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Minor issues

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Under "lowering cholesterol" what is meant by the unfolding of carbohydrates to glucose. Isn't this language a little bit confusing. Does he mean the break down of carbohydrates. "unfolding is not a very good word. —Preceding unsigned comment added by Cag66 (talkcontribs) 05:49, 6 June 2008 (UTC)[reply]

I'm not even going to attempt to flesh this page out, since I'm not able to follow most of the links I can find on the subject, certainly not at the end of a work day (I'm a marine biologist dang it18:40, 27 December 2016 (UTC)18:40, 27 December 2016 (UTC)18:40, 27 December 2016 (UTC)18:40, 27 December 2016 (UTC)65.27.230.232 (talk) 18:40, 27 December 2016 (UTC)Cite error: A <ref> tag is missing the closing </ref> (see the help page).</ref></ref>, not a doctor.. or whatever ;). However, if someone could kindly point out what the 'it' in the stub means that might help a \bit (I kind of assume cholesterol, but not sure). Rgamble[reply]


I'm not sure how to convert the units to European ones (mmol/l) but I'm sure it needs to be done (the same goes for HDL and triglyceride). JFW | T@lk 19:52, 15 Apr 2004 (UTC)


This isn't my specialty, but according to google, it's Friedwald, not Freidwald. - ganaaaa 2-9-2006

Low carbohydrate diet

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I removed the statement (written by an IP) that a low carbohydrate diet correlates with a healthy LDL distribution - there is no reference for it and it seems to be dubious. Icek 21:21, 30 March 2007 (UTC)[reply]

Ads

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looks like this page may have just been flooded with ad placement. A cleanup/revert, if someone has time? Snellios 23:31, 10 June 2007 (UTC)[reply]

Citations

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In the part (Recommended range; changing targets) I have added request for citation; there is mentioned scientific research in general instead of direct citation or reference and this creates false appearence that it has valid source. 213.215.88.108 16:28, 30 October 2007 (UTC)[reply]

In the section "Lowering LDL-cholesterol", the paper cited for the following statement makes no mention of LDL cholesterol, but rather, describes effective approaches to reducing abdominal visceral fat:

The most effective approach has been minimizing fat stores located inside the abdominal cavity (visceral body fat) in addition to minimizing total body fat.

I will update this if I find a source that more directly supports it. --Steliotron (talk) 02:52, 14 December 2017 (UTC)[reply]

Incomprehensible

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This article is loaded with far too many technical terms and jargon to be easily understandable for the average reader. —Preceding unsigned comment added by 72.66.249.231 (talk) 17:06, 3 November 2007 (UTC)[reply]

I agree that the dietary part is especially useless to the layman... maybe add some examples of food which would upregulate or downregulate LDL synthesis, or which foods may contain high levels of B3 (niacin). I also recall learning that moderate alcohol consumption may help regulate LDL (by means of HDL level regulation??). Might want to mention that too much alcohol would have the opposite effects, as metabolizing lots of EtOH would increase your triglyceride levels. —Preceding unsigned comment added by 137.122.149.212 (talk) 15:10, 7 November 2007 (UTC)[reply]
Strongly Agree — The dietary portion presently reads: "Dietary Insulin induces HMG-CoA reductase activity, whereas glucagon downregulates it.[5] While glucagon production is stimulated by dietary protein ingestion, insulin production is stimulated by dietary carbohydrate. The rise of insulin is, in general, determined by the unfolding of carbohydrates into glucose during the process of digestion. Glucagon levels are very low when insulin levels are high." Upregulates? Downregulates? Unfolds? Does this just mean increase or decrease? I have a doctorate (not in medicine) and I still don't understand these four sentences. Will a medical person please put this in lay terms? And make some distinction between "dietary insulin" and what, injected insulin? -- LisaSmall T/C 11:26, 19 May 2008 (UTC)[reply]

the above lines tells the relation between insulin and glucagon .These are hormones which oppose each other.Insulin anticipates HMG-coA reductase activity whereas glucagon decreases.Dietry carbohydrate is what we take from food ie.orally.when there is low production of insulin in body we need to decrease the rise in glucose level as insulin controls its level.Orally taken insulin is degraded in stomach and is of no use so artificially synthesized insulin is used for it.When carbohydrates breaks down in our body to simpler molecule eg. glucose for easy digestion, insulin is secreted from pancreas.

Heterogeneity

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PMID 6827999 - historical reference on the heterogeneity of LDL particles. JFW | T@lk 07:27, 16 March 2008 (UTC)[reply]

Blame it on small dense LDL JFW | T@lk 07:28, 16 March 20

'Fructose, a component of sucrose as well as high-fructose corn syrup, upregulates hepatic VLDL synthesis'

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Can someone translate that into english, please? Does that mean we should increase or decrease fructose intake to reduce LDL? Thanks. --220.253.29.116 (talk) 12:34, 20 June 2008 (UTC)[reply]

Yeah, there's a lot of jargon in this article with little common-language synthesis. Compare to high-density lipoprotein, which is actually intelligible. 149.10.148.229 (talk) 14:39, 26 February 2009 (UTC)[reply]
Whoops, I see that its actually discussed two sections up. 149.10.148.229 (talk) 14:41, 26 February 2009 (UTC)[reply]

No graphics or models?

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No image? Why?--69.155.111.122 (talk) 23:16, 15 January 2009 (UTC)[reply]

LDL cholesterol?!?

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I suggest there be a section explaining the terms "LDL cholesterol" and "HDL cholesterol". Since LDL and HDL are lipoproteins, they cannot be cholesterol. I guess that in this case, LDL and HDL are used as adjectives: "LDL cholesterol" -> "cholesterol, that is carried by LDL proteins". Is this correct? If yes, it should be evident in the article, as well.

And phrases like 'as opposed to HDL, which is frequently referred to as "good cholesterol" or "healthy cholesterol"', which appears in the first paragraph of the article, should be avoided as they are nonsense.

- Tom —Preceding unsigned comment added by 193.77.126.73 (talk) 09:24, 5 August 2009 (UTC) I agree that LDL and LDL-C need to be differentiated in the article. Of course, LDL does contain cholesterol and triglycerides. Blood tests actually report HDL-C and LDL-C: the amount of cholesterol (C) in each of the fractions. Mac John Concord (talk) 19:30, 9 September 2010 (UTC)[reply]

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I was listening to Audio Digest (an audio CME for healthcare professionals) the other day and it has been suggested that ldl levels below 80 mg/dl can arrest atherosclerosis, while levels below 70 mg/dl can even reverse it. I don't have enough time to find documentation for this, but if anyone is interested, it would be useful to have this in the article. It would seem that the current guidelines for LDL are out of date given new information and research into realistically healthy levels. —Preceding unsigned comment added by 72.44.99.254 (talk) 18:49, 4 September 2009 (UTC)[reply]

These recommended levels are extraordinary. The current (Nov 2009) recommended level in Europe is "no more than 160 mg/dl". It might be pointed out that even this is regarded in many quarters as suspect, i.e. ratcheted down by the pharmaceutical industry, and that a figure of 180 might be more realistic. Escoville (talk) 18:16, 8 November 2009 (UTC)[reply]


The whole concept of "good" and "bad" cholesterol is completely flawed and has been refuted endlessly in recent years, so I'm not sure why it is still sat atop the wikpedia page for LDL. Hopefully an editor can go about rectifying this. One source of many: http://www.canibaisereis.com/download/ldl-bad-science-colpo.pdf(188.222.85.110 (talk) 16:39, 14 December 2010 (UTC))[reply]

As with all things chemistry and health related, there are those exclaiming science, and those exclaiming myth. I don't presume to judge this particular topic, but this article seems well written, and the source sited by above does not exist. Iglam (talk) 18:06, 9 January 2012 (UTC)[reply]

At the same time low levels of LDL-C are associated with cancer and infectious disease in the elderly, so .. — Preceding unsigned comment added by 78.195.84.105 (talk) 15:17, 1 September 2018 (UTC)[reply]

Triglycerides & VLDL

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I've tagged the following sentence with {{vague}}:

Lowering the blood lipid concentration of triglycerides helps lower the amount of LDL, because VLDL gets converted in the bloodstream into LDL.

because it seems to assume that readers will already know the implied connection between triglycerides and VLDL. Reading Triglyceride, I see that the former is a "major component" of the latter, but that still doesn't really explain why lowering triglycerides would necessarily lower VLDL, let alone LDL. (From all the reading I've done – only a tiny fraction of what's known – on these health-related biochemical articles, one thing I've learned is that one cannot assume that lowering molecule A that's a building block of molecule B doesn't necessarily lower B, as there seem to be many ways to assemble any given molecule B, even assuming metabolism doesn't shift to accommodate the change.) Could someone knowledgeable add a brief, explicit connection? Thanks. ~ Jeff Q (talk) 07:23, 13 December 2009 (UTC)[reply]

Look it up! According to Wikipedia, VLDL particles are produced in the liver in order to deliver newly made triglycerides and cholesterol to the cells that need them. After delivering part of their load, the (now smaller) VLDL remnants are called IDL particles. About half of the IDL particles are taken up and destroyed by the liver. The other half continue to deliver their contents to the cells. After that the (now even smaller) IDL remnants are called LDL particles. They are small enough to sneak into the spaces between the cells lining the blood vessels, which is how the trouble begins. I infer that anything that increases or decreases VLDL is likely to do the same for LDL.
(Actually, Wikipedia is much clearer and more detailed on lipoproteins now than it was 5 years ago when heart troubles first impelled me to these pages. I don't mean to diss you if it was not so clear in 2009.)
-- Solo Owl 02:46, 17 September 2013 (UTC) — Preceding unsigned comment added by Eall Ân Ûle (talkcontribs)

Synthesis?

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It seems like a pretty major gap in this article is a complete absence of where, why and how LDL are synthesized. — Preceding unsigned comment added by 137.43.188.136 (talk) 20:37, 22 February 2012 (UTC)[reply]

I second the motion. -- Solo Owl 02:52, 17 September 2013 (UTC) — Preceding unsigned comment added by Eall Ân Ûle (talkcontribs)

Illustrations

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Some pretty snazzy illustrations appeared in this article a few years ago: "Three-Dimensional cryoEM Reconstruction of Native LDL Particles to 16Å Resolution at Physiological Body Temperature" by a Finnish group, published on-line at

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0018841

It is licensed Creative Commons Attribution, so there is no obvious reason not to use one or two of the TIFFs or MPEGs (I lack the skill to do it myself). Of interest is the fact that the ApoB100 protein molecule is 1/6 of the total mass, and almost surrounds the lipid core. The thing is almost spherical at body temperature.

-- Solo Owl 03:02, 17 September 2013 (UTC) — Preceding unsigned comment added by Eall Ân Ûle (talkcontribs)

Average LDL levels, by age

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The words and table format are mine and original. The information is attributed to "Controlling Cholesterol The Natural Way."

Before age 30: 136 mg/dL (men) and 126 mg/dL (women)

Age 30 to 39: 149 mg/dL (men) and 129 mg/dL (women)

Age 40 to 49: 162 mg/dL (men) and 136 mg/dL (women)

Age 50 to 59: 165 mg/dL (men) and 159 mg/dL (women)

Age above 60: 164 mg/dL (men) and 159 mg/dL (women)

This table underscores that "average" does not mean "healthy," as well as the sharp rise of risks with age. Even before age 30, average male levels are already borderline unhealthy, and LDL levels and risks rise sharply afterward. The rising trend in men is followed 10 or 20 years later by women (who in later life are actually more at risk for coronary events than men).

Raised LDL is strongly linked to artery calcification.

This table suggests a benefit to consideration of a lifelong primary coronary prevention lifestyle, and heightened vigilance to check and respond to cholesterol rise after age 30 for men and age 40 for women.

rewriting introduction

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Just rewrote the introduction so that first paragraph a. explain what lipoproteins do - for people who want a one sentance answer b. where LDL stands in relation to other lipoproteins c. recognises that their are two types of LDL

the subsquent two paragraphs introduce aspects of the issues in research, testing and clinical use of tests that are covered in greater detail in subsquent sections.

Health is a very emotive subject - with multiple schools of scientific thought, it is not bad to recognise this complexity in the text. It is important though that the text remains focused on LDL not on what inputs, outputs and diets effect LDL, those other focuses are for other articles where those focuses can be expanded upon. X-mass (talk) 23:11, 6 July 2014 (UTC)[reply]

LDL-P

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LDL-P would be VERY important to add to article. http://www.docsopinion.com/health-and-nutrition/lipids/ldl-p/ ee1518 (talk) 18:28, 8 August 2014 (UTC)[reply]

Garcinia section (now including entire Plant Remedies section)

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Does the bit about Garcinia belong here? Based on the page itself, http://en.wikipedia.org/wiki/Garcinia_gummi-gutta, it sounds pretty bogus. Also, the study it links to seems... suspect at best. Thoughts? 216.80.69.8 (talk) 19:41, 21 October 2014 (UTC)[reply]

I agree and removed the mention. The WP page supports no such claim and the citation is just a supplement maker's product page (i.e., not a credible source for this sort of claim).
While I was at it I looked at the citation regarding green tea and removed that from the section as well (now there is no section on Plant Remedies). The citation was based on a study of FIVE women (way too small of a sample) who were given some extract of the tea (not the tea itself) and even then the actual claim is of an increase in vasodilation and a decrease in serum oxidizability. I can't see where either of these directly supports the claim of lowering LDL. Vasodilation refers to increasing the diameter of the vessel, not a reduction in something that might be blocking it. Lastly, the abstract/summary of the paper does not mention how long (if at all) the effect persisted after the consumption of the tea extract. Arbalest Mike (talk) 19:17, 9 October 2015 (UTC)[reply]

LDL-C vs Total Cholesterol

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The most commonly used predictors of adverse health outcomes are both LDL-C and Total Cholesterol. Presumably LDL-C is more specific and targeted, and has greater predictive value than Total Cholesterol? The article should address this issue.-71.174.175.150 (talk) 15:27, 6 November 2014 (UTC)[reply]

dimensions of LDL inconsistent

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in the introduction, it is written"A single LDL particle is about 260-300 nm in diameter (submicroscopic )..." further down, the diameter of LDL is given as 22 nm, which according to the given reference should be correct. I guess the first value is actually in Angstrom. As 10 A = 1 nm, 220A = 22nm. — Preceding unsigned comment added by 132.187.23.115 (talk) 13:41, 15 January 2016 (UTC)[reply]

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Introductory paragraph

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There was an introductory paragraph explaining that LDL-C is not necessarily the "bad" cholesterol and is important for regular functioning, etc. There were no citations and it did not have a neutral tone--I removed it for that reason. — Preceding unsigned comment added by 24.48.69.87 (talk) 13:37, 9 February 2020 (UTC)[reply]

LDL and risk of cardiovascular diseases

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This content and source (excerpt below) were removed because there is no prevailing clinical standard to indicate that LDL is not a significant risk factor for cardiovascular diseases. The removed content is a minority position with undue weight for inclusion in the article, WP:RSUW. No major clinical organization, regulatory agency, or scientific consensus on systematic reviews or meta-analyses concludes that the LDL evidence as a risk factor is "inaccurate" or "flawed".

Excerpt - "This view has been challenged as inaccurate and based on flawed research methodology.[1] The issue remains controversial and vigorously contested in the literature."

References

  1. ^ Ravnskov U, de Lorgeril M, Diamond DM, Hama R, Hamazaki T, Hammarskjöld B, Hynes N, Kendrick M, Langsjoen PH, Mascitelli L, McCully KS, Okuyama H, Rosch PJ, Schersten T, Sultan S, Sundberg R (2018). "LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature". Expert Rev Clin Pharmacol. 11: 959–970. doi:10.1080/17512433.2018.1519391. PMID 30198808.{{cite journal}}: CS1 maint: multiple names: authors list (link)

Best to discuss here for consensus if warranted for reinstatement in the article, WP:CON. Zefr (talk) 20:39, 27 April 2021 (UTC)[reply]