arterycloggingsaturatedfat" listed at Redirects for discussion

The redirect Arterycloggingsaturatedfat has been listed at redirects for discussion to determine whether its use and function meets the redirect guidelines. Readers of this page are welcome to comment on this redirect at Wikipedia:Redirects for discussion/Log/2023 August 28 § Arterycloggingsaturatedfat until a consensus is reached. Mdewman6 (talk) 22:57, 28 August 2023 (UTC)

"Cardiovascular disease and saturated fat" listed at Redirects for discussion

The redirect Cardiovascular disease and saturated fat has been listed at redirects for discussion to determine whether its use and function meets the redirect guidelines. Readers of this page are welcome to comment on this redirect at Wikipedia:Redirects for discussion/Log/2023 August 28 § Cardiovascular disease and saturated fat until a consensus is reached. Mdewman6 (talk) 23:08, 28 August 2023 (UTC)