Talk:Cholesterol

misc

Haven't the AMA guidelines been updated to include minium HDL levels of 40mg/dl of serum (blood)? Kstailey I love joe harry frederick thompson

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Since it is likely that many people will come to this page because they have high cholesterol, is it reasonable to include a checklist for lowering cholesterol? e.g.

The American Heart Association suggests the following steps to reduce cholesterol levels:

• Watch your caloric intake by eating a wide variety of foods low in saturated fat and cholesterol.
• Eat at least five servings of fruits and vegetables every day.
• Eat six or more servings of cereals, breads, pasta and other whole- grain products.
• Eat fish, poultry without skin and leaner cuts of meat instead of fatty ones.
• Eat nonfat or 1% milk dairy products rather than whole-milk dairy products.
• Enjoy 30–60 minutes of vigorous activities on most (or all) days of the week.
• Maintain a healthy weight.

These 7 points are copied verbatim from a page linked from the American Heart Association page that this article already links to. In theory people can find it, but only if they follow the external link, scroll to the bottom, and follow the next link. (Perhaps we can't include these for copyright reasons, even though it is fully attributed and not very large? I'm not sure of the limits on fair use.) Nanobug 18:54, 12 Nov 2003 (UTC)

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Total cholesterol to any other cholesterol ratio is unit-less, so why is it expressed in mg/dl? This needs clarification. Geoff97 21:32, 1 Jan 2004 (UTC)

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The quantity of cholesterol in foods is clearly wrong. Egg yolks can't have cholesterol 1234 mg/g, as that would be more than 100% cholesterol. A quick search on the internet implies that this is off by a factor of 100, but I have no good data source I can cite. --David Manthey 16:36, 15 December 2006 (UTC)

The Great Cholesterol Con (book)

Source[1] This book talks about a Cholesterol conspiracy theory.--Can Not 21:34, 30 October 2007 (UTC)

Units

http://www.fatfreekitchen.com/cholesterol/cholesterol_units.html

This page gives conversion to mmol/L data. How about we mention the European units as well? JFW | T@lk 19:59, 15 Apr 2004 (UTC)

Cholesterol intake

On suggestion, this has been removed from the Rosuvastatin article:

Roughly 50% of the body's cholesterol is derived from dietary sources, while the remaining 50% is from this de novo synthesis.

yet on the same page, "Normal healthy adults synthesize cholesterol at a rate of approximately 1g/day and consume approximately 0.3g/day." Is 23% "roughly 50%", or is there something else going on here? Furthermore, the page indicates that synthesis varies to maintain a "relatively constant level of cholesterol in the body (150 - 200 mg/dL)", indicating that changes in dietary cholesterol should have a minor effect on serum cholesterol, i.e. that cholesterol consumption is a non-issue. I've seen mention of similar effects in other lit reviews. Evidence suggests, to me, that dietary cholesterol should only be mentioned as to the effect that it has to reduce synthesis. Heresiarch 18:28, 28 June 2006 (UTC)

Perhaps it would be appropriate to change the synthesis section to emphasize proportions of cholesterol obtained from internal synthesis and dietary intake rather than specifically stating milligram amounts? Courtland 14:09, 2005 Mar 26 (UTC)

The Cholesterol Myth

The section on atheromatosis is utterly wrong. It ought to be excised. A dicussion of *why* it is wrong would not even belong on this page: imo there should be a link to a separate page on "The Cholesterol Myth."

Cholesterol Myth

I am uneducated about cholesterol, but wondered if anyone who knows more read this article by Uffe Ravnskov, M.D., Ph.D.? The Cholesterol Myths - Section 1 At least as he puts it, it's bad science to claim HDL- and LDL- cholesterol levels have any correlation whatsoever to atherosclerosis and CHD. I'm out of my league so I'll just see if this piques anyone's interest or offers further insight. --TheRedFall 00:09, 20 August 2006 (UTC)

It seems to me that cholesterol is a symptom of heart disease rather than a cause.

Why would heart disease cause high cholesterol? Also: it is known that patients with familial hypercholesterolemia, a well-understood genetic form of high cholesterol, develop heart disease at a young age. How do you explain this? JFW | T@lk 23:20, 14 July 2005 (UTC)

Some patents with FH die from CAD; about 3% of those under 40 over a 5-year period. However, FH is generally under-diagnosed, and diagnoses are biased towards those with personal or familial histories of vascular disease. Valve deformaties are also common among those with FH, and so atherosclerosis alone is not the sole nor major cause of CAD deaths among FH patients (Sijbrands EJG et al. BMJ 322). If serum cholesterol alone is causal, then I reckon that it can't be too causal. (NB I've indented this further than the below anon reply to separate it. -Heresiarch)

"Cholesterol is not the cause of heart disease but rather a potent antioxidant weapon against free radicals in the blood, and a repair substance that helps heal arterial damage (although the arterial plaques themselves contain very little cholesterol.)."

"High serum cholesterol levels often indicate that the body needs cholesterol to protect itself... just as a large police force is needed in a locality where crime occurs frequently, so cholesterol is needed in a poorly nourished body to protect the individual from a tendency to heart disease and cancer. Blaming coronary heart disease on cholesterol is like blaming the police for murder and theft in a high crime area."

http://www.westonaprice.org/knowyourfats/skinny.html#chol

Good. That is in contradiction with what basically every health researcher in the area believes. You have also not addressed my point that patients with LDL receptor mutations develop severe cardiovascular disease despite healthy lifestyle. JFW | T@lk 23:22, 13 February 2006 (UTC)

No, actually it isn't in direct contradiction. Health researchers believe that high serum cholesterol levels lead to heart disease. They are claiming a causation. However, it is simply a correlation. How do people lower their serum cholesterol levels? By eating healthy, whole, natural foods such as oatmeal, etc... It wasn't their high cholesterol that was increasing their risk of heart disease, it was their poor diet. Reducing your serum blood cholesterol does reduce your risk of heart disease, not because it's the cause, but rather because it signifies poor general health. Secondly, I didn't address your "point" about familial hypercholesterolemia because it is a genetic mutation and therefore does not represent, in any way, the general population. We are talking about regular people with high cholesterol. familial hypercholesterolemia causes a malfunction of the liver. The excess LDL oxidizes in the blood and accumulates in macrophages in the arteries and tendons because it is not cleared out. Normal people would not have this happen, even if they had high serum LDL, because it would be cleared out at the regular rate. Also, isn't LDL the "good" cholesterol? HDL is the one we're told causes heart disease. Lastly, you indicate that these people live a "healthy lifestyle". What does that mean? The media tells us a healthy lifestyle is one low in dietary cholesterol and saturated fat. However, time and again, research has shown that people with what would be considered a diet high in cholesterol and saturated fat by today's standards don't get heart disease. Take the Inuit for example, their diet consists of fish, seal meat, and blubber and yet heart disease is unheard of in their population [Price, Weston, DDS, Nutrition and Physical Degeneration, 1945, Price-Pottenger Nutrition Foundation, San Diego, CA, 59-72]. Why is it that dietary intake of cholesterol and saturated fat has been on a rapid decline for the last 100 years, but heart disease is on a rapid incline? If lowering dietary intake of cholesterol and saturated fat is the cure for heart disease, why isn't it cured? The lipid hypothesis was wrong 50 years ago, and it's still wrong today. Perpetuating it now, 50 years after it was proven wrong, is a disservice. 23 March 2006

Your ignorance is shocking. You claim to know a lot about cholesterol, yet confuse LDL and HDL and fail again to grasp the point that I have been making: in patients with FH, the atherosclerosis is caused purely by high LDL cholesterol. It confirms that LDL is atherogenic, and therefore that there is probably a lot of truth in the "lipid hypothesis".

No, that shows that 'in patients with FH, LDL causes atherosclerosis.' I don't know enough about the biochemistry to know how true that is or isn't.. But what happens in 'FH patients' says 'nothing' (or certainly less than certainty) about what happens in people without it. People with FH have vascular changes and other organ changes early in life (different from non-FH), and have cholesterol deposits in places other than the vascular system as well (again, different from non-FH). The action of cholesterol as a pathogenic factor in FH may suggest a possible mechanism of pathogenesis in people without FH, but it says nothing about whether that mechanism actually happens - there could very well be some regulatory mechanism that is also impaired by the the genes involved in FH.

From what I know, LDL is considered the bad cholesterol and HDL the good. But there are also two (at least) types of LDL (pattern A and B), one of which is worse than the other, at least for some things. Almost no-one has a sub-pattern analysis done. There is also the research on people who have a genetic mutation for large HDL particles having less atherosclerosis than people without [need ref]. Oxidization of LDL in the blood of FH patients and the action of macrophages sounds similar to the changes Dr. Richard K. Bernstein claims happen in uncontrolled diabetes. As for references, I could find them, but excess glycation of LDL particles and receptors (leading to non-activation of said receptors due to particle/receptor shape) seems quite logical, considering we already know about glycation of hemoglobin.. And accumulation of glycated proteins in kidney disease (similar process) has been shown, although I don't have the reference handy.

I have still to hear evidence that anyone takes Weston Price seriously as a nutritional researcher. I've never heard of him outside Wikipedia, and I don't expect I will. JFW | T@lk 15:44, 23 March 2006 (UTC)

http://www.spiked-online.com/Articles/0000000CAE78.htm

http://www.second-opinions.co.uk/cholesterol_myth_1.html

Cholesterol Myth

Dear Dr. Wolff,

Respectfully, I submit that familial hypercholesterolemia should not be seen simply as a disease of high serum cholesterol. This disease involved a dysfunction of the LDL receptor, and is therefore qualitatively different from the general population, not just quantitatively different with respect to cholesterol levels. Thus, it isn't clear whether health defects in this population are due to high serum cholesterol levels, or low intracellular levels, or the necessity of LDL oxidation for cell entry.

To draw an analogy, I would point out that hyperinsulinemia affects memory in exactly the way deficient insulin does, rather than representing a greater magnitude of insulin's effects. There is a similarity in the sense that the serum insulin levels are high in insulin resistance because the insulin can't perform its function properly. Likewise, in familial hypercholesterolemia, the cholesterol can't interact with the LDL receptor appropriately.

Many studies have suffered from failing to classify familial hypercholesterolemia in a category of its own, and instead improperly assimilating this population into the general population, giving false indications of correlations between cholesterol and heart disease.

It's true that familial hypercholesterolemics have much greater relative risks of dying from heart disease in early age, but the number of people who do in the general population is so small that in fact most familial hypercholesterolemics survive this period. The greater the age, the more this increased risk drops in magnitude, until at a certain threshold age familial hypercholesterolemics actually have lower mortality. This might be due to a compensating effect of serum LDL protecting against infection and endotoxin.

User:Mr_Cholesterol August 27, 2005

Your science is fine, but long-term studies simply do not confirm your point. You can create the most fantastic theories about intracellular cholesterol, but it is known that reduction of cholesterol decreases the risk of cardiovascular disease, as supported by the S4, HPS, PROVE-IT/TIMI, TNT and basically every other large study. I'm not sure why you are singling out FH - were we discussing this? Could you cite any studies that document an increase of AD in people with low cholesterol? JFW | T@lk 07:19, 28 August 2005 (UTC)

The argument isn't that CAD happens independent of cholesterol levels, but rather that the relationship is not causal (specifically in the cholesterol->CAD direction). If AD causes high cholesterol levels, or if there is a third, common cause to both, then it would be quite difficult to demonstrate AD in people with low cholesterol. Also, my understanding is that those studies did not show either dose-response or a decrease in all-cause mortality, the former of import for the role that cholesterol plays and the latter for the benefits of statins. -Heresiarch

11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels (over 50 years of age) [PMID: 3560398]

Yes, I was directly replying to your own example of familial hypercholesterolemia. I will get back to you soon with references, but many of the studies showing a decrease in CHD with statins do not show a dose-response relationship to the cholesterol levels, and as the Wikipedia page you edit yourself discusses, statins have numerous effects that would be expected to lower CHD independent of cholesterol. Yes, in fact, AD is associated with decreased levels of cholesterol in brain membranes, brain lipid rafts, and CSF levels. My point wasn't about insulin, but it is quite clear that AD is associated with lower levels of cholesterol in certain areas, which is probably related to the cholinergic systems reliance on membrane cholesterol. ApoE4 might be less efficient at delivering cholesterol to tissues, which is perhaps why it is associated with higher free brain cholesterol and serum cholesterol.

I will supply references for this within a day or two.

Mr. Cholesterol

Fluidity

What does this term mean in this context?

Reply

The polar (water-soluble) hydroxyl group of cholesterol aligns with the polar phosphate heads of phospholipids, while the beginning of the steroid ring interacts with the first few carbons of the fatty acid chains of the phospholipids, acting to partially immobilize them. This acts to grant integrity to the membrane, preventing excessive fluidity. By the same token, membranes very rich in cholesterol are also protected from deficient fluidity because the cholesterol placed between the phospholipids inhibits them from crystallizing. So cholesterol helps to maintain the proper degree of fluidity-- basically, not too liquid and not too solid.

Mr. Cholesterol August 27, 2005.

I.e. pretty much the same as viscosity, which fluidity redirects to. I understand that this can be confusing, though, and will try and make a clarification. // Habj 18:57, 21 January 2006 (UTC)

Plantsterol

On Belgian and Dutch television, Becel, a producer of margarine products and such, has currently commercials running on their pro-active product line. Their products contain a "plantsterol" element that is supposed to reduce cholesterol levels. The ad is very vague, but it is suggested that this is a scientific fact. However, I am not able to find any scientific references of this "plantsterol" element, so I'm wondering whether the commercial is indeed scientifically sound. Most of the information I can find on the net seem to be aimed at either families on one hand, and a business oriented audience on the other. Can anyone confirm the existence of this compound, and if such a thing is for real, should it be added to the Cholesterol page, or elsewhere on wikipedia? --Anthony Liekens 21:08, 7 October 2005 (UTC)

Hm, this Nature article seems to be a good reference. Seems like there's also some information at Sterol ester, but not using the "plantsterol" (or "plant sterol") name. --Anthony Liekens 21:23, 7 October 2005 (UTC)

I would put this info in hypercholesterolemia and not here, as this article is about physiology and links nominally to the pages on high cholesterol. JFW | T@lk 08:43, 9 October 2005 (UTC)

Latest Cholesterol News

Because this subject is an area of science that so much research is going into I felt that people with high cholesterol levels might like to keep abreast of all the latest findings with regards to cholesterol that may be too numerous to put in an article here. I have put a link to a page where the very latest cholesterol research is reported daily on a website Cholesterol Doc as I think it would be a useful resource for people. 81.105.228.63 (talk · contribs)

What makes this site more authoratitive than other sites in this area? I looked it over and was very unimpressed with the quality of the information. What "people with high cholesterol" need is not endless news that some plants make phytosterols that improve TG levels in mice. What these people need is the basics. Every day people are overrun with news until they are so completely lost they give up with healthy living altogether. Please don't reinsert the link. JFW | T@lk 00:16, 16 November 2005 (UTC)

reply

The site in question contains all the basics. I have put together there all I learnt in my battle against heart disease. I have tried to present it in a very clear fashion and to expand on areas that I found when I was looking were briefly mentioned in passing on other sites and I had to visit many places to get the full picture. Your opinion is not in line with the opinion of most people who have reviewed the site, they have all commented that they found it very useful and well laid out and informative, it is in no way a site that is focussed on what plants do to mice, the subject of natural alternatives to statin drugs is covered there but it is in now way the main focus. And anyway the site as a whole was not what I was linking to here, it was the latest news. And maybe the day you looked the latest news was about phytoserols, but that changes daily and many of the articles that can be accessed are about general cholesterol research and I read at the top of this page the lady who wanted to hear more about what good cholesterol can do, tha is in the news, the subject is being studied and new facts coming up all the time. The resource answers her request. But maybe I am a little hurt you didnt like my efforts and am being overly defensive.

I am afarid that you may think that it is a commercial move on my part to want a link from here. However if you look at the site it is an informational site it provides up to date resources and I work on it daily to meet the needs of visitors. I thought maye because there is a page on the site that offers a home cholesterol test you thought it was a way to exploit people, but I dont actually make any money even if someone were to buy that home cholesterol test, I put the resource there only because it was suggested by someone and many people pay alot of money to get their cholesterol levels checked and dont realise that they can do it very cheaply at home.

I seriously believe that this is a worthwhile resource, I am not saying the site as a whole is any better or more authorative I am only saying that that in particular page page offers something that other sites do not and your reason for dismissing it is not based on any solid foundation. In the news today you will see an article as follows

A New Focus: "Good Cholesterol"

Statins have worked well in fighting LDL, the "bad cholesterol," but beyond a point, benefits may be slim. So attention is turning to raising HDL. In the cardiology world, the last 10 years are often referred to as the age of the statins. These drugs, which lower low-density lipoprotein (LDL), often known as "bad cholesterol," were introduced in 1995. They have been so successful at reducing heart attacks and other adverse events of heart disease that they are now the best-selling medicines in the world.......

This is the latest news and what someone on this very discussion page was asking for.

Please I ask you to reconsider, I do agree with you entirely that knowing what plant extracts do to mice is not helpful to anyone, but the news there is not about that even if sometimes there are articles on such subjects in the main the important news is there. Also please recognise that the page I have linked too, all the news stories are external links, people wont be staying on the cholesteroldoc site but will click through to the news sites to read the articles there, so it isnt a promotional thing I am trying to do here.

I have not replaced the link out of courtesy to you, but I would appreciate a discussion on the matter before my suggestion is dismissed out of hand. I can if you like look for better resources for the news stories, and try and filter out the ones that as you say are about the plants and mice type thing. Your critisisms are appreciated because all too often people wont tell me what is not good, but please can we address the faults you find and improve on them rather than throw the idea out all together, as I sincerely believe the idea is a good one and will be of benefit to people visiting this page.

Thankyou, I look forward to your reply

Clare

Clare, I did not mean to offend you, but Wikipedia actually aims to replace sites like yours. You must have put an awful lot of work into it, but the good thing about Wikipedia is that it is being edited by literally 100s of people, gradually and steadily improving the quality of the articles.

This article (cholesterol) covers the molecule. Your quote above concerns HDL, on which we have a seperate page. The HDL page should link to combined hyperlipidemia and the fact that low HDL and high TG levels are extremely prevalent. We haven't covered CETP inhibitors yet, but this is something we need to cover, especially since the trials were fairly disappointing.

There are literally 100s of sites that discuss cholesterol in some way or another. If I had to choose, I would insert an external link to a site with known authoratitive information (such as the American Heart Association[2]) over a private collection of information. I am not targeting you in particular - with Wikipedia becoming a prime work of reference, we have to be very selective in what we link to. JFW | T@lk 21:54, 16 November 2005 (UTC)

Feedback and advice

Could I please get some advice on how to best contribute to this article. We will be adding numerous videos, articles, and key opinion leader insites in the upcoming month. We have learned not to directly submit to the article and just want some help in contributing value. Thanks,

Ryan Cholesterol Treatment

It is a secondary source and hence not very useful compared to directly cited journal articles. Please review Wikipedia:Reliable sources. JFW | T@lk 22:27, 21 January 2006 (UTC)

Membranes and cholesterol in spinal cord and atheroma

I altered the statement that atheroma is something full of membranes - that is not why atheroma is full of cholesterol. On the spinal chord, I hesitate. Sure it's full of fat, but does it contain a lot of membranes? // Habj 18:46, 21 January 2006 (UTC)

Chylomicrons => LDL

Chylomicrons go into the liver and LDL comes out - but is it correct to say that chylomicrons are converted into LDL? // Habj 20:37, 21 January 2006 (UTC)

I am by no means an expert in this field, but off the top of my head, don't Chylomicrons contain intestinal-derived ApoB-48 while LDL particles primarily use ApoB-100? Perhaps if someone has time, an article on ApoB (or apolipoprotein B) would be something of use on Wikipedia. I could only find a generic article on apolipoproteins. Andrewjuren 23:31, 4 February 2006 (UTC)

Intended audience

What is the intended audience for such articles? I think in places this article will be difficult for the layperson to read/understand, and would suggest that the low-level technicalities are perhaps moved to the ends of paragraphs, or perhaps into a subarticle. What does anyone else think? --Rebroad 10:52, 25 February 2006 (UTC)

Overdosed on Statins

Dr JFW, If you want an eye-opener regarding the use of statins check out "Overdosed America" by John Abramson,MD. His book makes a compelling argument for the case that the US pharmaceutical industry has coopted and corrupted the medical research establishment in order shape data and outcomes to fit their marketing goals. Everyone should lower their cholesterol levels by reducing animal products in their diet, not by taking a pill. To that end, "The China Study" by Campbell is a stunning work by a seasoned researcher. I highly recommend it those who care about their health and are willing to do something about it. Dr JCS

I wonder why you are addressing me personally. Moreover, I wonder why you presume I need an eye-opener on statins. I tend to favour well-designed peer-reviewed studies over sensation-seeking works of art such as the book you are suggesting. I am also weary of suggestions that "the medical research establishment [has been] corrupted". If your views are based on honest science, why attack the messengers? Let the facts speak for themselves.

As you will probably know, reducing animal product intake gives a minimal improvement, as insulin resistance and many other factors play a role in the production of LDL cholesterol from VLDL. I am also in favour of dietary approaches, but not exclusively. There are good clinical guidelines for prescribing statins, such as those from the Framingham Heart Study, and as long as physicians adhere to these your comments are quite unfounded.

You did not provide a reference for "The China Study", so I should not be expected to comment on it. JFW | T@lk 11:23, 2 April 2006 (UTC)

Oxidized cholesterol

I'm far from being a doctor or scientist but have became interested in nutrition through dieting and training. I've read some articles on cholesterol that state that there are indeed different forms of cholesterol, mainly one form known as oxidized cholesterol which is cholesterol molecules influenced to heat before intake. Some say that it's actually this cholesterol that is bad (toxic and less functional), and that an excessive intake of non-oxidized cholesterol (such as raw egg yolk, in opposite to cooked eggs) can be handled by the body without problem. Have anyone else heard of this? Wintran 15:41, 19 May 2006 (UTC)

Here are some sources that discuss oxidized cholesterol.

Some interesting articles:

• Scandalous Lies About Cholesterol by Wai Genriiu
• The Cholesterol Scam by Eric Armstrong
• Oxycholesterol versus cholesterol, Gabe Mirkin, M.D.
• Cholesterol - A predictor of heart disease? by Norman Scherer

Some random PubMed articles regarding oxycholesterol (there are loads more):

• Oxidized cholesterol in the diet accelerates the development of aortic atherosclerosis in cholesterol-fed rabbits.
• Effect of cholesterol-rich diets with and without added vitamins E and C on the severity of atherosclerosis in rabbits.

Wintran 00:38, 29 June 2006 (UTC)

Cholesterol in Plants

Added a section based on some research to settle a debate about whether plants have cholesterol or not. It seems they do, so I added a section. Perhaps someone who knows more about the physiology of plants and cholesterol could add some more technical details. Chaleur 23:53, 1 June 2006 (UTC)

I have removed ", and require it to construct membranes" from the section because the source does not state that (unless I misread it). It states that cholesterol is found in some plants, and in higher concentrations in some sections of some plants.

I'm also intrigued about the content. I was unable to find much on PubMed to back any of this info up as many of the citations used in the article are books, and a few of the papers mentionned I can't find. I find it very weird that the authors (Berhman and Gopolan) stated the "methods for the detection of cholesterol in this range were not well developed until recently", 1991 (recent enough, I suppose), but are using data from 20 years ago in their table of cholesterol qty. Anyone know more about cholesterol in plants with newer sources? --jag123 05:23, 8 August 2006 (UTC)

The units of measure were inconsistant in the section on food sources of cholesterol (and in the cited study). Also, the cited study had an error in the table of plant oils (Table 2) -- the footnote had an inconsistent number of quantities compared with the number of example animal sources provided. Assuming the quantities in the table were correct, I added a comparision between an egg (213 mg) and peanut oil (24mg/kg, 213mg/19.5693 lbs.) (peanut oil was the closest item in the list to the statistical mean of all examples. Near the top of the wikipedia article, I changed the words "Lesser amounts" to "Trace amounts" to more accurately convey the relationship. Darana 07:37, 15 March 2007 (UTC)

misc 2

My nutritional instructor says that about 85% of cholesterol in the body is produced by the body, and only 15% is absorbed from food, anything more is not absorbed; peed out or something. But since I know nothing about cholesterol, I'll ask here, can someone include it into the article? I don't want to make any mistakes Nastajus 16:34, 16 April 2006 (UTC)

It IS mostly produced in the body, and the extra is NOT peed out, unfortunately -- that is why it is such a worry! 69.87.202.5 01:37, 9 June 2006 (UTC)

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This article needs the positive aspects of cholesterol also. (I don't have time right now...) It is NOT just a Bad Thing - it is absolutely required for the proper structure and fluidity of cellular membranes (which is why so much is found in nerve cells). -- Marj Tiefert, Tuesday, June 11, 2002

It makes cells squishy so they can fit through tiny openings. Nastajus 16:34, 16 April 2006 (UTC)

Yes, it also needs a section on the fallacy that cholesterol causes heart disease. I'm adding a link to Dr. Uffe Ravnskov's work, 'The Cholesterol Myths', but really there should be a section in the main text which addresses the strong opposition to the widely held "lipid hypothesis". - John P. Speno

Yes, it is required for our life/health -- but at lower levels than hardly any of us achieve. 69.87.202.5 01:37, 9 June 2006 (UTC)

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Right on, cholesterol is not at all a 'bad' substance. The LDL/HDL hypotheses are speculative. 'Lowering cholesterol' is a major mistake - in 2004 it was discovered that the brain produces its own cholesterol crucial for memory, and who has heard of that? Statins hamper the memory process, as does any attempt to 'lower cholesterol'. Wake up, people, can't you smell the interest of the pharmaceutical industry in this? An encyclopedic article should certainly not include such speculative information as that posted below here. Simoon

Simon, the LDL/HDL hypothesis is proven firmly by large population and intervention studies, most of which were not actually funded by the pharmaceutical industry, which is of course the root of all evil. Please be reasonable. And next time you pop a antihistamine for your hayfever, be grateful for the pharmaceutical industry for bothering to develop these drugs.

The Heart Protection Study was conducted by the MRC for this purpose. Yes, Merck payed the bill, but I think we can take Richard Doll and his time on their word when they say MSD did not influence the trial results.

What is your evidence that inhibition of HMG CoA reductase impairs memory? JFW | T@lk 09:38, 20 July 2005 (UTC)

Yes, taking strong drugs like statins population-wide for many years has risks. But the risks from high cholesterol are also certain -- about as certain as almost anything in medical science. There are also people who do not believe that HIV causes AIDS, but the rest of us in the "reality-based" world have to muddle through as best we can with the messy, inconvenient facts. (Get as healthy as you can if you want to avoid the bad side effects of drugs. Or just take your chances.) 69.87.202.5 01:37, 9 June 2006 (UTC)

I've seen many articles and studies that state that excessive pure cholesterol (not "HDL") can be handled by the body without problem, and does more good than bad. However, oxycholesterol, because of its influence with heat, is what eventually leads to clogged arteries, which makes it a type of "bad" cholesterol. I find this very interesting as it seems to make a lot of sense and I haven't heard any serious argument against it. I'm hoping that these studies and theories get more attention among the mainstream science. Wintran 12:11, 9 June 2006 (UTC)

Don't confuse dietary cholesterol with serum cholesterol. There's no statistical correlation between the two. I, likewise, have heard bad things about oxycholesterol, but I haven't seen research on it, and would appreciate any information that can be dug up. -Heresiarch

Check out the section on oxidized cholesterol above, I've posted some links there to some articles and researches about oxycholesterol. Wintran 00:38, 29 June 2006 (UTC)

Serum cholesterol

There's no page for serum cholesterol. Should this be explained in the Cholesterol article, and a redirect made? Badagnani 09:59, 3 December 2006 (UTC)

Invalid numbers, footnote

How can egg yolks have ~1234mg/g of cholesterol? This is saying that there is more than a gram of cholesterol in each gram of egg yolk. The article cites footnote 6 (a Web site) as being the source of this data, but I couldn't find these numbers anywhere on the site they supposedly came from.

Chaos in Cholesterol- Mevlüt Durmus-Biologist

SUMMARY OF BOOK

INTERPARTICULAR CHANGE BETWEEN THE MAJOR COMPONENTS OF LIPOPROTEIN AND TOTAL LİPOPROTEİN PARTİCULAR (TLP): BIOMATHEMATICAL STUDIES ON TOTAL CHOLESTEROL (TC), TRIGLISERIDES (TG), APOLIPOPROTEIN A-1 (APO A-1) AND APOLIPOPROTEİN B (APO B): AND COMBİNED TOTAL LIPOPROTEİN PARTICULAR HYPOTHESİS (CTLPH).

MEVLÜT DURMUŞ BIOLOGIST (MS)

GİRNE MAH. 403 SOK. NO: 11/1 100.YIL Balgat/Ankara/TURKEY

In this work, relations between the transported (lipids) and transporters (apolipoproteins) are biomathematically examined throug theroies and hypothesis of present lipoprotein, and theoric Total Lipoprotein Particular (TLP) model including major lipoprotein components is established. In this model, apolipoprotein B (apo B), apolipoprotein A-1 (apo A-1), total cholesterol (TC) and TLP model which includes triglycerid (TG) are defined. In the Combined Total Lipoprotein Particular Hypothesis (CTLPH), major components of LDL, VLDL and HDL are taken into consideration to make together rewerse transport system and endogenous transport system, then theoric biomathematically CTLPH formula is attained. Minor apolipoproteins and phosfolipids (PL) which are changed in lipoprotein are not included in TLP. According to CTLPH, TLP is expressed with the biomathematical formula as it is show below:

(apoA1/apoB).(TK/2.ApoB).(apoA1+TG/3.ApoB)=1.1.1 Small Text

(Ç constand)

Total Cholesterol: TK, Trigliserid: TG, Apolipoprotein A-1: Apo A-1, Apolipoprotein B: Apo B

According to CTLPH, apo B has an effect on highness and lowness of major lipid components, primer effect on lipoprotein and whatever reason every changes in apo B effect other major lipoprotein (TC, TG and apo A-1) components. Major component units’ determined values in lipoprotein partuculars are in fact total measurements (TC, TG,apo B and apo A-1), and a particular created with major components based on mathematical theory, is a different expression of total particular.

This hypothesis, which we assume that explain firstly coronary artery disease (CAD) which depends on Atherosclerosis originating from disorder of lipoprotein metabolism, then the uneasiness caused by lipoprotein metabolism, evaluates interparticular movements of major components. According to CTLPH formula: increasing TG and TC are single parametrical relativeincreases when apolipoproteins are not included. For conclusion; lipid protein ratio, especially apo B ratio in lipoprotein particular should be taken into consideration.

According to CTLPH, it is possible to evaluate relative TC and TG increasing, and to explain the change that occurs through interparcular movements by Ç constand. For CTLPH, values above and below constand Ç should be evaluated again by considering TC and TG increases. In our work, TLP,created an mathematical ground, appears in 3 main groups, and is named according to Ç constand and plasma concentration (mgdl):

1. Ç 1.00 particular occurs throug pathological case, is named as Hypolipemic Minor Particular (HLMP) according to CTLPH, and HLMP’s plasma concentrations, TC andor TG200, Apo B  100 and Apo A-1 100 (mgdl) are accepted. In that kind of particulary, decreasing in the amount TC, TG and apo A-1, increasing of levels of plasma (mgdl) TC and TG are presented biomathematically (single parametrical).(Mean Ç=0.84)

2. The particular in Ç1.00 is named as Normolipemic Normo Particular (NLNP). Plasma concentrations of NLNP called as TC and TG  200, apo A-1 100 and apoB 100 (mgdl). (Mean Ç=1.39)

3. For CTLPH, Ç 1.00 particular meaning transition, (for us it is a pathological case

          before) which occurs in the particular constructions including TC and-or TG 200, 
          apo A-1 100 and apo B 100 (mgdl) plasma concentrations, on which we suppose 
          that scientific depates will increase, is named Caotic Undetermined Lipoprotein 
          Particular (CULP)(Mean Ç=1.20)

NOTİCE: THIS HYPOTHESIS, WHICH CHOLESTEROL AND TRIGLYCERİD ARE

                 INNOCCENT.

E-mail; mevlutdurmus@hotmail.com

       mevlutdurmus@yahoo.com  

Mevlüt Durmuş

Kolesteroldeki Kaos (Chaos in Cholesterol) Nisan 2003 . Nobel Yayın No:487 . Ankara (Publication in Turkey) ISBN 975-591-466-8

aditional link on the function section second paragraph

Where you read:

"It also reduces the permeability of the plasma membrane to hydrogen ions (protons) and sodium ions."

I would sugest to link the word permiability to the corresponding wikipedia page, or alternativelly to the "Semipermeable membrane" entry dedicated solely to the biochemical concept.

Luis Oliveira (luisfpoliveira at g mail, Portugal) —The preceding unsigned comment was added by 217.129.188.43 (talk) 10:12, 13 February 2007 (UTC).

Mechanism of reduction

How is bad cholesterol removed from the blood stream and how are plaque particles removed from the artery walls? How does exercise help reduce cholesterol? --Apathy 10:51, 13 February 2007 (UTC)

Etymology

Surely steroid is derived from sterol, and not the other way round? Cholesterol was originally called cholesterine (or cholesterin) and the name was changed when it was identified as an alcohol. Similar molecules became known as sterols (the name implies "solid alcohol", which is fair enough), and molecules derived from sterols became known as steroids. SpikeMolec 07:28, 27 February 2007 (UTC)

Effect of Blood Pressure Meds on Cholesterol Measurements

What are the effects of Blood Pressure Meds on Cholesterol measurements?

For example, if one was taking Microzide, aka Hydroclorothiazide, which is described as a "water pill" for reducing salt up-take and therefore the amount of water in the blood, for a period of time (say a week) prior to having blood drawn, would that effect the measurement?

As a first pass, wouldn't one presume that a reduction in the amount of water would increase the concentration of everything else in the blood, including cholesterol?

Would the regulatory mechanism respond to the reduction in water by reducing the overall amount of cholesterol?

How fast would the regulatory mechanism respond to this. Is the set point of that mechanism based on concentration in the blood, or as indicated, on intracellular concentrations?

If it is based on intracellular concentrations, would those concentrations respond to the presumed change in concentration due to water level reduction?

If there is an effect on the measurement from Microzide, is there a way to estimate a pre-Microzide level based on dosage and the measured concentrations and other relevant factors (e.g. body weight etc?)?

anon64.0.112.24 11:17, 18 March 2007 (UTC)

Thiazides are well known for their role in gout and possibly insulin resistance. This is generally outweighed by its effects on blood pressure. There is not much of an effect on cholesterol. JFW | T@lk 07:52, 15 April 2007 (UTC)

Thanks for the reply. However, my question is about the effect on Cholesterol MEASUREMENT. If you can, please respond the the reduction in water leading to and increase in the concentration of everything else issue.

Critics

Can we have a degree of consensus on how to address the ongoing attempts of "cholesterol critics" to get their theories on this page? JFW | T@lk 07:58, 15 April 2007 (UTC)

There needs to be a balance in the article and an acknowldgement that there are differing points of view on cholesterol by members of the scientific medical community, both supporting and opposing the lipid hypothesis. I would propose that

a) the section on Hypercholesterolemia be shortened, as it is practically long enough to be an article on its own and the subject already has its own page. Non-redundant information in that section could be incorporated into the Hypercholesterolemia article.

b) the section containing the information on Hypercholesterolemia (summarised) and that on Hypocholesterolemia be re-entitled "Clinical Conditions"

c) a new section entitled "Clinical Significance" be created, which contains a summary of the scientific mainstream and the scientific minority viewpoints on the lipid hypothesis.

Suppression of the existence of valid scientific debate from an article (the members at www.thincs.org are qualified in appropriate fields) represents a violation of Wikipedia's NPOV policy. Impartiality demands fair treatment of both sides of the case. However, as the article is to do with the subject of cholesterol the substance, discussion of the scientific debate regarding the lipid hypothesis should be kept to a minimum. A more appropriate place would be a new article entitled "Cholesterol controversy". Bezapt 13:25, 15 April 2007 (UTC)

Cholesterol information Link

I tried to add this website I found, [www.ldlhdl.info], to the external links section, but it keeps getting deleted. I believe this site should be added to the article, as it provides easy to understand information for users who might want to explore further on the subject. Futhermore, the site is a non-for-profit...— Preceding unsigned comment added by Dherna01 (talk • contribs)

Wikipedia is an encyclopedia, not a linkfarm (also see our external links guideline). External links do not necesseraly improve the encyclopedia, if you think the link provides more information on the article, try to improve the article, using the information from the page as a reference (see our citation guideline, and our how to add citations guideline). Hope this explains. --Dirk Beetstra ^{T C} 16:03, 16 August 2007 (UTC)

Umm, out of curiosity, why is this link (compared to the other links) inappropriate to this article? You don't really say, Beetstra. Certainly the other links are to sites whose information that could also be integrated into the article. I'd just like some clarification.— Preceding unsigned comment added by Friarslantern (talk • contribs)

Thank you for taking this discussion to the talkpage. The difference between your site and the present links is enormous. The WHO and American Heart Association are important bodies that disseminate scientific knowledge. In contrast, ldlhdl.info does not claim to be authoritative, makes tentative claims about functional foods, and perpetuates the rather doubtful idea that cholesterol must be linked purely to dietary causes (ignoring genetics, sedentary lifestyle, comorbidities etc). I support Beetstra in the removal of the link. Wikipedia is not an advertising medium, and its contributors tend to get a bit peeved when their studiously written content is used as a vehicle to promote traffic to other people's websites. JFW | T@lk 22:36, 16 August 2007 (UTC)

In answer to your 'why is this link (compared to the other links) inappropriate to this article?', I did answer that with the links to our 'what wikipedia is not' policy and our external links guideline. And, that other links are similar is not an excuse to add more links, in those cases, it is better to start a discussion on talkpages. Hope this explains, have a nice day! --Dirk Beetstra ^{T C} 09:26, 17 August 2007 (UTC)

JFDWolff: this is not ~my~ site addition, btw, someone ~else~ added it; I am commenting on the deletion, though, and hear your appreciating my keeping this issue on the discussion page (for now, at least ;-) ). I don't dispute that adding site simply to advertise the site (as opposed to the ideas that may be exposed in the site) is against the rules -- and I'm sure that is rampant on Wikipedia -- but this doesn't appear so clear in this case. I support the user who added it in including it; I hope you're not saying that the ~studious~ authors of Wikipedia don't also hope that people will traffic sites whose views the American Heart Association endorses when ~they~ include an AHA site in the external links. Nevertheless, pure advertisement is clearly forbidden, but I suspect you are using the fact that this site advocates an ~alternative approach~ to reflexively argue that it is pure advertisement. If what you're saying is the approach detailed in the site needs to be written about in the article first before adding a link, fair enough, but I'm skeptical that you wouldn't object to any ~alternative~ approaches appearing here, no matter how widely held or well-sourced they are.

Beetstra: Today I'm not so sure about it being so great a day, but, your reference to the guideline about not deleting or keeping an article for the reason that articles on other similar articles don't or do exist is well taken. Again, as I stated above, I was not the one who added this site, but a review of it did indicate to me that it is fairly simple and straightforward, representing the yes, alternative views held by yes, a minority of experts, but that shouldn't disqualify it from being included in this article. Also, see my comments to JFDWolff above. Friarslantern 19:15, 17 August 2007 (UTC)

Large-scale study showing that low cholesterol does not seem to be a proxy for frailty occurring with age

Dear Jfdwolff, why do you feel the conclusion of a particular study involving ~150K persons needs special treatment compared with the other sources cited in the article? You have removed this reference because you claim that in the years following its publication this paper has received little citation. Probably this is the case because it does not support the Cholesterol-Heart Disease hypothesis. Also, you ask if it has it been replicated elsewhere. I have provided references to two large scale studies: a follow-up from the Framingham Heart Study and the Vorarlberg Health Monitoring and Promotion Programme. I respectfully disagree with your attitude of removing my contributions, I would rather prefer to see you adding large-scale studies that refute these findings. 128.61.146.11 22:06, 5 September 2007 (UTC)

I have a few problems with your approach. Firstly, wouldn't you prefer to get a username, given that you seem to know Wikipedia's workings pretty well (using templates, undoing edits etc)?

My second problem is that one single study is simply inadequate to undermine a hypothesis that is adhered to by the vast majority of the medical profession. The journal in which it was published does not have a high impact factor, while all other relevant studies are making it into the core journals. I am fully aware of the "cholesterol skeptics" and I suspect you are amongst them, and you will probably argue that the journal editors are in the pay of the drugs lobby. A circular argument is likely to ensue.

For my information, did the Vorahlberg study include only healthy people that then went on to develop cardiovascular disease, cancer, liver disease etc? Because otherwise one can argue that those people with low cholesterol already had active cancer, a knackered liver or an eating disorder when their baseline cholesterols were determined. JFW | T@lk 14:08, 6 September 2007 (UTC)

• Speaking here as a medical doctor with almost 30 years experience (and a sufferer of hypercholesterolaemia) I must take exception to the idea of the opinion of the "vast majority" of the medical profession as to the place of cholesterol in heart disease. It has been internationally recognised that the cholesterol hypothesis for heart disease is based on the wrong model. 75% of cholesterol arises not from diet, but from the liver. Why? What is the protective mechanism sought by the liver? Obviously there is a good reason for excess production. Why is it that we have known since the mid-50s that CRP is a better predictor of CHD than cholesterol? What is the role of homocysteine in predicting heart disease, and what biochemical process does it represent? These are indisputable findings. Remember that the "vast majority" of the medical profession disputed Semmelweiss' approach to hygiene and puerperal fever. I appreciate your adherence to orthodoxy, but there is a large and growing body of doctors who doubt that approach. Yes, Framingham is excellent and must be used to assess risk, yes cigarette smoking is really dumb, yes there are issues with poor nutrition and lack of exercise. Cholesterol is, however, not the most important issue for CHD. Otherwise, the biochemical references here are excellent. docboat 00:33, 6 October 2007 (UTC)

I honestly don't see why the anonymous editing, if done properly, constitutes a problem. The only reason I have never bothered getting a username (up to this day) is that Wikipedia does not force you to do it (which I think is one of the things that makes Wikipedia great). I take it as a compliment that I seem to know Wikipedia's workings pretty well, but in reality I may have anonymously corrected about 10 things here and there, in mathematics, biochemistry and bioinformatics. To make clear that I have no intention to hide and to keep the discussion focused in what really matters (the science), I just created a username, which is actually my real name.

Let us pass to the second problem you mentioned. Before to comment on the issue of the number of studies supporting one hypothesis or the other, I would like to state that I am not a "cholesterol skeptic", I try to be a good scientist so I am a skeptic period. Whether the journal editors are in the pay of the drugs lobby or not, whether most of the favorable trials are sponsored by the pharmas or not, etc, are all valid points of debate, but I am not interested in that kind of arguments. I prefer to discuss the scientific evidences, trying not to be biased by what the majority of the medical profession believes.

Now to your scientific question: the Vorahlberg study included more than two thirds of a whole Austrian province. Quoting from the Materials and Methods section of the paper: "Participants. In Vorarlberg, the westernmost province of Austria, population-based documentation of cardiovascular risk factors has been performed routinely since 1970 by the Agency for Social- and Preventive Medicine. From the outset, this ongoing extensive risk factor surveillance and treatment referral program has conducted medical examinations of more than two thirds of the entire population of this province. A total of 149,650 individuals, 67,413 men (44.9%) and 82,237 women (55.1%), participated in the VHM&PP between 1985 and 1999. During this period, men underwent 191,629 examinations (42.2%), and women underwent 262,819 examinations (57.8%), a total of 454,448 in all. Informed consent to store and process the data was obtained from all participants at each examination time, and ethical approval was obtained. A total of 5,393 persons died in the course of follow-up, and cause of death was linked to the database using a validated record-linkage procedure."

I'll be happy to send you the PDF if you want, I cannot post it publicly because of copyright issues. There are other large studies showing association between low cholesterol and increased risk of death (e.g. see PMID 9229204, published in Epidemiology and PMID 12397569, published in the Journal of Cardiac Failure). This issue was even the subject of a conference in 1990 (PMID 1355411, published in Circulation), although the conclusion of that meeting was more in the line of what you are arguing; "most participants considered it likely that many of the statistical associations of low or lowered TC level are explainable by confounding in one form or another.". The problem I have with that view is the double standard when interpreting the epidemiology: 1) HIGH cholesterol -> CAUSES -> CVD, but 2) LOW cholesterol -> IS A CONSEQUENCE OF -> cancer, etc. AK Arakaki 19:34, 6 September 2007 (UTC)

Anonymous editing: of course anons are free to edit, but when a long discussion ensues, working with a clearly identifiable handle is much more straightforward. Thanks for registering, anyway.

You say that you prefer to discuss evidence rather than consensus. That is fine, but radical reinterpretations of the evidence (unsupported by consensus) may be in violation of WP:NOR (original research) and WP:WEIGHT (disproportionate emphasis). I'm sure you get my point, and I support the skeptical stance in general.

I did not question the Vorahlberg study methodology, apart from the basic question: were those with low cholesterol not already ill from their cancer/liver disease/malnutrition at baseline? I don't see a double standard here at all. Cholesterol is found in atherosclerotic plaque, and in LDL receptor mutations patients develop premature coronary artery disease. Can't get much more convincing evidence. In contrast, a sick liver will not synthetise cholesterol (but see Zieve's syndrome) and a cachectic cancer patient has a neoplasm that gobbles up all available energy. These are widely held views. In contrast, the supposition that low cholesterol causes liver disease and cancer is highly innovative (liver disease) or has for all intents and purposes been disproven (cancer). JFW | T@lk 19:37, 10 September 2007 (UTC)

Hi Jfdwolff, I have a few comments in regard to the link between low cholesterol and cancer. First, the relationship doesn't need to be strictly causative, it may be that low cholesterol supports the progress of cancer, i.e. yet another out of many other factors that contributes to cancer without being an initiating factor per se. It is now accepted that changes in intracellular concentrations of certain metabolites (having other important cellular functions not related with cancer) can influence the rate of cancer cell growth by acting as signaling molecules (e.g. diacylglycerol [1], ceramides and sphingosines [2], NAD+ [3,4] and arginine [5]). Considering that the signaling role of most of the aforementioned biomolecules was not even suspected ten years ago, it is likely that other metabolites acting as second messengers are yet to be discovered. There are other cases where the significance of a metabolic phenotype observed in cancer cells have been very controversial, e.g. the shift in energy production from oxidative phosphorylation (respiration) to aerobic glycolysis known as the Warburg effect [6]. For long time, the mainstream viewpoint have been that the Warburg effect is a consequence of the cancer process (secondary events due to hypoxic tumor conditions), rather than a mechanistic determinant of it, as was originally hypothesized by the biochemist Otto Warburg. However, it has been recently shown that the dichloroacetate-induced reversion from a cytoplasm-based glycolysis to a mitochondria-located glucose oxidation effectively inhibits cancer growth, supporting the idea that the glycolytic shift is a fundamental requirement for cancer progression [7]. This is an example of evidence contradicting what the majority of the medical profession believed, and my interpretation of the published literature makes me believe that we may find a similar situation with respect to the low cholesterol and cancer correlation. I grant you that cancer-induced cachexia would in principle explain such association, but if cholesterol levels are simply the effect of the disease, how to explain the persistence of statistical association between cancer and low cholesterol after excluding early deaths (within 5 years after study baseline) in many of the epidemiologic analyses? [8]. Moreover, in a recently published meta-analysis of 23 statin treatment arms with 309,506 person-years of follow-up, there was a highly significant inverse relationship between achieved LDL-cholesterol levels and rates of newly diagnosed cancer (R2=0.43, p=0.009) [9]. The authors conclude: "Furthermore, a concerning inverse relationship between achieved LDL-cholesterol levels in statin-treated patients and risk of cancer was observed, and requires further investigation". I contrast that conclusion with these statements from the companion editorial article by John C. LaRosa "Withholding cholesterol-lowering therapy is itself very harmful. These current findings provide insufficient evidence that there is any problem with LDL lowering that outweighs its significant benefits on vascular disease" [10]. IMHO, higher incidence of cancer IS a significant problem.

1. Carrasco S, Merida I: Diacylglycerol, when simplicity becomes complex. Trends in biochemical sciences 2007, 32(1):27-36.

2. Ogretmen B: Sphingolipids in cancer: regulation of pathogenesis and therapy. FEBS letters 2006, 580(23):5467-5476.

3. Yang T, Sauve AA: NAD metabolism and sirtuins: metabolic regulation of protein deacetylation in stress and toxicity. The AAPS journal 2006, 8(4):E632-643.

4. Ashraf N, Zino S, Macintyre A, Kingsmore D, Payne AP, George WD, Shiels PG: Altered sirtuin expression is associated with node-positive breast cancer. British journal of cancer 2006, 95(8):1056-1061.

5. Grabon W: [Arginine as a crucial amino acid in carcinogenesis and tumor growth]. Postepy higieny i medycyny doswiadczalnej (Online) 2006, 60:483-489.

6. Warburg O, Posener K, Negelein E: Ueber den Stoffwechsel der Tumoren. Biochemische Zeitschrift 1924, 152:319-344.

7. Bonnet S, Archer SL, Allalunis-Turner J, Haromy A, Beaulieu C, Thompson R, Lee CT, Lopaschuk GD, Puttagunta L, Bonnet S et al: A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth. Cancer cell 2007, 11(1):37-51.

8. Jacobs D, Blackburn H, Higgins M, et al. Report of the Conference on Low Blood Cholesterol: Mortality Associations. Circulation 1992;86:

9. Alsheikh-Ali AA, Maddukuri PV, Han H and Karas RH. Effect of the Magnitude of Lipid Lowering on Risk of Elevated Liver Enzymes, Rhabdomyolysis, and Cancer: Insights From Large Randomized Statin Trials. Journal of the American College of Cardiology 2007, 50:409-418

10. John C. LaRosa. Means and Ends of Statins and Low-Density Lipoprotein Cholesterol Lowering. Journal of the American College of Cardiology 2007, 50:419-420.

AK Arakaki 22:32, 26 September 2007 (UTC)

Controversy

A user removed the link to the Lipid hypothesis article. I believe the user did this in good faith but the user cited WP:WEIGHT, commenting that the "controversy" exists largely in the mind of the skeptics, who "comprise <1% of all scientists looking into this." I don't believe the user can substantiate the "1%" claim; and WP:WEIGHT doesn't say that there is a "1%" cutoff or anything on the number of people who agree. There was a time when 99% of the people in the world thought the Earth was flat, or that HIV was a homosexual-only disease. Moreover, it was just a link to the controversy article, and did not contain not any data or claims regarding the controversy at all; hence I believe the link is appropriate for the article on cholesterol. Even WP:WEIGHT says if the "viewpoint is held by a significant minority, then it should be easy to name prominent adherents" and there are many named on the Lipid hypothesis page -- as proof, see the extensive list of citations by prominent doctors and researchers there. -- GeĸrίtzĿ._..•˚^˚ 21:39, 20 October 2007 (UTC)

I have responded to your post on my talkpage. JFW | T@lk 21:44, 20 October 2007 (UTC)