Talk:Lipid hypothesis/Archive 1

Spelling
Seeing how I misspelled it and it is more commonly called the cholesterol hypothesis I agree the best way forward would be to delete the article. Apologies to any mods/admins for the extra work! --Starquin 13:18, 31 July 2006 (UTC)


 * Ha, I hadn't even noticed the misspelling in the title. Moved to "hypothesis." With the change to NPOV article text, this is a perfectly legitimate article. It has a significant number of hits in Google, so it's deserving of an article. I'll leave it to people who know what they're talking about to make it more than a stub. eaolson 14:28, 31 July 2006 (UTC)

NPOV
According to the AfD discussion, this is a nonneutral term. It's used by one side in the debate to convey a particular POV. We can still have an article about it, but, like other such articles (e.g., Chickenhawk (politics)), this one must make clear that the term proceeds from a particular orientation. I've rewritten it along those lines. JamesMLane t c 10:55, 27 February 2007 (UTC)

"Lipid hypothesis" is a term used in peer-reviewed scientific literature describing a hypothesis proposed by Virchow in 1856. As such, it is a perfectly valid scientific term and the article could have a section on the development of the hypothesis from a science history perspective. As scientific hypotheses go, they make testable predictions that can be proven or disproven by studies. Therefore, the article should contain a section on studies that have been done to address this question. In the case of the lipid hypothesis, controversial discussion started in the 1970s and 1980s that questioned the interpretation of data that some scientists consider to be solid proof of the lipid hypothesis. This could be worked into a controversy section. It appears that the term was "hijacked" into this discussion by people arguing that the "proof" for the hypothesis is flawed and unscientific and therefore it is still nothing but a theory, but that doesn't change the validity of the term itself.

What this article needs is solid, scientific references from peer-reviewed publications. There are scientific papers that question the lipid hypothesis, but from what I can tell right now, they appear to be mostly single-author review papers written by one person in the scientific community whose main point of argument is that other scientists and NIH are working unscientifically and misinterpreting the data. As such, I feel the controversy section should not be the main part of the article as it does not reflect "mainstream" view. The critical articles are counter-balanced by a number of reviews detailing proof for the lipid hypothesis, which should be part of the article as well, if not its main body.

Looking over the article history, I have to agree that apparently this article was originally created on Wikipedia to support a certain POV. I do believe though that it could be worked into a neutral and informative article about a 150-year-old scientific hypothesis that became a controversial topic towards the end of the 20th century. The article should aim at allowing readers to understand the data produced in studies based on predictions made by the hypothesis and form an educated opinion about its conflicting interpretations. - tameeria 16:57, 27 February 2007 (UTC)

NPOV tag
What are the reasons for the NPOV tag? Currently the intro IS POV, in that it doesn't state that the "lipid hypothesis" is accepted by scientific consensus and only a small number of scientists hold a dissenting view. Please see WP:WEIGHT, which this article is violating by presenting the "lipid hypothesis" and its detractors as if they had somewhere near equal footing in the scientific community. They don't. The article needs to make clear the relative acceptance of the "lipid hypothesis" vs its alternatives, particularly in the lead, which User:Bezapt has removed. MastCell Talk 15:48, 15 April 2007 (UTC)
 * OK point taken re the lead paragraph and have added balance there. However the article certainly contains POV. See section "The lipid hypothesis and cholesterol controversy of atherogenesis": in answer to "lack of proof that lowering blood cholesterol levels results in decreased risk for atherosclerosis", article quotes NIH consensus development conference as squashing all objections. Truth by decree is not truth by scientific questioning, research and impartial argument about the observations. The pronouncement of that conference was criticised by several scientists at the time, and notes criticising the proceedings published by Thomas J Moore, Heart Failure, (Random House NY, 1989). He asserts criticism from the conference audience was ignored, critics were cut off by panel chairman Daniel Steinberg, and that there was no unanimity about the treatment the conference was to recommend - so it recommended all three proposals. Ravnskov notes that while violently criticised by his opponents, Moore's description of the events at the conference was not questioned. The article then breezes on with "Nonetheless, criticism persisted.." as if this contentious conference decree had actually proved something scientifically. Quite frankly: weasel words. While yes, I acknowledge WP:WEIGHT, the case for the majority should be more convincing than the poor effort that presently stands. There should be references to scientific studies, not a politically charged conference. The article also makes no reference to important considerations such as the traditional diets of the Masai and the Inuit, which are laden with animal fats, the so-called "French Paradox", or the interesting case of Ancel Key's fundamental 1953 paper which examined the correlation of fat consumption with heart disease mortality in six countries - when at the time data was available from 22 countries: inclusion of the omitted contemporary data has been shown by Ravnskov to seriously undermine Keys' conclusions. But be this as it may, perhaps the subject of debate is best moved to a new page entitled "Cholesterol controversy", while this article is reduced to a more neutral description, with a wiki-link to the controversy page if the reader wishes to follow it. Bezapt 16:43, 15 April 2007 (UTC)


 * Re the dispute on neutrality of the title brought up again by User:MastCell, tameeria has already commented on this: "Lipid hypothesis is a term used in peer-reviewed scientific literature describing a hypothesis proposed by Virchow in 1856. As such, it is a perfectly valid scientific term". Are you proposing to censor an historical term simply because it is still used by a minority of scientists and others? Bezapt 17:17, 15 April 2007 (UTC)


 * The NIH conference consensus is actually a secondary source from a reliable entity, which is the preferred source even for medical articles (as opposed to citing the primary literature and giving our own interpretation). It's only "politically charged" because a small number of contrarians refuse to accept it. NIH consensus documents carry a lot of weight on Wikipedia, as well they should per our sourcing policies and guidelines. As to the title, I guess it's a bit of a gray area, as it was once a widely used term, but my point was this: "lipid hypothesis" is no longer used in the scientific literature, except by the small minority who vehemently disagree with it. It's like referring to the pro-choice movement as the "anti-life movement" - it's a POV title because it's been appropriated by one side of the debate to try and cast doubt on the acceptance of the idea, which has moved beyond a "hypothesis". MastCell Talk 20:56, 15 April 2007 (UTC)


 * On researching the matter a little further I must admit I was wrong to be influenced by the unverified assertion that the term "lipid hypothesis" is only used by a minority who oppose it. Here is a selection of URLs pointing to publications made by those supporting and indeed currently investigating the hypothesis, who actually use the term. You will note that there is still an open trial, with further results due in 2010, which currently adds to the 18 or so other trials mentioned by Colpo in his book which indicated no statistical significance. With regard to your NIH conference remarks, an "appeal to authority" argument doesn't hold the same scientific weight as the actual examination of the research data. A committee can decree what it likes and rely on its aura of respectability to push an agenda over the criticisms of individual detractors. An appeal to authority is not science. Ad hominem attacks are not science. And yet detractors are dismissed as "a small minority" with the implication that they are misguided. The Wright Brothers  were members of a small minority - powered flight was not possible. Christopher Columbus was a member of a small minority - of course the earth was flat. Of course ships made out of metal would sink - metal cannot float. For well over a century the proponents of the idea that citrus fruits and fresh food would combat scurvy were vehemently opposed by members of the medical profession who had ideas which had also "moved beyond an hypothesis" - and yet sailors still died from their officially approved treatments. Can you see my point? The number of detractors is immaterial if a valid scientific question is asked of an hypothesis. To suppress an idea, as you seem to be suggesting, can be contrarian to the advancement of human knowledge. The resolution of scientific argument should be settled with science - not with dogma.  The term "lipid hypothesis" as seen below is used by both sides of the argument. If the lipid hypothesis is beyond doubt, and has moved beyond being an hypothesis to a "law", then trial results surely should be overwhelmingly convincing - but as shown again by the 2007 paper mentioned below, they are not even statistically significant.
 * http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2073909&dopt=Abstract
 * Dec 1990


 * http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2182981&dopt=Abstract
 * Feb 1990


 * http://www.cardiosource.com/rapidnewssummaries/index.asp?EID=15&DoW=Mon&SumID=98
 * refers to "the prevailing lipid hypothesis" - 7 Mar 2005


 * http://www.eurekah.com/chapter/3070
 * chapter in a book published (December 12, 2006)


 * http://www.jpands.org/vol12no1/ottoboni.pdf
 * Journal of American Physicians and Surgeons Volume 12 Number 1 Spring 2007
 * Abstract from the Women's Health Initiative Randomized Controlled Dietary Modification Trial (trial still open with further results due in 2010). Results puzzlingly inconclusive - no statistically significant benefits found deriving from a low fat diet. Lipid hypothesis is specifically mentioned, indeed used as the title of a section. (authors of this one are members of THINCS, just included this as it is a trial still in progress). Bezapt 03:19, 16 April 2007 (UTC)

No. The article doesn't dismiss the views of the minority - it presents them in the context of their acceptance by the scientific community, per WP:WEIGHT - or at least it should. You're essentially describing core Wikipedia policies like WP:V and WP:RS derisively as "appeal to authority". Citing papers from 16 years ago using the phrase "lipid hypothesis" only proves my point - this term used to be widely used (say, 16 years ago), but as the "hypothesis" is now considered proven, the term is loaded and used primarily by the minority who dispute it. Arguing that there's some kind of equivalence to Christopher Columbus or the Wright Brothers is off-topic - this is about how Wikipedia presents the topic, and it needs to be based on WP:V, WP:RS, and WP:WEIGHT. Citing the Journal of American Physicians and Surgeons pretty much proves conclusively that the idea in question is fringe and outside the mainstream - you may want to look beyond the vanilla title at what that particular journal actually represents, and why it's not indexed on MEDLINE or anywhere else. MastCell Talk 03:35, 16 April 2007 (UTC)


 * I fail to see how an NIH consensus development conference that set out to critically examine the available scientific data at the time and invited experts to present this data to a panel of yet more experts can be construed as having "decreed" something. As far as I can see, it merely confirmed an already existing consensus as a guideline for NIH. As for disregarding the voice of skeptics during the conference: Three of the invited speakers were actually known critics of the lipid hypothesis, which means that the critical side was even overrepresented (on purpose and by invitation) in comparison to the 1-8% of experts skeptical of the lipid hypothesis in the survey of 1978. Regardless of the conference outcome and its criticism, both are now just historical anecdotes two decades into the past and superseded by newer studies. While there is no doubt that skepticism still persists, it appears to come from a vocal minority of maybe 1% or even fewer "experts" within the medical community that rely on popular literature, news stories and interviews, and their own websites to make their points. I have yet to find any truly critical papers within the scientific community (PubMed) published within the last five years. - tameeria 13:48, 16 April 2007 (UTC)


 * OK, separating the text from the argument, yes, the NIH matter is verifiable, and yes reliable journal sources are quoted. In that respect WP:V and WP:RS are satisfied. A concern however is that the construction of the article places an odd prominence on reports of academic "consensus", rather than the results of the medical trials. In fact there is a lacuna from 1953 and the survey from 1978. No studies are mentioned. The article states "During the 70s and 80s, a fair number of researchers and practitioners were questioning the lipid hypothesis", and "Predictions were made that further research during the 80s and 90s would help settle this controversy". These statements are inconsistent with the verifiable fact from a reliable source which states that in 1978 an overwhelming majority of surveyed researchers and practitioners supported the lipid hypothesis by an impressive vote of 189 to 2. Why the 70s & 80s questioning if the general mood was so supportive? Colpo cites 18 trials and studies which were conducted during the period from 1955 to 2006, 12 of which did not produce statistically significant results (total mortality benefit from intervention), and 1 which had mixed results. the remaining 5 supporting the lipid hypothesis are not beyond query, and include the Finnish Mental Hospitals trial of 1972, which was extensively criticised in The Lancet in 1973 by staff of the NHBLI. Perhaps these are factors which could explain the "questioning" of the 70s and 80s? Regarding reference dates, the article states the lipid hypothesis was considered validated by the end of the 1980s. The articles that are 16 years or so old are around or just after the time of lipid hypothesis "validation" (per article). While I only supplied a small selection of more recent references, I am sure as you are familiar with www.pubmed.gov you could easily find the 72 hits for that text string. Note that 10 of these respectable articles, many of which support the lipid hypothesis, are using the term from 2002 (a date with relevance, according to the article) to the present (although the likes of Steinberg seems to prefer to quarantine the term from the rest of his prose with inverted commas). The title is a valid term, still in use by both sides of the question. As it has been mentioned in the literature for at least the last 30 years (as per www.PubMed.gov) it has an historical validity also. Bezapt 17:49, 16 April 2007 (UTC)


 * Moore, Thomas J., Heart Failure (Random House, 1989) describes how the 2.5-day NIH conference made its pronouncement at the end of the second day and, before concluding for the day the panel announced that a printed national cholesterol plan would be available at 8:30 the next morning, with a press conference three hours later to announce the plan to the general public, such readiness suggesting a pre-orchestrated outcome to the conference. Despite inviting known opponents, the announcement would appear to have been pre-planned, regardless of the matters raised during the conference. Yes it is an historical anecdote, (and verifiable from responsible sources both for and against), but does it deserve so much prominence as being a powerful factor in the debate, while discussion of some 18 medical trials is omitted? The addition of the 1978 survey is opinion - from relevent professionals, to be sure - but opinion nonetheless. What trial evidence did they base their overwhelmingly positive opinion on, especially during a time when "a fair amount of questioning" was going on? Regarding the lipid hypothesis opponents using websites and popular literature to get their point across, why shouldn't they? The NIH conference panel was keen to announce their national cholesterol plan to a wider audience too -the last half-day of the conference appears to have been occupied significantly by promotional matters. The THINCS members do also publish in the scientific literature, and you can find various items listed at www.thincs.org/public.htm listed in PubMed as well (I checked a few). Bezapt 17:49, 16 April 2007 (UTC)


 * Parsing the above: you say, "the construction of the article places an odd prominence on reports of academic "consensus", rather than the results of the medical trials." Yes, this is exactly what we're enjoined to do by WP:OR - see here - where secondary sources (e.g. NIH consensus conference) are preferred to having us list primary sources (trials) and provide our own interpretation of what they mean. Bottom line: the NIH's interpretation of the data is more "reliable" than yours or mine, so far as Wikipedia is concerned. Also, it's not "odd" to give prominence to academic consensus - it's actually mandated by WP:WEIGHT. Impugning the motives of the NIH and citing an apparently out-of-print book does not override those considerations. MastCell Talk 18:08, 16 April 2007 (UTC)


 * You appear to have missed my point, MastCell. I have been writing for Wikipedia for a while now and am quite aware of the WP:No original research rule. My point is that primary and secondary sources exist which can explain the article's statement "During the 70s and 80s, a fair number of researchers and practitioners were questioning the lipid hypothesis". However these primary and secondary sources have been omitted for a large number of years - the article's chronology has a big hole in it from 1953 until a 1978 survey confidently supporting the hypothesis even though the article notes it was a time of doubt. Readers are left to wonder about the inconsistency. This selective choice of verifiable, Reliable sources, while omitting others which are equally verifiable and reliable, distorts the article, i.e. displays the effect of a point of view. It appears that the justification for the omission of opposing sources is seen as justifiable in the name of WP:Weight. While not giving the arguments of the hypothesis opponents WP:Undue_weight (to reflect that there are more lipid hypothesis proponents than opponents), there needs to be a little more balance to the article. If points supporting the hypothesis are included, then at least some points opposing it should also be included, not just a few mentions that there are some opponents. Erasing opposing voices was what the Ministry of Truth was about... what a coincidence that the NIH conference occurred in 1984! Regarding the motives of the NIH, these were speculated upon by the source quoted above, which is freely available for purchase if you wish to pick up a copy at amazon.com. Virchow's book from 1856 has been out of print for considerably longer and is probably harder to get hold of, not to mention being written in an older style of German and printed in that gothic font they used to use - yet it is quoted as a source. Surely you are not implying that if a book is out of print it is unreliable? Further criticism of the NIH conference's National Cholesterol campaign was published in reliable sources after its release, appearing in The Lancet 1:633-634 (1984) & 1:1087-1089 (1985) & 1:503 (1987), JAMA 256:2779-2780 (1986) and Mayo Clinic Proceedings 63:88-90 (1988), so while there might have been consensus amongst the NIH conference panel of 14 members, consensus was certainly not achieved in the medical community of the time. When I have some more time I will make an attempt at providing some balance while trying not to upset the dominant position held by the hypothesis proponents. Bezapt 15:38, 18 April 2007 (UTC)


 * Basically, the entire article is a POV fork - it's as if the article on AIDS was entitled "HIV/AIDS hypothesis". If you re-read the AfD discussion, the article was kept on grounds of tameeria's excellent rewrite and provided that it covers the "lipid hypothesis" as a historical dispute now considered settled (with the exception of a small but vocal fringe). I don't see how citing letters to the editor from 20 years ago suggests that the lipid hypothesis is currently controversial in the scientific community, and as you probably know, letters to the editor are not peer-reviewed and are generally selected to foment discussion - therefore, they should not be taken as evidence of a weight of scientific opinion. The difference between Virchow's monograph (which is cited for its historical importance) and Thomas Moore's book is obvious, and the fact that Moore's book is out of print suggests that perhaps its impact has not been particularly profound - although of course this is indirect evidence. Finally, please leave the Orwell analogies at home, as they tend to undercut one's credibility in the same manner as a reference to Nazi Germany. MastCell Talk 16:09, 18 April 2007 (UTC)


 * Sorry, your analogy is not quite congruent. There exists a main cholesterol article, and this one is merely supplementary to the main subject, providing information about a term with a valid historical existence for at least 50 years if not more, as well as being in use still by some and, as tameeria notes, being employed in other contexts too. Consider the student using Wikipedia to help with research, or a school project. They may have seen "lipid hypothesis" in some publication and wish to investigate it further. Surely they have a right to expect Wikipedia will have some sort of article or section explaining said term?
 * Your confusion regarding submissions from approximately 20 years ago has resulted from your overlooking the fact that I was discussing the NIH conference, which occurred 20 years ago, and not the present. The differences between Virchow's and Moore's publications include: one is relatively much harder to obtain than the other; even if both were obtained, one is less accessible and liable to have a profound impact on those unfamiliar with antique scientific German; one proposed the lipid hypothesis and the other includes an eyewitness account of a conference related to the subject (which, as Ravnskov notes in The Cholesterol Myths (2000), p.295, n.1, "(Moore's) views have been violently criticised by the diet-heart proponents. However, no one has questioned his description of the conference.") Sorry if my Orwellian reference offended, I must have touched a nerve.. Bezapt 18:29, 18 April 2007 (UTC)


 * This is a POV fork because the history of the "lipid hypothesis", as well as the fact that a small fringe of dissenters exists, should both be covered under cholesterol, atherosclerosis, and/or coronary heart disease. Creating an article using a (now)-partisan title to expand on the views of that small fringe of dissenters smacks of POV-pushing and violates WP:WEIGHT. But those are my 2 cents. No, the Orwell thing hasn't touched a nerve. I've heard the same before from editors who are convinced that Wikipedia is a soapbox upon which one can expound uncritically on fringe views and challenge scientific "dogma" - but a reliance on conspiracism is generally not an effective persuasive tool here, I've found. MastCell Talk 19:26, 18 April 2007 (UTC)
 * Including the term in another article is certainly an option, but if you continue to feel so strongly about the title, what about us renaming this article "Cholesterol controversy", with "lipid hypothesis" pointing to it via redirect link? Then it would, for example, parallel the arrangement of the "Evolution" article which has a "Theory of evolution" redirect and also separate subsidiary artcles Creation-evolution controversy, and Objections to evolution. This precedent would appear to be a way forward. Thanks for the advice re conspiracy theories, but I am relying on the authors I have quoted (with the exception of Colpo, who provides extensive citations) rather than a single lighthearted literary reference (suggested to me by Moore's viewpoint and the date); while not holding to the mainstream view, they are medically qualified. They are not hippies, or sensation-seeking journalists, but the professional peers of the proponents. Bezapt 15:55, 20 April 2007 (UTC)

I can see that the PubMed sources appear to be inconsistent and lacking in original data. Part of this may be because "lipid hypothesis" as a search term preferentially pulls up reviews from the two opposing sides in the argument. As a matter of fact, all the articles after the 1996 introduction of the Diabetes Atherosclerosis Intervention Study that the PubMed search brings up are review articles (and one interview). (The non-review of 1999 is regarding the lipid hypothesis of osteoporosis, and the 2007 paper deals with the lipid hypothesis of cold tolerance. Both are thus off-topic in this context.) Of course, they will place different weights and emphases on consensus and interpretation of results, thus the apparent inconsistency. Going backwards, the first articles with actual data date from 1987 (Effects of fenofibrate on plasma lipoproteins in hypercholesterolemia and combined hyperlipidemia) and 1986 (In vivo effect of a high-cholesterol diet on the endothelial integrity of rat aorta). Why is that and where is the data that has been generated since then? It appears to me that all primary sources containing data on the topic published since the late 80s consistently avoided using the term "lipid hypothesis" and it has since then only been used by those who argue about it. - tameeria 20:52, 16 April 2007 (UTC)
 * Why do articles with data not use the term lipid hypothesis these days? A very good question indeed. I did find a few articles referring to the 2006 Women's Health Initiative trial, but they slipped by my search as they apparently do not refer to "that" hypothesis by name. Perhaps the term is now too politically incorrect in mainstream medical circles but, since I do not move in them, this is pure speculation of course.
 * Howard BV, et al., "Low-fat dietary pattern and risk of cardiovascular disease: the Women's Health Initiative Randomized Controlled Dietary Modification Trial.", 1: JAMA 2006 Feb 8;295(6):655-66. PMID: 16467234. "CONCLUSIONS: Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved only modest effects on CVD risk factors, suggesting that more focused diet and lifestyle interventions may be needed to improve risk factors and reduce CVD risk."
 * There are number of other articles cross referenced to that one in PubMed, but one item alleges that debate has been stirred again in the mainstream:
 * Twombly R, "Negative Women's Health Initiative findings stir consternation, debate among researchers", J Natl Cancer Inst 2006 Apr 19;98(8):508-10. PMID: 16622115.


 * Perhaps those other uses of the term "lipid hypothesis" that you spotted should be added to the article in an additional section. Bezapt 18:29, 18 April 2007 (UTC)


 * Interesting citation. Hopefully you have the whole article available to look at, particularly the last paragraph of the Results section and the entire Comment section. The Howard study's main conclusion was that reducing total fat intake had no discernible effect. However, the "lipid hypothesis" specifically identifies saturated fat (and more recently, trans-fat) as the bad actor in atherogenesis. So when Howard et al. looked at this, what did they find? A trend toward reduction in heart disease risk in those with the lowest intake of saturated fat and trans-fat, along with a decrease in LDL-cholesterol in those with the lowest saturated fat intake. Even though these were not pre-specified objectives of the study, the p values were pretty good - 0.05 for saturated fat and 0.10 for trans-fat.


 * The authors concluded, "Collectively, these analyses, despite their inherent limitations, suggest that a diet lower in saturated and trans fat intake and higher in intakes of vegetables and fruits and polyunsaturated fat than what was achieved in this trial might show significant benefit in preventing CHD." Hence, "more focused" dietary interventions, rather than dealing with total fat intake alone. Doesn't sound like a challenge to the "lipid hypothesis" to me. MastCell Talk 19:26, 18 April 2007 (UTC)


 * I've tried to address some of the points raised by rewriting a bit, adding more references (e.g. Science coverage of NIH conference criticism) and verifying sources. Does this address the issues for the NPOV tag, and can it be removed? Or are there other points? - tameeria 17:35, 19 April 2007 (UTC)

Thanks for the excellent work. I think the tag could be removed, from my perspective, but the article needs to continue to be watched closely. MastCell Talk 18:21, 19 April 2007 (UTC)


 * Ok, I've removed the NPOV tags for now. It appears to me that the only section under dispute may be the controversy section. Therefore, I would suggest using a section tag if you think the NPOV tag removal was premature. I think though that this is not really the place for detailed discussions of experiments and their criticism. Also, the section's references include seven reviews summarizing criticism and seven reviews from proponents/neutral sources now. I think that's as much balance as we can get without tipping the scale into the other direction. Maybe criticism voiced by THINCS members could go onto the THINCS page? Or should there be an extra page with more details on the cholesterol controversy that is then linked from the summary section in this article? - tameeria 14:54, 20 April 2007 (UTC)


 * Jacqueline Walker MD, from THINCS, has questioned that last paragraph of the results section in a forum discussion. "The study found no significant increase in CVD outcomes in the low-fat group EXCEPT, they found the hazard ratio for women in the low-fat intervention group who already had CVD to increase 1.26 (CVI 1.03-1.54) and this was significant (P=0.006). Interestingly they put this bit in at the end of a section in a sentence which completely omits to mention the direction of the 'interaction between the intervention and the [baseline] disease'). However, they did do some fancy calculations on CHD risk and found some groups where this fell where saturated fat and trans fat consumption was lowered. Now this can usually safely be ignored because 'risk' usually just means the application of a model incorporating LDL levels, triglycerides, diabetes, BP etc. However, it's not clear how this was calculated. The paper says: "Trends for changes .... were examined by evaluating CHD risk for individuals stratified by quartiles of achieved levels of key nutrients in year 1, using the rate in the comparison group as reference. Analyses were adjusted for age, baseline CHD, ... randomization group.." My question is - is this using actual CHD outcomes for the intervention individuals or not? It's not clear because then they talk about a 'CVD risk model' which includes the usual suspects (BP, cholesterol level etc.). And then they compare each quartile intervention group with the WHOLE comparison group!" Perhaps, as Howard's paper says, "more focused" dietary interventions might add clarity, rather than using data with "inherent limitations" and not in a situation "where the additional analyses are subject to residual confounding". Not really a completely confident statement, but hedged and qualified.


 * A pertinent posting relating more confident observations re saturated vs unsaturated fats: "Half a century ago, CHD was rare in India. It was only after the West told them that their diet was 'unhealthy' and the Prudent Diet introduced them to polyunsaturated vegetable oils that CHD took off in that country. A population comparison was reported in 1967. Dr S L Malhotra, Chief Medical Officer for the Western Railway system had reason to question the Prudent Diet. (Malhotra S L. Serum lipids, dietary factors and ischemic heart disease. Am J Clin Nutr. 1967; 20: 462-75.) He reported that in Madras, in the south of India, the population was vegetarian, living mainly on rice. Although they had a relatively high-fat diet, it was mainly of peanut oil. As vegetarians, there was practically no animal fat in their diet. In effect they were living on the Prudent Diet more strictly than were the Americans. Malhotra compared these Madrassis with a population who lived in the north near Udaipur. Their religion allowed them to eat meat and their fat intake was almost entirely from animal sources and highly saturated. They cooked in ghee (clarified butter) and had what was probably the highest butterfat consumption in the world. Present-day 'wisdom' would predict that the vegetarian Madrassis would have the lower rate of heart disease but the opposite was true. Malhotra found that the Madrassis who adhered so well to the precepts of the Prudent Diet had fifteen times the death rate from heart attacks compared to the northern Indians even though those in the north ate nine times as much fat - and that fat was saturated animal fat. Twenty years later the Lancet noted an increase in heart-attack deaths amongst the northern Indians. By this time the northerners diet had also been made 'healthier' by the replacement of the traditional ghee in their diets with margarine and refined vegetable oils. ((No authors listed) Ghee, cholesterol, and heart disease. Lancet. 1987; 2 (8568):1144-5.)".
 * A paper from before the results of the Women's Health Initiative trial (L.A. Corr, "The low fat/low cholesterol diet is ineffective", European Heart Journal (1997) 18, 18-22, PMID: 9049510), stated "Remarkably, no primary prevention trial of sufficient size or sensitivity to examine the effect of a low total and saturated fat diet alone has ever been conducted". With the Women's Health Initiative trial, now total fat intake has' now been studied, without finding significant beneficial results from lowering total fats in the diet. The same 1997 paper referred to two other trials (Research Committee to the Medical Research Council, "Low fat diet in myocardial infarction. A controlled trial" Lancet 1965: ii: 501-4 ('the MRC Trial'); and an Australian trial by Woodhill JM et al., "Low fat, low cholesterol diet in secondary prevention of coronary disease", Adv Exp Med Biol'' 1978: 109: 317-30.) which were conducted to study the effect of a low saturated fat diet *alone* in patients with coronary heart disease - neither produced significant results to support the lipid hypothesis either.
 * While the Women's Health Initiative trial paper does not set out to "challenge" the lipid hypothesis (instead shoring it up with some qualified and results which could do with further clarification as to their derivation), it does usefully provide results that Corr stated were missing from the scientific research - low *total* fat intake does not appear to have a significant effect on heart disease prevention. To get back to the article itself, it needs more information. By careful selection of sources and omitting commentary on the conflicting for-and-against trial results conducted over the half century since 1953, a reader of the article would gain little idea about why in the 70s and 80s there was doubt about the hypothesis and also why statins are perceived as the proof of it (as statins have other effects besides stopping the formation of cholesterol, that these considerations should be discounted should be explained with appropriate citations, if the cholesterol effect alone is the reason for statins "proving" the hypothesis). While acknowlegding WP:Weight, there is certainly room for a little more balancing information in the article without overpowering the majority viewpoint. When I have a moment to attend to it, be assured I will proceed with as neutral a flavour as possible. Tameeria, I noticed the new extra sections for other use of the term - perhaps the NPOV tag about the article title can go now. Bezapt 14:27, 20 April 2007 (UTC)

What, exactly, is unbalanced about the article? The consensus view is presented as the consensus view (with references to back up its wide acceptance), and the THINCS view is presented as that of a small but vocal minority, which it is. It looks like it follows WP:WEIGHT pretty closely. I think adding a bunch of outdated primary sources from the 70's and 80's only confuses the general reader, gives undue weight to the cholesterol "skeptics" (as their ideas are much more marginal now than in the 70's/80's), and violates WP:RS and its injunction to avoid outdated primary sources and use secondary sources (e.g. NIH consensus conference, review articles) where possible. MastCell Talk 18:17, 20 April 2007 (UTC)

For starters, the phrase "small but vocal minority" is not neutral point of view. It's not intending to inform people about true dissent in the medical community, but to make it sound like those "fringe" folks (another non-neutral term) are wacko crackpots. Those who edit this article need to take a look at The Skinny on Fats. Here's a teaser: "These "experts" assure us that the lipid hypothesis is backed by incontrovertible scientific proof. Most people would be surprised to learn that there is, in fact, very little evidence to support the contention that a diet low in cholesterol and saturated fat actually reduces death from heart disease or in any way increases one's life span." This article has 73 references and is CLEARLY much more than unscientific opinion by uninformed "vocal fringe crackpot theorists." Second, peer review is tricky--it is a social phenomenon, not a scientific one. Peer review cannot detect fraud, nor can it catch errors of belief which the reviewers share with the researchers. And it is uniquely powerful in keeping out "fringe beliefs" whether they are that way because they're truly crackpot ones or whether they are good science but unpopular and not with the current fad of "medical consensus." —Preceding unsigned comment added by 76.213.201.56 (talk) 07:32, 7 November 2008 (UTC)

Palm oil and blood cholesterol controversy
It appears this section was orginally copied straight from the palm oil article. There was some confusion about "palmitic oil." (Palm oil or palmitic acid? The two are not identical, palm oil is a mix containing palmitic acid. I looked up the WHO report and it says palmitic acid, not oil.) I tried to verify the sources and rewrote the section based on PubMed references, but I couldn't find a copy of the Vessby paper and it is not on PubMed. Can anyone verify it? - tameeria 23:20, 18 April 2007 (UTC)

This section (aplm oil) feels really out of place and breaks the flow of the argument. How about simply deleting it? Uffish 13:14, 11 November 2007 (UTC)

Freeze in Quotes
Under the section "Lipid hypothesis of cold tolerance" the word "freeze' is double quoted. Why ?  Does the author not accurately understand the melting/freezing point of fats and the variation wrt degree of de-saturation ? This is not some special use of the term freeze, and does not deserve the special interpretation implied by the quotes.  —Preceding unsigned comment added by 173.89.175.101 (talk) 06:21, 18 August 2010 (UTC)

Virchow' defintion?
The article looks like Virchow proposed the defintion of the lipid hypothesis. Glossing over the google books excerpt this is very far from truth, in fact he may have been criticising other researchers for their undifferentiated approach to "atheromatöser Process".. whatever that may have been in the 1860ies. Richiez (talk) 22:52, 5 August 2011 (UTC)

I found this articles which could be used to sketch the early history? Richiez (talk) 22:47, 8 August 2011 (UTC)
 * http://circ.ahajournals.org/content/102/suppl_4/IV-94.full
 * http://pmj.bmj.com/content/76/899/542.extract
 * http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116370/

People who disagree with the hypothesis.
To the list of people who disagree with the lipid hypothesis should be added Mary Enig who is hardly a quack, having been the voice who warned of the problems of trans-fats 40 years or so before the rest of the nation caught up. Mary Enig has documented some pretty horrifying shenanigans by the AHA to force through an apparent consensus for the hypothesis where none existed. A short summary of her views can be found at http://www.westonaprice.org/know-your-fats/the-oiling-of-america with lecture of the same content available at www.youtube.com/watch?v=fvKdYUCUca8 — Preceding unsigned comment added by 75.142.52.46 (talk) 03:50, 14 December 2012 (UTC)


 * Now, really. If you take a good look at westonaprice.org, you will see that it is an advocacy site for "nutrient-dense" foods, by which they mean meat and dairy products. They have a blog named "butter buddies". This is not WP:RS. --  Solo Owl   20:04, 24 August 2013 (UTC) — Preceding unsigned comment added by Eall Ân Ûle (talk • contribs)

Dated consensus
How relevant is a 'dated' scientific consensus. Its of no consequence that in 1978 there was scientific consensus about this hypothesis being probably correct if the hypothesis was falsified long after that time. Like with any hypothesis, its falsifyability is essential to it being a good hypothesis. This particular hypothesis appears to have been falsified this in multiple what appear to be solid and statistically sound scientific experiments. While in any other branch of science a single counter experiment would be sufficient to consider the hypothesis false, in medical science this (for reasons I do not understand) isn't sufficient. In order to proof the claim of consensus, a post-falsification experiment poll might be of consequence. Without a more recent poll, the claim of consensus is an empty one. I would propose this article be stripped of all (apparently unfounded and/or outdated) claims of consensus unless a more recent source of such consensus is provided. — Preceding unsigned comment added by 92.70.45.2 (talk) 13:05, 1 April 2014 (UTC)


 * It's quite difficult for us to declare a scientific consensus in the presence of ongoing respectable, albeit minority, disagreement. Supporters were quite happy to declare a consensus in their favour of course. Maybe we should use the word "orthodoxy" instead? It certainly was that.
 * As for being "falsified", I don't think that's quite correct. There was never one simple "lipid hypothesis", and some things about cholesterol are universally acknowledged. Cholesterol is the main substance that makes up atheromatous lesions. People with hereditary very high cholesterol do have a strong tendency to die young of heart problems. Cholesterol levels are a risk factor associated with the chances of heart problems, at least between individuals within societies, in most major studies, though not always very good between societies. And, in good-quality randomized controlled trials, statins do reduce cholesterol levels and (possibly by other mechanisms) they do reduce the chances of heart attack and (in high-risk groups) all cause mortality. Richard Keatinge (talk) 17:26, 1 April 2014 (UTC)


 * Its not a matter of disagreement, its a matter of the falsifications either being disputed or not. The 'consensus' about the 'hypothesis' is outdated by multiple claims of falsifications (I could provide references if you like). Normaly, if these claims are not disputed the hypothesis would be considered falsified. If there is post-publication consensus about the falsifications being unfounded, than we might again have consensus. Currently there is no talk about the claims of falsification or their disputed state, only about consensus that aparently pre-dates the claims of falsification. There are no arguments about there being correlation, the hypothesis however is about causality. The existence of post-consensus papers (either disputed or not) showing a clear lack of a causal link makes the claim of consensus a hollow one if its based on such a pre-falsification-paper poll. — Preceding unsigned comment added by 2001:980:4962:1:5604:A6FF:FEF1:6202 (talk) 06:21, 2 April 2014 (UTC)


 * References can only be a good thing! We need, I suggest, to be careful what we mean by the "lipid hypothesis". The lede refers to Rudolf Virchow as its originator; looking at the reference the only relevant mention of lipids appears to be "nebstdem kommt eine faulige Schmelzung der Thromben, Bildung von Fettkrystallen und endlich Krebsumwandlung vor." Feel free to improve on my attempt at translation: "afterwards comes a foul melting /fusion of the clot, buildup of fat crystals, and finally development of cancer." It doesn't seem much of a "hypothesis" to me. We really should find a good secondary reference to the start of the idea.
 * We should also find references for what the "lipid hypothesis" actually is. I don't know if anyone has formally stated it but clarity can only help. I note that the reference for a scientific consensus relies on the fact of statins being effective as the crushing piece of evidence, and I'm fairly sure that Virchow, for example, didn't have statins in mind, nor details of particular kinds of dietary fat. Only when we know what the hypothesis is can we really even consider falsifying it, and of course, we are here to report secondary sources, not our own opinions.
 * I look forward to your references and ideas. In the meantime I propose to change the word "consensus" to "orthodoxy" as appropriate. Richard Keatinge (talk) 09:30, 2 April 2014 (UTC)


 * I have tried a little early clarification on the nature of the various hypotheses concerned. Here is a quotation from Duff and Macmillan (http://www.sciencedirect.com/science/article/pii/0002934351900113), just to make clear that they are not making any assertions about aetiology but do describe the pathogenesis from fatty streak onward:
 * "The word “atherosclerosis” is not capable of definition except in descriptive morphologic terms, since knowledge, which may in the future permit a clinical or etiologic definition, is still inchoate. Atherosclerosis denotes a pathologic change affecting the intima of arteries that is characterized by focal thickenings of the intima in which stainable lipids can readily be demonstrated in and between the cellular elements. The larger lesions show, at the one extreme, an almost exclusively fibrous composition with only minimal quantities of lipid material while, at the other extreme, they contain lipid accumulations of massive proportions with extensive necrosis of the central parts of the lesions commonly culminating in disruption of the intimal lining... While opinion has not been unanimous in the past, it is now generally accepted that the so-called fatty flecks or streaks of arteries are the early lesions of atherosclerosis and that they may develop into the more advanced lesions of the disease." Richard Keatinge (talk) 11:50, 2 April 2014 (UTC)


 * I think the most important thing to fix is that the section 'Wide scientific acceptance' lacks neutrality. It uses old pre-falsification-claims consensus amongst 'prominent researchers' and links this to claimed current day 'medical profesional' knowledgability to convey a POV about the critics aparently not accepting 'facts' for almost 40 years. When it states: 'A minority of the medical community still argue that the lipid hypothesis has not yet been scientifically validated as having identified a cause of heart disease', there are multiple falicies at work in that sentence:


 * 1) The medical community exists for a large part of practitioners. In any field, practitioner knowledge will lag that of scientists by many years. This could swing both ways, it could be that today all the scientific specialist are convinced of the validity of the hypothesis, but some practitioners havn't gotten the message yet, or it could mean a large minority or even a majority of the specialist scientists are now convinced the falsification is genuine, but most of the practitioners are, as some claim based on the sheer ecconomic size of the statin market, basing their knowledge on the subject on marketing rather than science.
 * 2) It ignors the fact that not only does a minority (that may be much larger than implied) argue insignificant validation, a minority actualy argues the hypothesis has been falsified.


 * Think of it as a retrile. We have a suspect that has been sentencend for murder many years back, and the case has been promenently in the media. Now the defense prenents new evidence and asks for a retrile. The paragraph is currently like the procecutor would quote the old trile jury and shows the current public oppinion that both show consensus about the defendant being guilty of murder. The procecuror is basically asking the judge to forget about asking the current jury, given that the old jury and the public oppinion together show how the current jury would rule.


 * Based on this, I don't think there is a strong case being presented about current day 'Wide scientific acceptance' or current day 'scientific consensus'. There may still be consensus, but without asking the new jury, and without seriously adressing the independence issues raised by the other side regarding statin revenues, I don't think we can use the current section content in any way to claim such consensus still exists.


 * OK. This is Wikipedia and the "jury" is reliable sources. I have done a major rewrite, ensuring that a primary source (Virchow) is used with suitable caution, that we have unimpeachable definitions from RS for what the lipid hypothesis actually is, and that our text addresses those definitions using the literature appropriately. I hope everyone likes it. Richard Keatinge (talk) 13:03, 4 April 2014 (UTC)

Controversy: independence claims
I'm not fully sure, but many publications that claim falsification of the hypothesis seem to bring up the funding argument. Shouldn't this article hold a short statement of the kind regarding the ecconomic size of the statins market, and the role of statin vendors in the funding of accademic research. This could possibly balance the current overselling of the 'hypothesis is proven' POV in the article. IMO the article should not take sides with the 'hypothesis is proven' POV neither with the 'hypothesis is falsified' POV, and assume both sides to be equally important. Providing a reference regarding the controversy surounding research funding might somewhat ballance the currently rather dismisive tone of the article regarding the 'hypothesis is falsified' POV. — Preceding unsigned comment added by 2001:980:4962:1:5604:A6FF:FEF1:6202 (talk) 08:47, 3 April 2014 (UTC)

4 rather than 2 POVs
I believe there are 4 rather than 2 POVs regarding this hypothesis, and the article should reflect this:


 * The point of view that the hypothesis is still a hypothesis.
 * The point of view that the hypothesis is no longer a hypothesis but is now a proven fact (the POV that currently seems to dominate this article).
 * The point of view that the hypothesis is no longer a hypothesis but has now been falsified (reasoning like in the 'The truth about statins' book and the 'The falicies of the lipid hypothesis' article)
 * The point of view that the hypothesis is currently not a relevant hypothesis as a more likely suspect has been identified (the fructose hypothesis and reasoning like in the 'why we get fat' book)

I think all 4 views should be presented and be treated as equal without being dismisive about any one of the 4. There are significant long term experiments and other arguments and valid scientific reasonings for each one of these 4 POVs, and there are significant groups of scientists, medical professionals and nutritional experts in each \ of the 4 camps to make it clear that the jury is still out on this issue. — Preceding unsigned comment added by 2001:980:4962:1:5604:A6FF:FEF1:6202 (talk) 08:59, 3 April 2014 (UTC)

Other causative factors
What is the point of this section? The sources fails MEDRS (first one is not peer reviewed, is way too old; second fails as a primary study), and what does this have to with the lipid hypothesis? That there are other risk factors doesn't have any direct correlation as to the validity of the lipid hypothesis. If this isn't meant to be a commentary about the validity of the lipid hypothesis, this material is off topic, as it is not meant to be a general discussion of atherosclerosis. Yobol (talk) 16:42, 4 April 2014 (UTC)

Statins
What exactly is the point of this section? That there are other mechanisms besides lipid lowering for statins doesn't mean that the lipid lowering effects of statins are not also important. Yobol (talk) 16:44, 4 April 2014 (UTC)
 * It does not, but it does mean that statin trails that concluded statistically significant correlation between lowering cholesterol levels and lowering heart disease are in fact tainted and should not be considered as (part of) proof for the hypothesis. — Preceding unsigned comment added by 92.70.45.2 (talk) 11:35, 14 April 2014 (UTC)

Statins and sugar
Yobol asks what these issues have to do with the lipid hypothesis. This is a good question, and thanks also for removing the overciting - I'd normally leave all the refs in after a big edit, but only temporarily. In fact the refs could do with a bit more pruning.

Other possible mechanisms for the effects of statins are relevant because the fact that they work has been taken as proof of the lipid hypothesis - which it isn't necessarily. Just to make the point that there are other hypotheses, it may be worth making some brief comment about risk factors other than lipids; Cleave is a classic, to which I've added a much more recent citation.

I haven't seen the movie Fat Head (documentary), but it does seem to be some part of the popular presentation of the lipid hypothesis. I've left it out for the time being, but perhaps it justifies a See Also?

I look forward to your comments. Richard Keatinge (talk) 17:27, 4 April 2014 (UTC)
 * See my question above. The point being, that the statins have other possible mechanisms of affecting athrogenesis doesn't mean that lipid lowering is also an important mechanism. This is classic WP:SYNTH; the article is presenting other mechanisms to suggest it doesn't work through lipid lowering mechanism, when that is not what the source itself says (the source appears to suggest that statins work better than expected than through lipid lowering alone, not in spite of the lipid lowering mechanisms, as it appears the article is implying. In effect, we are using a source that says nothing explicitly against the lipid hypothesis to support the position it might not work, which would seem to be dishonest. Yobol (talk) 17:35, 4 April 2014 (UTC)


 * To quote the ref "Statins, were initially designed as cholesterol-lowering drugs. However, these drugs, besides their lipid-lowering properties, exert a number of protective effects on the cardiovascular system that emerged over the past years. The benefits observed with statin treatment appear to be greater than that might be expected from reduction in lipid levels alone, suggesting effects beyond cholesterol lowering. These cholesterol-independent effects have been called “pleiotropic”. The cholesterol-independent or “pleiotropic” effects of statins involve improvement of endothelial function, stability of atherosclerotic plaques, decrease of oxidative stress and inflammation, and inhibition of thrombogenic response. These pleiotropic effects of statins have been proposed as key properties of these drugs to reduce cardiovascular morbidity and mortality." Our report is at present "Statins also reduce other mechanisms that are a major part of the process of atherogenesis; these have been postulated to be at least part of the mechanisms by which statins reduce heart disease." That strikes me as quite a good encyclopedic sentence, honest and free of WP:SYNTH, but would you like to suggest some other form of words? Richard Keatinge (talk) 18:06, 4 April 2014 (UTC)
 * Besides the phrase "Statins also reduce other mechanisms" does not seem grammatically correct to me, I'm still wondering what the point of mentioning statins have other possible effects on atherosclerosis on this page is. How exactly is that sentence related to the lipid hypothesis? Why are we mentioning it at all here (this material is relevant in statins, where it already exists)? Yobol (talk) 18:13, 4 April 2014 (UTC)
 * There are alternative mechanisms, not dependent on the lipid hypothesis, by which statins may produce their observed effects. I've had another go at it: "Statins also have effects on other processes thought to be important in the development of heart disease; these have been postulated to be at least part of the mechanisms by which statins reduce heart disease, over and above the reductions expected from cholesterol-lowering effects." Any better? Richard Keatinge (talk) 18:29, 4 April 2014 (UTC)
 * No, what is the point? Statins may have many mechanisms by which it works. How is this relevant on this page? Detailed discussions about the mechanisms of statins occurs in statin, why is it here? Yobol (talk) 18:34, 4 April 2014 (UTC)
 * Without going into the actual mechanisms of statins, which I agree we don't need to do here, it makes the point that the fact of statins working does not necessarily imply the exclusive correctness of the lipid hypothesis. Richard Keatinge (talk) 18:57, 4 April 2014 (UTC)
 * So you are using a source that does not in any way discount the lipid hypothesis to imply that the lipid hypothesis is not necessarily correct? How is that not WP:SYNTH? Yobol (talk) 19:00, 4 April 2014 (UTC)
 * The source says "The benefits observed with statin treatment appear to be greater than that might be expected from reduction in lipid levels alone, suggesting effects beyond cholesterol lowering." I don't see that we are going beyond our source. We could make it all more explicit, perhaps adding, say, ? Richard Keatinge (talk) 19:24, 4 April 2014 (UTC)
 * The source says there are effects that might be there on top of the lipid lowering effects. It does not in any way create doubt about the lipid lower effects, which is the implication you are trying to make. It cannot be used in this manner, per WP:SYNTH. Journal of American Physicians and Surgeons is not a reliable source for medical claims, so that is not an appopriate source. I will remove the statin section per WP:SYNTH until an appropriate source is found.  I will also remove the "sugar" section per the same rationale. Yobol (talk) 19:33, 4 April 2014 (UTC)
 * You're right about JAPAS, I should have checked further. And I suppose there's an argument for removing all other hypotheses about atherosclerosis from this article - bearing in mind that they're not all in competition either with each other or with the lipid hypothesis, nobody disputes smoking or exercise as important and probably causal risk factors, and inflammatory mechanisms, plaque rupture, and so on, are fairly well established. As far as I know, nobody has ever suggested that the lipid hypothesis is the only risk factor or causal mechanism in atherosclerosis, but we probably don't need to mention the others. Anyway, I have tweaked your wording a little - mainly, removing mention of inflammatory processes as the only alternative to lipids. I have also given the other biological lipid hypotheses their own heading, I'd suggest as an intermediate step to their own stub articles and disambiguation page. Richard Keatinge (talk) 20:57, 4 April 2014 (UTC)
 * Given that the statistical significance of effect of statins (lowering both cholesterol and heart disease), information that decouples the two effects is very much relevant to the article. Statin trails have long been used as proof of the hypothesis, showing a statistical significant correlation between lowering blood cholesterol and suffering from heart disease that the hypothesis predicts. Showing that the two effects are in fact (partialy or completely) unrelated basically reduces what used to be solid proof to statistically inconclusive. — Preceding unsigned comment added by 92.70.45.2 (talk) 10:40, 14 April 2014 (UTC)
 * I tend to agree but we do need reliable sources that say so. On thinking about it, I also suggest that we should keep this article tightly focused on its subject. The place for a more comprehensive discussion, or at least systematic mention of all the main ideas, might be Atherosclerosis. Richard Keatinge (talk) 13:27, 14 April 2014 (UTC)

Widespread acception nonsense
The "Widespread Section" is problematic.

1. The 1978 study questions are seriously flawed and ridiculous. "Do you think there is a connection between plasma cholesterol level and the development of coronary heart disease?" does not imply you think that coronory heart disease is caused by plasma cholesterol levels if you answer yes to the question, since it can also be the case that the scientists think that coronary heart disease causes a rise in plasma cholesterol levels, and not the other way around, or simply that there is no causal relation at all. Even opponents of the lipid hypothesis think that cholesterol levels have something to do with cardiovascular disease. "Do you think that our knowledge about diet and coronary heart disease is sufficient to recommend a moderate change in the diet for the population of an affluent society?" This question only implies that a change in diet should happen, not what change or what the aim of this change in diet is or whether that change even has anything to do with cholesterol. This is not proof of "widespread acceptance" in any way.

2. The 1984 study is about only 14 researchers thus very irrelevant. 14 researchers from thousands is not considered statistically relevant nor proof for something to be "widely accepted".

3. It should be noted that even if the lipid hypothesis were to be considered widely accepted 30-40 years ago, that is no indication that it is widely accepted today.

4. Since 1984 there have been a lot of scholars that have started to doubt the Lipid hypothesis. Robert Lustig, Uffe Ravnskov, Gary Taubes, etc. Ravnskov and Taubes won prizes for their research. Even a BMJ editor, Richard Smith thinks it's a load of bullshit.

Since the sources of this subsection are either total crap or heavily outdated, I will remove it per WP:BOLD. And put the latest sentence, which seems to be better sourced, at the previous section since it goes there well. Feel free to disagree, but I ask you to rewrite the section instead of reverting my edit. 09I500 (talk) 18:37, 20 December 2014 (UTC)

Dated refs
Much of the dispute discussion seems to be based on outdated refs. Particularly egregious are instances of older papers used to support assertions that they contradicted newer ones. This is blatant wp:OR. LeadSongDog come howl!  02:35, 21 May 2016 (UTC)

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Lack of papers from 2016 to 2018
This article needs an update. Many of the sources are 1980s up until 2006. I will see if I can help, but needs an expert on the subject. Skeptic from Britain (talk) 11:12, 2 December 2018 (UTC)


 * This is recent "Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD." Skeptic from Britain (talk) 11:24, 2 December 2018 (UTC)

This paper here seems to suggest the contrary: https://www.amjmed.com/article/S0002-9343(18)30404-2/pdf — Preceding unsigned comment added by 96.233.56.141 (talk) 22:04, 15 April 2019 (UTC)

External links.
There are six entries in the "External links" and five are for Steinberg D. If these links can't be incorporated into the article the list needs to be trimmed. Three or four links are more than enough and too many is link farming. 10:10, 6 December 2018 (UTC)

This cannot conform to NPOV nor properly citing claims passed off as fact
"An accumulation of evidence has led to the acceptance of the lipid hypothesis by most of the medical community.[3] A small number of "cholesterol skeptics" take a contrary position, falsely claiming that heart disease is not caused by cholesterol, and demonizing the cholesterol-lowering drugs statins.[4] "

Really, "falsely claiming", "demonizing"? It doesn't even list any example of who does this, when, how or anything. (source does though the accusations here does not match what the source says, and the source deals with one person - which is clearly not everyone who may hold this hypothesis to be flawed.) This is clearly a biased opinion-based claim, and an absolute blanket statement to boot. It does not conform to NPOV in the slightest and obviously do not belong. 81.228.169.227 (talk) 21:16, 16 June 2019 (UTC)

✅ Checked the source (which is reliable), what we have seems like a good summary. Alexbrn (talk) 06:47, 17 June 2019 (UTC)

Article quality
This article is incredibly uninformative. It lacks basic details surrounding the science, and deliberately works to minimize detractors while neglecting to include broader, much more pertinent criticism. As such, I've tagged the article for a full rewrite.  —  C M B J   02:28, 29 June 2020 (UTC)
 * Adding to that, the text at Seven Countries Study is of very poor quality, but with some modifications for context, would still be much more informative than what's presently here right now.  —   C M B J   02:45, 29 June 2020 (UTC)

"Most of the medical community"
I'm a bit skeptical of the sourcing on the lede, specifically in regards to the statement that "An accumulation of evidence has led to the acceptance of the lipid hypothesis by most of the medical community." I don't deal with medical articles often but it feels like putting such a statement in wikivoice would require a bit more than 3 citations. Deku link (talk) 02:43, 2 May 2021 (UTC)
 * The problem is not the quantity of citations but the quality. All three argue some form of "Lowering LDL-cholesterol with statins reduces risk for cardiovascular events, providing ultimate proof of the cholesterol hypothesis" (with this being a direct quote of the last cite) when that argument is simply not sound.  The premise, that statins reduce risk, is more or less proven, but it does not follow that that proves the hypothesis.  What would prove the hypothesis is lowering LDL-cholesterol by any means not just statins.  An alternative argument, that people genetically predisposed towards high cholesterol such as those with familial hypercholesterolemia are at unusually high risk (or those genetically predisposed towards low cholesterol are at low risk) also doesn't prove the hypothesis in a pragmatic sense which would be that most people with high cholesterol will reduce their risk by taking cholesterol lowering drugs.  This article also currently overweights the view of a single group, namely the European Atherosclerosis Society, presenting its view as the global consensus.  I've left the consensus statement stand for the moment but added a citation to the New York Times which deals much more comprehensively with the various issues than this Wikipedia article as currently written.  Including another NYT piece the NYT has made the observations I've made above such that this is not original research on my part.--Brian Dell (talk) 18:46, 20 July 2021 (UTC)


 * The mechanism is irrelevant for the lipid hypothesis and does not need to be specified although most would certainly specify the mechanism. The lipid hypothesis is accepted by nearly all in the medical community and all public health agencies around the world. Hardly anyone in medicine disputes the fact that high blood cholesterol is a significant causative factor in atherogenesis. What is sometimes debated is the mechanism of this and how it can come about. So you can accept the fact of the lipid hypothesis but dispute the mechanism although there is a consensus on this as well. But hardly anyone apart from a few cranks (THINCS) dispute the fact of the lipid hypothesis.
 * Daniel Steinberg has a good definition: "The lipid hypothesis proposes specifically that a high level of cholesterol in the blood is a significant causative factor in atherogenesis and its clinical expression. It does not specify the nature of the hypercholesterolemia nor how it was brought about. It might be the result of genetic defects in lipid or lipoprotein metabolism; it might be the result of an endocrine disorder; or it might be the result of a diet that raises blood cholesterol levels".
 * There are a lot of papers that examine the role of oxidized LDL in atherosclerosis and the mechanism behind this. We can expand the article but mechanism does not need to be specified for one to accept the lipid hypothesis. This needs to be made more clear on the article. Obviously we need to expand more on the history of the lipid hypothesis. Psychologist Guy (talk) 13:01, 24 July 2021 (UTC)
 * If you've got no evidence for your proposed causal mechanism then all you've got is correlation. Which of course is not causation.  Where are the RCTs showing nonstatin lipid-lowering therapies reduce cardiovascular events?  Correct me if I'm wrong but the article makes no mention at all of the fact the ACC/AHA guideline on the treatment of blood cholesterol was changed in 2013 because of this lack of evidence.--Brian Dell (talk) 05:47, 27 July 2021 (UTC)
 * The 2013 comments about statins and LDL you have found are not relevant because they do not mention the lipid hypothesis. What you have added to the lead is a 2013 opinion piece in the New York Times which talks mainly about statin therapy it does not mention the "lipid hypothesis" so you are adding original research. The lipid hypothesis holds that high blood cholesterol is a significant causative factor in atherogenesis it is not up to us to debate the mechanisms of this on the talk-page here. I don't think we should start adding references that do not specifically mention the lipid hypothesis to the article and certainly not opinion pieces from a newspaper. Psychologist Guy (talk) 16:38, 27 July 2021 (UTC)
 * The cite is NOT an "opinion piece". If this isn an opinion piece then everything in the New York Times is an opinion piece.  It's a news article from a reliable source and apparently none of you can actually challenge what it reports so you're reduced to trying to dodge it by claiming the material you won't substantively engage with is from an unreliable source.--Brian Dell (talk) 16:58, 28 July 2021 (UTC)
 * Also, why does a source have to specifically "mention" the two words you've put in quotes there, "liquid hypothesis"? You've policed all the currently cited sources to ensure they use that exact term?  Does this article not define it as "postulating a link between blood cholesterol levels and the occurrence of cardiovascular disease" and does the cited reliable source not have something to say about that when it says "Drugs that only reduce LDL have not been shown to be effective in preventing heart attacks"?--Brian Dell (talk) 08:28, 1 August 2021 (UTC)
 * I was apparently reverting at the same time as XOR'easter so my edit summary is missing. My rationale: That is the lead of the article.  The other sources are higher quality and some even more recent than 2013 which is a bit old.  WP:MEDRS also matters.  This would be more relevant in a "management" section (this is currently missing); still, better and more recent sources would be available.  — Paleo  Neonate  – 19:23, 27 July 2021 (UTC)

Hypothesis IS NOT a theory
I can't undesrtand the first sentence! What's that even mean? When an hypothesis become a theory? It is clear in Wikipedia that science doesn't care no more. — Preceding unsigned comment added by 181.209.83.194 (talk) 07:31, 22 July 2021 (UTC)


 * It started out as a hypothesis. It became a theory over time because a lot of evidence supports it. It is no different than the general theory of relativity which was at one time a very weak hypothesis but is now accepted by the majority of the scientific community because it has been repeatedly tested and confirmed from experiments and observations. Psychologist Guy (talk) 13:10, 24 July 2021 (UTC)
 * My impression is that the general usage of theory is used here, that is acceptable to describe a hypothesis (since a scientific theory generally refers to an explanatory model, often resting on a number of working hypotheses, accumulated knowledge and data sets, practical formulas including for prediction, etc)... — Paleo  Neonate  – 03:54, 7 August 2021 (UTC)

Canadian Cardiovascular Society
,, , , ,

Content about the Canadian Cardiovascular Society has recently been added in the "dissenting views" section which is sourced to their 2021 guidelines. We can get full access to their 2021 guidelines, I highlight the following from the guidelines of which part was added to the article:

"'Previous versions of these guidelines have used LDL-C as the primary laboratory measurement for considering initiation of statin treatment and as a treatment target in low, intermediate and high-risk individuals. Beginning with the 2012 Guidelines, it has been recommended that non-HDL-C and ApoB could be used as alternate targets to LDL-C in any individual with triglyceride level > 1.5 mmol/L. The rationale for this is that above this level of triglyceride, some cholesterol in LDL particles is replaced by triglyceride, which promotes production of more atherogenic small dense LDL particles, and makes the amount of cholesterol in LDL-C an unreliable reflection of LDL particle number. In addition, other particles, such as remnants of chylomicrons and very low density lipoprotein (VLDL), as well as Lp(a), all accumulate in the artery wall and contribute to atherogenesis, whereas HDL-C does not. Therefore, estimation of the concentration of all atherogenic particles requires a broader focus than a measurement of LDL-C. Both non-HDL-C (indirectly) and ApoB (directly) provide a more accurate assessment of the total concentration of atherogenic particles than LDL-C. Non-HDL-C and ApoB are, for this reason, both better predictors of CV event risk and benefit of lipid lowering therapy when compared to LDL-C. Based on these previous recommendations, non-HDL-C is now routinely reported across Canada at no additional cost, based on the simple calculation of total cholesterol minus HDL cholesterol.'"

The above content does not challenge the lipid hypothesis, they are merely calling for advanced lipoprotein testing that goes beyond LDL-C. They say that Apolipoprotein B (apoB) may be more useful than LDL-C in coronary heart disease (CHD) because it captures greater information about atherogenic particles. ApoB is the main protein found in low-density lipoproteins (LDL). The same lifestyle measures that lower LDL cholesterol will lower ApoB. Apolipoprotein B (ApoB) is basically just an alternative LDL measure that gives us more detail.

This debate has been around for a few years now but even ApoB advocates admit that LDL-C is still an accurate predictor for CVD in many cases (up to 85%). I don't know about other countries but in the UK LP(a) is not routinely measured in general medical practice. , there are various reasons for this. Advanced Lipoprotein Tests are not routinely used in clinics they are impractical in some cases. Psychologist Guy (talk) 23:44, 5 August 2021 (UTC)

I do not oppose mention of apoB, there is even another review here but I am not convinced this challenges the lipid hypothesis and we now have this content in the "dissenting views" section directly below a bunch of quacks who work for the THINCS group. It seems random topics are being thrown together in that section. That section is very badly organized but I agree the article does need fixing but this is not the way to do it. What do other users suggest? Psychologist Guy (talk) 23:44, 5 August 2021 (UTC)


 * I like "quack" sections generally since in theory they should allow getting some more content into articles under a less demanding sourcing standard as it would be appearing appropriately weighted, criticized (if editors wish to add criticisms) and in context. That concept doesn't seem to carry any water with editors like, though, given his practice of reverting on sight all published research regardless of quality that doesn't take the form of a review.  I ended up calling this section "dissenting" because I felt non-endorsement of the "consensus" as stated should be treated rather less prejudicially as "dissent" as opposed to quackery or exclusive to THINCS.
 * I suggest the problem is defining the hypothesis in the "consensus" section solely in terms of LDL. It seems there was fairly adamant opposition to my adding "Drugs that only reduce LDL have not been shown to be effective in preventing heart attacks" to the article and my "dispute over whether... to particular target levels has been shown to prevent heart attacks" edit yet "no clear target to which LDL-C or non HDL-C or ApoB levels should be lowered is clearly identified in RCTs" is a similar sort of statement in my view, just more nuanced.  If you don't broaden the definition of what constitutes the consensus view or add nuance I think it remains necessary to note that the notion that LDL-C level is the metric most closely related to mortality risk is subject to legitimate dissenting views.  See also remnant cholesterol.  Rewrite the consensus view and the way criticism to the Ravnskov study is expressed in order to bring the Canadian guidelines into the consensus and the Canadian guidelines would no longer need to be classed as dissenting!--Brian Dell (talk) 20:49, 6 August 2021 (UTC)
 * What currently remains is this: https://www.onlinecjc.ca/article/S0828-282X%2821%2900165-3/fulltext how is this dissenting to the link between elevated blood lipids and heart disease risk? "those with low-density lipoprotein cholesterol ≥ 5 mmol/L, statin therapy continues to be recommended", "Lipoprotein(a) measurement is now recommended once in a patient's lifetime, as part of initial lipid screening to assess cardiovascular risk", "Health behaviour modification, including regular exercise and a heart-healthy diet, remain the cornerstone of cardiovascular disease prevention." — Paleo Neonate  – 04:14, 7 August 2021 (UTC)
 * I also see no conflict between these select snippets and the "consensus".--Brian Dell (talk) 08:13, 7 August 2021 (UTC)
 * Then why is this source used to support statements in the "dissenting" views? "the best measure of cardiovascular", who claimed that it was the most important reason anyway?  My impression is a misrepresentation of the source to claim that a link is seriously in question.  — Paleo  Neonate  – 05:36, 8 August 2021 (UTC)
 * Because what you've quoted on this Talk page is not on the table here but what is quoted in the article. If I cite a particular source to say someone is X years old have I misrepresented the source if the thesis of the source concerns something other than the person's age?  The details matter here.  I see no reason to read into this edit more than is there... it doesn't say it rejects the lipid hypothesis, it simply says what it says which is a limited statement.  It dissents on a narrow, particular point: The "consensus" claims LDL is the best measure because no other measure is mentioned.  Why do do you want to delete this reliably sourced material when you could just broaden the definition of the consensus so that it doesn't solely revolve around LDL?  Is it not generally agreed that the "lipid hypothesis" does not stand ot fall on LDL levels?  I don't understand why you can't concede anything on LDL's primacy.--Brian Dell (talk) 02:31, 11 August 2021 (UTC)
 * Just please be sure not to use unreliable medical sources to air biomedical claims (as here). There are ample really good sources in this topic area, so no need to stoop. Alexbrn (talk) 05:38, 7 August 2021 (UTC)
 * Question: if all the research in the world is "unreliable", how are guidelines based on that research reliable? If the argument is we don't know which research is unreliable until we see guidelines developed and/or reviews done, that'd be understandable, but that's not your position, your position being that you KNOW that this RCT I cited is "unreliable" and if I cited any other RCT that'd be "unreliable" too.--Brian Dell (talk) 08:00, 7 August 2021 (UTC)
 * What is unreliable in the context of Wikipedia editing (where the goal is to reflect accepted knowledge ) is useful in the hands of experts, who can sift, analyze and synthesize to create that accepted knowledge, and publish it in secondary/tertiary sources, where it becomes of use to us. RCTs are "unreliable" for us in part because Wikipedia editors are prohibited from assessing their worth. Alexbrn (talk) 08:07, 7 August 2021 (UTC)
 * Looks to me like you assessed the worth of this RCT, which finds no association between LDL cholesterol and cardiovascular disease, when you declared it "unreliable". I'll add that I find it a little odd that you are citing a policy that says "Deciding whether primary, secondary, or tertiary sources are appropriate in any given instance is a matter of good editorial judgment and common sense, and should be discussed on article talk pages" when you see no role for either editorial judgment or Talk page discussion when you encounter a citation like this.--Brian Dell (talk) 08:25, 7 August 2021 (UTC)
 * WP:MEDRS gives specific guidance on what sources are reliable for WP:Biomedical content. Alexbrn (talk) 08:34, 7 August 2021 (UTC)
 * We must be reading different versions because where I see "often" you apparently see "always" and where I see "Ideal sources" you apparently see "The only reliable sources". The RCT at issue here is from December 2020 (so not considered by the sources presently cited for the current state of knowledge) and I find "If conclusions are worth mentioning (such as large randomized clinical trials with surprising results), they should be described appropriately as from a single study" whereas you seem to find conclusions are not worth mentioning and may not be described.--Brian Dell (talk) 09:37, 7 August 2021 (UTC)
 * There's some bold text in the lede you should pay attention to, and WP:MEDFAQ has some additional background. If in doubt, ask at WT:MED. Alexbrn (talk) 10:56, 7 August 2021 (UTC)
 * Not sure why you refer to MEDFAQ when "Primary sources aren't completely banned" explicitly contradicts your position. This particular situation is a rather classic example of the uncommon situation where a mention may be appropriate in that it may render the currently presented state of knowledge obsolete. Not saying inclusion is obvious, I'm rather saying it's not "obviously unreliable" and is worthy of discussion as opposed to a knee-jerk rejection.  The context of where this appears is critical and the context here happens to be "having established the consensus view, not all specific elements of the consensus view are beyond controversy, so looking briefly at the other direction, we find this and that (such as Ravnskov, DuBroff, etc), which has this or that problem, problems which may include being preliminary and not guaranteed to stand the test of time".  If you argued undue weight (something that's rarely universally obvious) instead of "obvious unreliability", that would be much more convincing, not least because you do not actually know that it is unreliable under the common meaning of "unreliable".--Brian Dell (talk) 20:46, 7 August 2021 (UTC)
 * It's an obvious case. The source is not reliable for any assertion about biomedicine. If in doubt, ask at WT:MED. Alexbrn (talk) 05:41, 8 August 2021 (UTC)

Wikipedia medicine discussion
https://en.wikipedia.org/wiki/Wikipedia_talk:WikiProject_Medicine#Saturated_Fat,_shifting_consensus,_Cardiovascular_disease_(CVD)_,_and_general_health. Please feel free to participate. Thank you! FrederickZoltair (talk) 00:53, 15 August 2021 (UTC)

Mechanism?
So you are telling me, that scientists haven't found exact mechanism that would trigger cholesterol to build up and plaque the arteries, yet they somehow believe that just its high levels somehow lead to cardiovascular disease? On what basis? On just correlation? Correlation is not causation. The article doesn't explain about exact mechanism, so either my assumption is right, or this segment is missing.


 * The mechanism is discussed in the medical literature on this topic but that information is missing from the article. This is a very terrible article it needs a massive update with a section on the mechanism, I agree with Brian Dell we need a big update on this article. I would like to update the article at some point this year but it will takes days to complete. Psychologist Guy (talk) 23:51, 15 August 2021 (UTC)

Recent blanket removal
These sources have been on the cholesterol article for some time and it would need more arguments than "quackery sources" to blanket remove the entire paragraph. Altanner1991 (talk) 01:52, 8 April 2022 (UTC)


 * Where are they on the cholesterol article? You may be confused because those sources are not on that page. Many of those are unreliable primary sources, they fail WP:MEDRS Psychologist Guy (talk) 01:56, 8 April 2022 (UTC)


 * It seems you have been trying to add this same crap two years ago . The sources fail MEDRS. They are not good sources to be citing. I am not sure why you think we should include them. Psychologist Guy (talk) 02:00, 8 April 2022 (UTC)


 * Well uh it *very* clearly says in the edit summary from those Two years ago that it is being moved from the cholesterol article... umm so don't say that ok??!! Altanner1991 (talk) 02:12, 8 April 2022 (UTC)
 * Well they were from the cholesterol article. Altanner1991 (talk) 16:30, 8 April 2022 (UTC)
 * Why do you think the content was removed? It was likely a vandal or fringe pusher who added such content. The content was removed because it is unreliable or sources taken out of context. I can't be bothered right now to go through the cholesterol article and see who added it two years ago but the information is incorrect and many of those sources fail Wikipedia policy. The content has not been on Wikipedia for years, so I am not sure why you are putting it back on now on a different article.


 * Part of the text you added was "Recent meta-analysis has questioned the rigor of previous research on the effect of dietary cholesterol on cardiovascular disease risk, noting that dietary cholesterol had little impact on blood cholesterol level in about 60% of people" . This is a reliable source but it is not recent, it is from 2015. I have read over the paper. Nowhere does it say dietary cholesterol had little impact on blood cholesterol level in about 60% of people. I read over the conclusion of the paper in full, near the end it notes "In conclusion, the effect of dietary cholesterol on incident CAD and serum cholesterol outcomes remains unclear. In-tervention trials showed a statistically signiﬁcant increase in total,LDL, and HDL cholesterol when comparing intervention doses of 500–900 mg/d dietary cholesterol with control doses. . So what you are adding is a false citation, the paper calls for further research on the topic and notes the outcomes are "unclear" due to lack of methodologic rigor. It is obvious you are not reading over the sources you are citing. They were deleted for a very good reason. Just because these sources were on the cholesterol article two or three years ago is not a valid reason to re-add them here. Psychologist Guy (talk) 02:18, 8 April 2022 (UTC)


 * Sorry I think I didn't explain myself properly. These portions had been removed from the cholesterol article only by me to put them on this article. And aside from your analysis of the studies' methods, what about these sources is any less reliable than the others on the page? Altanner1991 (talk) 16:33, 8 April 2022 (UTC)


 * You are entirely correct regarding WP:MEDRS, thanks. Altanner1991 (talk) 17:26, 8 April 2022 (UTC)
 * I have restored but marked as deleted a reply above which was modified non transparently after it was replied to [//en.wikipedia.org/w/index.php?title=Talk:Lipid_hypothesis&diff=1081628688&oldid=1081543857]. I have left the modified reply intact except dating it according to when this modification was carried out. [//en.wikipedia.org/w/index.php?title=Talk:Lipid_hypothesis&diff=1082119582&oldid=1081636036] Nil Einne (talk) 12:39, 11 April 2022 (UTC)

Ansel Keys
I think it should be made more clear that Keys put forward the lipid hypothesis in order to protect sugar from coming into the spotlight. He was a sugar industry man. SCIdude (talk) 11:08, 26 September 2022 (UTC)