Low-density lipoprotein

Short description: One of the five major groups of lipoprotein

"LDL" redirects here. For other uses, see LDL (disambiguation).

Low-density lipoprotein

Medical diagnostics

Elevated LDL may result in atherosclerosis

Calculator| Template:LDL conversion

Low-density lipoprotein (LDL) is one of the five major groups of lipoprotein that transport all fat molecules around the body in extracellular water.[1] These groups, from least dense to most dense, are chylomicrons (aka ULDL by the overall density naming convention), very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL). LDL delivers fat molecules to cells.

Lipoproteins transfer lipids (fats) around the body in the extracellular fluid, making fats available to body cells for receptor-mediated endocytosis.[2][3] Lipoproteins are complex particles composed of multiple proteins, typically 80–100 proteins per particle (organized by a single apolipoprotein B for LDL and the larger particles). A single LDL particle is about 22–27.5 nanometers in diameter, typically transporting 3,000 to 6,000 fat molecules per particle and varying in size according to the number and mix of fat molecules contained within.[4] The lipids carried include all fat molecules with cholesterol, phospholipids, and triglycerides dominant; amounts of each vary considerably.[5]

Elevated LDL is an established causal factor for the development of atherosclerotic cardiovascular disease.[6][7][8][9] A normal non-atherogenic LDL-C level is 20–40 mg/dl.[10] Guidelines recommend maintaining LDL-C under 2.6 mmol/L (100 mg/dl) and under 1.8 mmol/L (70 mg/dL) for those at high risk.[10][11]

## Contents

* 1 Biochemistry
* 1.1 Structure
* 2 Physiology
* 2.1 Transport into the cell
* 2.2 Innate immune system
* 2.3 Size patterns
* 2.4 Oxidized
* 2.5 Acetyl
* 3 Testing
* 3.1 Estimation of LDL particles via cholesterol content
* 3.1.1 Normal ranges
* 3.2 Direct measurement of LDL particle concentrations
* 3.2.1 Optimal ranges
* 4 Lowering LDL-cholesterol
* 4.1 Pharmaceutical
* 4.1.1 Not approved as drugs
* 4.2 Lifestyle
* 5 See also
* 6 Notes and references
* 7 Further reading
* 8 External links

## Biochemistry

### Structure

Each native LDL particle enables emulsification, i.e. surrounding the fatty acids being carried, enabling these fats to move around the body within the water outside cells. Each particle contains a single apolipoprotein B-100 molecule (Apo B-100, a protein that has 4536 amino acid residues and a mass of 514 kDa), along with 80 to 100 additional ancillary proteins. Each LDL has a highly hydrophobic core consisting of polyunsaturated fatty acid known as linoleate and hundreds to thousands (about 1500 commonly cited as an average) of esterified and unesterified cholesterol molecules. This core also carries varying numbers of triglycerides and other fats and is surrounded by a shell of phospholipids and unesterified cholesterol, as well as the single copy of Apo B-100. LDL particles are approximately 22 nm (0.00000087 in.) to 27.5 nm in diameter and have a mass of about 3 million daltons.[12] Since LDL particles contain a variable and changing number of fatty acid molecules, there is a distribution of LDL particle mass and size.[4] Determining the structure of LDL has been difficult for biochemists because of its heterogeneous structure. However, the structure of LDL at human body temperature in native condition, with a resolution of about 16 Angstroms using cryogenic electron microscopy, has been described in 2011.[13]

## Physiology

LDL particles are formed when triglycerides are removed from VLDL by the lipoprotein lipase enzyme (LPL), and they become smaller and denser (i.e., fewer fat molecules with the same protein transport shell), containing a higher proportion of cholesterol esters.[14][15]

### Transport into the cell

When a cell requires more cholesterol than its HMG-CoA pathway can produce, it synthesizes the necessary LDL receptors as well as PCSK9, a proprotein convertase that marks the LDL receptor for degradation.[16] LDL receptors are inserted into the plasma membrane and diffuse freely until they associate with clathrin-coated pits. When LDL receptors bind LDL particles in the bloodstream, the clathrin-coated pits are endocytosed into the cell.[citation needed]

Vesicles containing LDL receptors bound to LDL are delivered to the endosomes. In the presence of low pH, such as that found in the endosome, LDL receptors undergo a conformation change, releasing LDL. LDL is then shipped to the lysosomes, where cholesterol esters in the LDL are hydrolysed. LDL receptors are typically returned to the plasma membrane, where they repeat this cycle. If LDL receptors bind to PCSK9, however, transport of LDL receptors is redirected to the lysosome, where they are degraded.[17]

### Innate immune system

LDL interferes with the quorum sensing system that upregulates genes required for invasive Staphylococcus aureus infection. The mechanism of antagonism entails binding apolipoprotein B to a S. aureus autoinducer pheromone, preventing signaling through its receptor. Mice deficient in apolipoprotein B are more susceptible to invasive bacterial infection.[18]

### Size patterns

LDL can be grouped based on its size: large low-density LDL particles are described as pattern A, and small high-density ("small dense") LDL particles are pattern B.[19] Pattern B has been associated by some with a higher risk for coronary artery disease.[20]: 1–10 This is thought to be because the smaller particles are more easily able to penetrate the endothelium of arterial walls. Pattern I, or intermediate, indicates that most LDL particles are very close in size to the normal gaps in the endothelium (26 nm). According to one study, sizes 19.0–20.5 nm were designated as pattern B and LDL sizes 20.6–22 nm were designated as pattern A.[21]

Some evidence suggests the correlation between pattern B and coronary artery disease is stronger than the correspondence between the LDL number measured in the standard lipid profile test. Tests to measure these LDL subtype patterns have been more expensive and not widely available, so the standard lipid profile test is used more often.[20]

There has also been noted a correspondence between higher triglyceride levels and higher levels of smaller, denser LDL particles and alternately lower triglyceride levels and higher levels of the larger, less dense ("buoyant") LDL.[22][23]

With continued research, decreasing cost, greater availability, and wider acceptance of other lipoprotein subclass analysis assay methods, including NMR spectroscopy, research studies have shown a stronger correlation between clinically evident human cardiovascular events and quantitatively measured particle concentrations.[24]

### Oxidized

Oxidized LDL (oxLDL) is a general term for LDL particles with oxidatively modified structural components. As a result, from free radical attack, both lipid and protein parts of LDL can be oxidized in the vascular wall. Besides the oxidative reactions in the vascular wall, oxidized lipids in LDL can also be derived from oxidized dietary lipids.[25][26] Oxidized LDL is known to associate with the development of atherosclerosis, and it is therefore widely studied as a potential risk factor of cardiovascular diseases.[27] Atherogenicity of oxidized LDL has been explained by lack of recognition of oxidation-modified LDL structures by the LDL receptors, preventing the normal metabolism of LDL particles and leading eventually to the development of atherosclerotic plaques.[27] Of the lipid material contained in LDL, various lipid oxidation products are known as the ultimate atherogenic species.[28] Acting as a transporter of these injurious molecules is another mechanism by which LDL can increase the risk of atherosclerosis.[26][29]

The LOX-1 scavenge receptor does take up oxLDL, but the liver does not naturally express it.[30] It is instead expressed by endothelial cells, platelets, macrophages, smooth muscle cells, and cardiomyocytes as an innate immune scavenge receptor. When activated, pro-inflammatory signals are generated in the cell, and damaging compounds are released as well. As a result, these cells are most sensitive to the effects of oxLDL.[31] SR-BI and CD36, two class B scavenge receptors, also take up oxLDL into the macrophage.[32]

Despite lower recognition efficacy by the LDL receptor, the liver does remove oxLDLs from the circulation. This is achieved by Kupffer cells and liver sinusoidal endothelial cells (LSECs). In LSECs, stabilin-1 and stabilin-2 mediate most of the uptake. Uptake of oxLDLs causes visible disruption to the structure of the LSEC in rats.[33] Doing the same also damages human LSEC cultures.[34]

### Acetyl

Acetyl LDL (acLDL) is a construct generated in vitro. When scientists produced such a modified version of LDL, they found that a class of scavenge receptors, now called SR-A, can recognize them and take them up. Because scavenge receptors work much faster than the downregulated native LDL receptor of a macrophage, oxLDL and acLDL can both fill up a macrophage quickly, turning it into a foam cell.[35]

## Testing

Blood tests commonly report LDL-C: the amount of cholesterol that is estimated to be contained with LDL particles, on average, using a formula, the Friedewald equation. In a clinical context, mathematically calculated estimates of LDL-C are commonly used to estimate how much low-density lipoproteins drive the progression of atherosclerosis. The problem with this approach is that LDL-C values are commonly discordant with both direct measurements of LDL particles and actual rates of atherosclerosis progression.[citation needed]

Direct LDL measurements are also available and better reveal individual issues but are less often promoted or done due to slightly higher costs and are available from only a couple of laboratories in the United States. In 2008, the American Diabetes Association (ADA) and American College of Cardiology (ACC) recognized direct LDL particle measurement by NMR as superior for assessing individual risk of cardiovascular events.[36]

### Estimation of LDL particles via cholesterol content

Chemical measures of lipid concentration have long been the most-used clinical measurement, not because they have the best correlation with individual outcomes but because these lab methods are less expensive and more widely available.

The lipid profile does not measure LDL particles. It only estimates them using the Friedewald equation[23][37] by subtracting the amount of cholesterol associated with other particles, such as HDL and VLDL, assuming a prolonged fasting state, etc.:

L≈C−H−kT

where H is HDL cholesterol, L is LDL cholesterol, C is total cholesterol, T is triglycerides, and k is 0.20 if the quantities are measured in mg/dL and 0.45 in mmol/L.

L is often reported as CLDL-C (calculated low-density lipoprotein cholesterol). This is the most common way of estimating the amount of cholesterol carried by low-density lipoprotein.[38]

There are limitations to this method, most notably that samples must be obtained after a 12 to 14 h fast and that LDL-C cannot be calculated if plasma triglyceride is > 4.52 mmol/L (400 mg/dL). Even at triglyceride levels of 2.5 to 4.5 mmol/L, this formula is considered inaccurate.[39] If both total cholesterol and triglyceride levels are elevated then a modified formula, with quantities in mg/dL, may be used

L=C−H−0.16T

This formula provides an approximation with fair accuracy for most people, assuming the blood was drawn after fasting for about 14 hours or longer, but does not reveal the actual LDL particle concentration because the percentage of fat molecules within the LDL particles, which are cholesterol, varies as much as 8:1 variation. There are several formulas published addressing the inaccuracy in LDL-C estimation.[40][41][42] The inaccuracy is based on the assumption that VLDL-C (very low density lipoprotein cholesterol) is always one-fifth of the triglyceride concentration. Other formulae address this issue by using an adjustable factor[43] or using a regression equation.[44] There are few studies which have compared the LDL-C values derived from this formula and values obtained by direct enzymatic method.[45] Direct enzymatic methods are found to be accurate and must be the test of choice in clinical situations. In resource-poor settings, the option to use the formula has to be considered.[45]

However, the concentration of LDL particles, and to a lesser extent, their size, has a stronger and consistent correlation with individual clinical outcomes than the amount of cholesterol within LDL particles, even if the LDL-C estimation is approximately correct. There is increasing evidence and recognition of the value of more targeted and accurate measurements of LDL particles. Specifically, LDL particle number (concentration) and, to a lesser extent, size have shown slightly stronger correlations with atherosclerotic progression and cardiovascular events than obtained using chemical measures of the amount of cholesterol carried by the LDL particles.[46] It is possible that the LDL cholesterol concentration can be low, yet LDL particle number high and cardiovascular events rates are high. Correspondingly, it is possible that LDL cholesterol concentration can be relatively high, yet LDL particle number is low, and cardiovascular events are also low.[citation needed]

#### Normal ranges

In the US, the American Heart Association, National Institutes of Health (NIH), and National Cholesterol Education Program (NCEP) provide a set of guidelines for fasting LDL-cholesterol levels, estimated or measured, and risk for heart disease. As of about 2005, these guidelines were:[47][48][49]

Level mg/dL | Level mmol/L  | Interpretation

|
|

25 to <50  | <1.3  | Optimal LDL cholesterol levels in healthy young children before onset of atherosclerotic plaque in heart artery walls
<70  | <1.8  | Optimal LDL cholesterol, corresponding to lower rates of progression, is promoted as a target option for those known to have advanced symptomatic cardiovascular disease clearly
<100  | <2.6  | Optimal LDL cholesterol, corresponding to lower, but not zero, rates for symptomatic cardiovascular disease events
100 to 129  | 2.6 to 3.3  | Near-optimal LDL level, corresponding to higher rates of developing symptomatic cardiovascular disease events
130 to 159  | 3.3 to 4.1  | Borderline high LDL level, corresponding to even higher rates for developing symptomatic cardiovascular disease events
160 to 199  | 4.1 to 4.9  | High LDL level, corresponding to much higher rates for developing symptomatic cardiovascular disease events
>200  | >4.9  | Very high LDL level, corresponding to the highest increased rates of symptomatic cardiovascular disease events

Over time, with more clinical research, these recommended levels keep being reduced because LDL reduction, including to abnormally low levels, was the most effective strategy for reducing cardiovascular death rates in one large double blind, randomized clinical trial of men with hypercholesterolemia;[50] far more effective than coronary angioplasty/stenting or bypass surgery.[51]

The 2004 updated American Heart Association, NIH, and NCEP recommendations for people with known atherosclerosis diseases are for lowering LDL levels to less than 70 mg/dL. This low level of less than 70 mg/dL was recommended for primary prevention of 'very-high risk patients' and secondary prevention as a 'reasonable further reduction'. This position was disputed.[52] Statin drugs involved in such clinical trials have numerous physiological effects beyond simply the reduction of LDL levels.

From longitudinal population studies following the progression of atherosclerosis-related behaviors from early childhood into adulthood,[53] the usual LDL in childhood, before the development of fatty streaks, is about 35 mg/dL. However, all the above values refer to chemical measures of lipid/cholesterol concentration within LDL, not measured low-density lipoprotein concentrations, which is the accurate approach.[46]

A study was conducted measuring the effects of guideline changes on LDL cholesterol reporting and control for diabetes visits in the US from 1995 to 2004. It was found that although LDL cholesterol reporting and control for diabetes and coronary heart disease visits improved continuously between 1995 and 2004,[54][55] neither the 1998 ADA guidelines nor the 2001 ATP III guidelines increased LDL cholesterol control for diabetes relative to coronary heart disease.[56]

### Direct measurement of LDL particle concentrations

There are several competing methods for measuring lipoprotein particle concentrations and size. The evidence is that the NMR methodology (developed, automated and significantly reduced in costs while improving accuracy as pioneered by Jim Otvos and associates) results in a 22-25% reduction in cardiovascular events within one year,[57] contrary to the longstanding claims by many in the medical industry that the superiority over existing methods was weak, even by statements of some proponents.[58]

Since the later 1990s, because of the development of NMR measurements, it has been possible to clinically measure lipoprotein particles at lower cost [under $80 US (including shipping) and is decreasing versus the previous costs of >$400 to >$5,000] and higher accuracy. There are two other assays for LDL particles; however, most estimate only LDL particle concentrations like LDL-C.[citation needed]

The ADA and ACC mentioned direct LDL particle measurement by NMR in a 28 March 2008 joint consensus statement,[59] as having advantages for predicting individual risk of atherosclerosis disease events, but the statement noted that the test is less widely available, is more expensive [about $13.00 US (2015 without insurance coverage) from some labs which use the Vantera Analyzer[60]]. Debate continues that it is "...unclear whether LDL particle size measurements add value to the measurement of LDL-particle concentration", though outcomes have continuously tracked LDL particle, not LDL-C, concentrations.

Using NMR, the total LDL particle concentrations in nmol/L plasma are typically subdivided by percentiles referenced to the 5,382 men and women participating in the MESA trial who are not on any lipid medications.[61]

LDL particle concentration can also be measured by measuring the concentration of the protein ApoB, based on the generally accepted principle that each LDL or VLDL particle carries one ApoB molecule.[62]

#### Optimal ranges

The LDL particle concentrations are typically categorized by percentiles, <20%, 20–50%, 50th–80th%, 80th–95%, and >95% groups of the people participating and being tracked in the MESA trial, a medical research study sponsored by the United States National Heart, Lung, and Blood Institute.

MESA Percentile  | LDL particles nmol/L  | Interpretation

|
|

0–20%  | <1,000  | Those with the lowest rate of cardiovascular disease events and low (optimal) LDL particle concentration
20–50%  | 1,000–1,299  | Those with a moderate rate of cardiovascular disease events and moderate LDL particle concentration
50–80%  | 1,300–1,599  | Those with borderline-high rates of cardiovascular disease events and higher LDL particle concentration
89–95%  | 1,600–2,000  | Those with a high rate of cardiovascular disease events and even higher LDL particle concentration
>95%  | >2,000  | Those with a very high rate of cardiovascular disease events and the highest LDL particle concentration

Over time, the lowest incidence of atherosclerotic events occurs within the <20% group, with increased rates for the higher groups. Multiple other measures, including particle sizes, small LDL particle concentrations, large total and HDL particle concentrations, along with estimations of insulin resistance pattern and standard cholesterol lipid measurements (for comparison of the plasma data with the estimation methods discussed above) are also routinely provided.

## Lowering LDL-cholesterol

Markers indicating a need for LDL-C Reduction

(Per 2004 United States Government Minimum Guidelines[63][64])

If the patient's cardiac risk is...  | then the patient should consider LDL-C reduction if the count in mg/dL is over...  | and LDL-C reduction is indicated if the count in mg/dL is over...
High, meaning a 20% or greater risk of heart attack within 10 years or an extreme risk factor

* United States Department of Health and Human Services; National Heart, Lung, and Blood Institute; National Institutes of Health (June 2005). "NHLBI, High Blood Cholesterol: What You Need to Know". http://www.nhlbi.nih.gov/health/public/heart/chol/wyntk.htm. </ref>

| 100[65]
moderately high, meaning a 10-20% risk of heart attack within 10 years and more than 2 heart attack risk factors  | 100[65] | 130[65]
moderate, meaning a 10% risk of heart attack within 10 years and more than 2 heart attack risk factors  | 130[65] | 160[65]
low, meaning less than 10% risk of heart attack within 10 years and 1 or 0 heart attack risk factors  | 160[65] | 190[65]

The mevalonate pathway serves as the basis for the biosynthesis of many molecules, including cholesterol. The enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA reductase) is an essential component and performs the first of 37 steps within the cholesterol production pathway, and is present in every animal cell. Statins block this first step.[66]

LDL-C is not a count of actual LDL particles. LDL-C represents how much cholesterol is being transported by all LDL particles, which is either a smaller concentration of large particles or a high concentration of small particles. LDL-C itself can be estimated by subtraction (Friedewald's method)[67] or directly measured; see the section Testing above to see how it's measured.[68] LDL particles carry many lipid molecules (typically 3,000 to 6,000 lipid molecules per LDL particle); this includes cholesterol, triglycerides, phospholipids and others. An LDL-C measurement cannot account for differences in size and composition between types of LDL.[69]

### Pharmaceutical

Main article: Chemistry:Lipid-lowering agent

* PCSK9 inhibitors, in clinical trials, by several companies, are more effective for LDL reduction than the statins, including statins alone at high dose (though not necessarily the combination of statins plus ezetimibe).[citation needed] They have been approved and are recommended in patients not receiving enough reduction from their maximally tolerated dose of statins + ezetimibe.[70]
* Statins reduce high levels of LDL particles by inhibiting the enzyme HMG-CoA reductase in cells, the rate-limiting step of cholesterol synthesis. To compensate for the decreased cholesterol availability, synthesis of LDL receptors (including hepatic) is increased, resulting in an increased clearance of LDL particles from the extracellular water, including of the blood.[66]
* Ezetimibe reduces intestinal absorption of cholesterol, thus can reduce LDL particle concentrations when combined with statins.[71]
* Niacin (nicotinic acid), lowers LDL by selectively inhibiting hepatic diacylglycerol acyltransferase 2, reducing triglyceride synthesis and VLDL secretion through a receptor HM74[72] and HM74A or GPR109A.[73] Introduced in 1955.
* Clofibrate is effective at lowering cholesterol levels, but has been associated with significantly increased cancer and stroke mortality, despite lowered cholesterol levels.[74] Other developed and tested fibrates, e.g. fenofibric acid[75] have had a better track record and are primarily promoted for lowering VLDL particles (triglycerides), not LDL particles, yet can help some in combination with other strategies.
* Probucol, introduced in the 1970s. Now known to work through, among other ways, changing the shape and size of the LDL particle so they can be taken up by the liver without involving the LDL receptor. It has been discontinued in the west due to HDL-C decreases that were not explainable at the time. It's now known that it enhances the reverse cholesterol transport and antioxidant functions of HDL despite decreasing HDL-C.[76]

#### Not approved as drugs

* Several CETP inhibitors have been researched to improve HDL concentrations, but so far, despite dramatically increasing HDL-C, have not had a consistent track record in reducing atherosclerosis disease events. Some have increased mortality rates compared with placebo.
* Some tocotrienols, especially delta- and gamma-tocotrienols, are being promoted as statin alternative non-prescription agents to treat high cholesterol, having been shown in vitro to have an effect. In particular, gamma-tocotrienol appears to be another HMG-CoA reductase inhibitor, and can reduce cholesterol production.[77] As with statins, this decrease in intra-hepatic (liver) LDL levels may induce hepatic LDL receptor up-regulation, also decreasing plasma LDL levels. As always, a key issue is how benefits and complications of such agents compare with statins—molecular tools that have been analyzed in large numbers of human research and clinical trials since the mid-1970s.[citation needed]
* Phytosterols are widely recognized as having a proven LDL cholesterol lowering efficacy'[78] A 2018 review found a dose-response relationship for phytosterols, with intakes of 1.5 to 3 g/day lowering LDL-C by 7.5% to 12%,[79] but reviews as of 2017 had found no data indicating that the consumption of phytosterols may reduce the risk of CVD.[80] Current supplemental guidelines for reducing LDL recommend doses of phytosterols in the 1.6-3.0 grams per day range (Health Canada, EFSA, ATP III, FDA) with a 2009 meta-analysis demonstrating an 8.8% reduction in LDL-cholesterol at a mean dose of 2.15 gram per day.[81]

### Lifestyle

LDL cholesterol can be lowered through dietary intervention by limiting foods with saturated fat and avoiding foods with trans fat.[82] Saturated fats are found in meat products (including poultry), full-fat dairy, eggs, and refined tropical oils like coconut and palm.[83] Added trans fat (in the form of partially hydrogenated oils) has been banned in 53 countries.[84] However, trans fat can still be found in red meat and dairy products as it is produced in small amounts by ruminants such as sheep and cows.[85][86] LDL cholesterol can also be lowered by increasing consumption of soluble fiber and plant-based foods.[87] Canned baked beans, whole chickpeas, navy beans, pinto beans and peas decrease total and LDL cholesterol.[88][89]

Another lifestyle approach to reduce LDL cholesterol has been minimizing total body fat, in particular fat stored inside the abdominal cavity (visceral body fat). Visceral fat, which is more metabolically active than subcutaneous fat, has been found to produce many enzymatic signals, e.g. resistin, which increase insulin resistance and circulating VLDL particle concentrations, thus both increasing LDL particle concentrations and accelerating the development of diabetes mellitus.[citation needed]

## See also

* Catechin
* Cholesterol
* Lysosomal acid lipase deficiency
* Cholesteryl ester storage disease
* Coenzyme Q10
* Flavonoid
* Glutathione
* Health effects of tea
* High density lipoprotein
* LDL receptor
* Lipid profile
* Lipoprotein(a)
* Lipoprotein-X
* Melatonin
* Polyphenol antioxidant
* Saturated fat
* Stanol ester
* Sterol ester
* Triglyceride
* Vitamin A
* Vitamin C
* Vitamin E

## Notes and references

1. ↑ "LDL and HDL: Bad and Good Cholesterol". CDC. https://www.cdc.gov/cholesterol/ldl_hdl.htm.
2. ↑ Dashti, Monireh; Kulik, Willem; Hoek, Frans; Veerman, Enno C.; Peppelenbosch, Maikel P.; Rezaee, Farhad (7 November 2011). "A Phospholipidomic Analysis of All Defined Human Plasma Lipoproteins". Scientific Reports 1 (1): 139. doi:10.1038/srep00139. PMID 22355656. Bibcode: 2011NatSR...1..139D.
3. ↑ Dashty, Monireh; Motazacker, Mohammad M.; Levels, Johannes; Vries, Marcel de; Mahmoudi, Morteza; Peppelenbosch, Maikel P.; Rezaee, Farhad (2014). "Proteome of human plasma very low-density lipoprotein and low-density lipoprotein exhibits a link with coagulation and lipid metabolism". Thrombosis and Haemostasis 112 (3): 518–530. doi:10.1160/TH13-02-0178. PMID 24500811.
4. ↑ 4.0 4.1 "Structure of apolipoprotein B-100 in low density lipoproteins". Journal of Lipid Research 42 (9): 1346–67. September 2001. doi:10.1016/S0022-2275(20)30267-4. PMID 11518754.
5. ↑ Sira, Elevina E. Pérez (2021-10-05) (in en). Foods for Special Dietary Regimens. Bentham Science Publishers. ISBN 978-981-4998-07-9. https://books.google.com/books?id=MIROEAAAQBAJ&pg=PA208.
6. ↑ "Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel". European Heart Journal 38 (32): 2459–2472. August 2017. doi:10.1093/eurheartj/ehx144. PMID 28444290.
7. ↑ Mach, François; Baigent, Colin; Catapano, Alberico L; Koskinas, Konstantinos C; Casula, Manuela; Badimon, Lina; Chapman, M John; De Backer, Guy G et al. (2020-01-01). "2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk" (in en). European Heart Journal 41 (1): 111–188. doi:10.1093/eurheartj/ehz455. ISSN 0195-668X. PMID 31504418. https://academic.oup.com/eurheartj/article/41/1/111/5556353.
8. ↑ Borén, Jan; Chapman, M John; Krauss, Ronald M; Packard, Chris J; Bentzon, Jacob F; Binder, Christoph J; Daemen, Mat J; Demer, Linda L et al. (2020-06-21). "Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel". European Heart Journal 41 (24): 2313–2330. doi:10.1093/eurheartj/ehz962. ISSN 0195-668X. PMID 32052833. PMC 7308544. https://academic.oup.com/eurheartj/article/41/24/2313/5735221?login=false.
9. ↑ Jackson, Elizabeth J.; Willard, Kaye-Eileen (2025). "LDL Cholesterol Management Simplified in (Adults) - Lower for Longer is Better: Guidance from the National Lipid Association". Journal of Clinical Lipidology. doi:10.1016/j.jacl.2025.06.002. PMID 40713232. https://www.lipidjournal.com/article/S1933-2874(25)00317-4/fulltext.
10. ↑ 10.0 10.1 "There is urgent need to treat atherosclerotic cardiovascular disease risk earlier, more intensively, and with greater precision: A review of current practice and recommendations for improved effectiveness". Am J Prev Cardiol 12. 2022. doi:10.1016/j.ajpc.2022.100371. PMID 36124049.
11. ↑ "The importance of LDL-C lowering in atherosclerotic cardiovascular disease prevention: Lower for longer is better". Am J Prev Cardiol 18. 2024. doi:10.1016/j.ajpc.2024.100649. PMID 38576462.
12. ↑ Campos, Hannia (1992). "LDL Particle Size Distribution". Arteriosclerosis, Thrombosis, and Vascular Biology 12 (12): 1410–1419. doi:10.1161/01.ATV.12.12.1410. PMID 1450174.
13. ↑ "Three-Dimensional cryoEM Reconstruction of Native LDL Particles to 16Å Resolution at Physiological Body Temperature". PLOS ONE 6 (5). May 2011. doi:10.1371/journal.pone.0018841. PMID 21573056. Bibcode: 2011PLoSO...618841K.
14. ↑ Pirahanchi, Yasaman; Sinawe, Hadeer; Dimri, Manjari (8 August 2023). "Biochemistry, LDL Cholesterol". StatPearls. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK519561/.
15. ↑ Sun, Hung-Yu; Lin, Chun-Chieh; Lee, Jin-Ching; Wang, Shainn-Wei; Cheng, Pin-Nan; Wu, I.-Chin; Chang, Ting-Tsung; Lai, Ming-Derg et al. (July 3, 2013). "Very low-density lipoprotein/lipo-viro particles reverse lipoprotein lipase-mediated inhibition of hepatitis C virus infection via apolipoprotein C-III". Gut 62 (8): 1193–1203. doi:10.1136/gutjnl-2011-301798. PMID 22689516.
16. ↑ Zhang, Da-Wei; Garuti, Rita; Tang, Wan-Jin; Cohen, Jonathan C.; Hobbs, Helen H. (2 September 2008). "Structural requirements for PCSK9-mediated degradation of the low-density lipoprotein receptor". Proceedings of the National Academy of Sciences 105 (35): 13045–13050. doi:10.1073/pnas.0806312105. PMID 18753623. Bibcode: 2008PNAS..10513045Z.
17. ↑ "Inclisiran: a new milestone on the PCSK9 road to tackle cardiovascular risk". Eur Heart J Cardiovasc Pharmacother 7 (3): e11–e12. May 2021. doi:10.1093/ehjcvp/pvab014. PMID 33655296.
18. ↑ "Apolipoprotein B Is an innate barrier against invasive Staphylococcus aureus infection". Cell Host & Microbe 4 (6): 555–66. December 2008. doi:10.1016/j.chom.2008.10.001. PMID 19064256.
19. ↑ "When it comes to LDL, size matters" (in en-US). 2022-07-18. https://gethlth.com/when-it-comes-to-ldl-size-matters/.
20. ↑ 20.0 20.1 "Small Dense Low-Density Lipoprotein as Biomarker for Atherosclerotic Diseases". Oxidative Medicine and Cellular Longevity 2017 (10). 2017. doi:10.1155/2017/1273042. PMID 28572872.
21. ↑ Bhalodkar, Narendra C.; Blum, Steve; Rana, Thakor; Kitchappa, Radha; Bhalodkar, Ami N.; Enas, Enas A. (1 May 2005). "Comparison of high-density and low-density lipoprotein cholesterol subclasses and sizes in Asian Indian women with Caucasian women from the Framingham offspring study". Clin Cardiol 28 (5): 247–251. doi:10.1002/clc.4960280510. PMID 15971461.
22. ↑ "Small LDL and its clinical importance as a new CAD risk factor: a female case study". Progress in Cardiovascular Nursing 17 (4): 167–73. 2002. doi:10.1111/j.0889-7204.2002.01453.x. PMID 12417832.
23. ↑ 23.0 23.1 "Estimating low-density lipoprotein cholesterol by the Friedewald equation is adequate for classifying patients on the basis of nationally recommended cutpoints". Clinical Chemistry 36 (1): 15–9. January 1990. doi:10.1093/clinchem/36.1.15. PMID 2297909.
24. ↑ Otvos J (June 1999). "Measurement of triglyceride-rich lipoproteins by nuclear magnetic resonance spectroscopy". Clin Cardiol 22 (6 Suppl): II21–7. doi:10.1002/clc.4960221405. PMID 10376193.
25. ↑ Staprans, I.; Rapp, J. H.; Pan, X. M.; Feingold, K. R. (1996). "Oxidized lipids in the diet are incorporated by the liver into very low density lipoprotein in rats". Journal of Lipid Research 37 (2): 420–30. doi:10.1016/S0022-2275(20)37628-8. PMID 9026539.
26. ↑ 26.0 26.1 Ahotupa, Markku (2017). "Oxidized lipoprotein lipids and atherosclerosis". Free Radical Research 51 (4): 439–447. doi:10.1080/10715762.2017.1319944. PMID 28412863. https://figshare.com/articles/journal_contribution/4986497.
27. ↑ 27.0 27.1 Stocker, Roland; Keaney, John F. (2004). "Role of Oxidative Modifications in Atherosclerosis". Physiological Reviews 84 (4): 1381–1478. doi:10.1152/physrev.00047.2003. PMID 15383655.
28. ↑ Birukov, K. G. (2006). "Oxidized lipids: The two faces of vascular inflammation". Current Atherosclerosis Reports 8 (3): 223–31. doi:10.1007/s11883-006-0077-x. PMID 16640959.
29. ↑ Shao, Baohai; Heinecke, Jay W. (2009). "HDL, lipid peroxidation, and atherosclerosis". Journal of Lipid Research 50 (4): 599–601. doi:10.1194/jlr.E900001-JLR200. PMID 19141435.
30. ↑ Wang, Z; Guo, X; Zhang, Q; Du, G; Zeng, Z; Zheng, C; Wei, Y (2021). "Elimination of Ox-LDL through the liver inhibits advanced atherosclerotic plaque progression.". International Journal of Medical Sciences 18 (16): 3652–3664. doi:10.7150/ijms.63065. PMID 34790037.
31. ↑ Barreto, Joaquim; Karathanasis, Sotirios K.; Remaley, Alan; Sposito, Andrei C. (January 2021). "Role of LOX-1 (Lectin-Like Oxidized Low-Density Lipoprotein Receptor 1) as a Cardiovascular Risk Predictor: Mechanistic Insight and Potential Clinical Use". Arteriosclerosis, Thrombosis, and Vascular Biology 41 (1): 153–166. doi:10.1161/ATVBAHA.120.315421. PMID 33176449.
32. ↑ Sun, B; Boyanovsky, BB; Connelly, MA; Shridas, P; van der Westhuyzen, DR; Webb, NR (December 2007). "Distinct mechanisms for OxLDL uptake and cellular trafficking by class B scavenger receptors CD36 and SR-BI.". Journal of Lipid Research 48 (12): 2560–70. doi:10.1194/jlr.M700163-JLR200. PMID 17876058.
33. ↑ Mao, Hong; Kruse, Larissa D.; Li, Ruomei; Oteiza, Ana; Struck, Eike C.; Schürstedt, Jasmin; Hübner, Wolfgang; Cogger, Victoria C. et al. (23 October 2024). "Impact of oxidized low-density lipoprotein on rat liver sinusoidal endothelial cell morphology and function". npj Gut and Liver 1 (1). doi:10.1038/s44355-024-00009-5.
34. ↑ Zhang, Qi; Liu, Jing; Liu, Jia; Huang, Wenhui; Tian, Limin; Quan, Jinxing; Wang, Yunfang; Niu, Ruilan (October 2014). "oxLDL induces injury and defenestration of human liver sinusoidal endothelial cells via LOX1". Journal of Molecular Endocrinology 53 (2): 281–293. doi:10.1530/JME-14-0049. PMID 25057109.
35. ↑ Miller, Yury I.; Tsimikas, Sotirios (2009). "Lipoprotein Oxidation and Modification". Clinical Lipidology. pp. 93–110. doi:10.1016/B978-141605469-6.50012-3. ISBN 978-1-4160-5469-6.
36. ↑ Brunzell, John D.; Davidson, Michael; Furberg, Curt D.; Goldberg, Ronald B.; Howard, Barbara V.; Stein, James H.; Witztum, Joseph L. (April 2008). "Lipoprotein Management in Patients With Cardiometabolic Risk". Journal of the American College of Cardiology 51 (15): 1512–1524. doi:10.1016/j.jacc.2008.02.034. PMID 18402913.
37. ↑ "Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge". Clinical Chemistry 18 (6): 499–502. June 1972. doi:10.1093/clinchem/18.6.499. PMID 4337382.
38. ↑ Ntei Abudu and Stanley Levinson. "Calculated low-density lipoprotein cholesterol remains a viable and important test for screening and targeting therapy ". doi: 10.1515/CCLM.2007.291  2007.
39. ↑ "Triglycerides and small dense LDL: the twin Achilles heels of the Friedewald formula". Clinical Biochemistry 36 (7): 499–504. October 2003. doi:10.1016/S0009-9120(03)00117-6. PMID 14563441.
40. ↑ Anandaraja, S.; Narang, R.; Godeswar, R.; Laksmy, R.; Talwar, K.K. (June 2005). "Low-density lipoprotein cholesterol estimation by a new formula in Indian population". International Journal of Cardiology 102 (1): 117–120. doi:10.1016/j.ijcard.2004.05.009. PMID 15939107.
41. ↑ de Cordova, Caio Mauricio Mendes; de Cordova, Mauricio Mendes (January 2013). "A new accurate, simple formula for LDL-cholesterol estimation based on directly measured blood lipids from a large cohort" (in en). Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 50 (1): 13–19. doi:10.1258/acb.2012.011259. PMID 23108766.
42. ↑ Chen, Yunqin; Zhang, Xiaojin; Pan, Baishen; Jin, Xuejuan; Yao, Haili; Chen, Bin; Zou, Yunzeng; Ge, Junbo et al. (2010). "A modified formula for calculating low-density lipoprotein cholesterol values" (in en). Lipids in Health and Disease 9 (1): 52. doi:10.1186/1476-511X-9-52. PMID 20487572.
43. ↑ Martin, Seth S.; Blaha, Michael J.; Elshazly, Mohamed B.; Toth, Peter P.; Kwiterovich, Peter O.; Blumenthal, Roger S.; Jones, Steven R. (20 November 2013). "Comparison of a Novel Method vs. the Friedewald Equation for Estimating Low-Density Lipoprotein Cholesterol Levels From the Standard Lipid Profile". JAMA 310 (19): 2061–2068. doi:10.1001/jama.2013.280532. PMID 24240933.
44. ↑ Sampson, Maureen; Ling, Clarence; Sun, Qian; Harb, Roa; Ashmaig, Mohmed; Warnick, Russell; Sethi, Amar; Fleming, James K. et al. (May 2020). "A New Equation for Calculation of Low-Density Lipoprotein Cholesterol in Patients With Normolipidemia and/or Hypertriglyceridemia". JAMA Cardiology 5 (5): 540–548. doi:10.1001/jamacardio.2020.0013. PMID 32101259.
45. ↑ 45.0 45.1 Ramasamy, Jagadish; Job, Victoria; Mani, Thenmozhi; Jacob, Molly (May 2021). "Calculated values of serum LDL-cholesterol (LDL-C) – for better or worse?". Nutrition, Metabolism and Cardiovascular Diseases 31 (5): 1486–1493. doi:10.1016/j.numecd.2021.01.016. PMID 33744036.
46. ↑ 46.0 46.1 "Apolipoprotein B Particles and Cardiovascular Disease: A Narrative Review". JAMA Cardiology 4 (12): 1287–1295. December 2019. doi:10.1001/jamacardio.2019.3780. PMID 31642874.
47. ↑ "Cholesterol Levels". American Heart Association. http://www.americanheart.org/presenter.jhtml?identifier=4500.
48. ↑ "What Do My Cholesterol Levels Mean?". American Heart Association. September 2007. http://www.americanheart.org/downloadable/heart/119618151049911 CholLevels 9_07.pdf.
49. ↑ "Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Executive Summary". National Institutes of Health. May 2001. https://www.nhlbi.nih.gov/files/docs/guidelines/atp3xsum.pdf.
50. ↑ "Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group". The New England Journal of Medicine 333 (20): 1301–7. November 1995. doi:10.1056/NEJM199511163332001. PMID 7566020.
51. ↑ William E. Boden (April 2007). "Optimal Medical Therapy with or without PCI for Stable Coronary Disease". The New England Journal of Medicine 356 (15): 1503–1516. doi:10.1056/NEJMoa070829. PMID 17387127.
52. ↑ Hayward, Rodney A. (3 October 2006). "Narrative Review: Lack of Evidence for Recommended Low-Density Lipoprotein Treatment Targets: A Solvable Problem". Ann Intern Med 145 (7): 520–30. doi:10.7326/0003-4819-145-7-200610030-00010. PMID 17015870.
53. ↑ Cybulska, Barbara; Kłosiewicz-Latoszek, Longina; Penson, Peter E.; Nabavi, Seyed Mohammad; Lavie, Carl J.; Banach, Maciej (July 2021). "How much should LDL cholesterol be lowered in secondary prevention? Clinical efficacy and safety in the era of PCSK9 inhibitors". Progress in Cardiovascular Diseases 67: 65–74. doi:10.1016/j.pcad.2020.12.008. PMID 33383060. https://researchonline.ljmu.ac.uk/id/eprint/14560/1/How low should you go with LDL cholesterol lowering in secondary prevention.pdf.
54. ↑ Wolska, Anna; Remaley, Alan T. (2020). "Measuring LDL-cholesterol: what is the best way to do it?". Current Opinion in Cardiology 35 (4): 405–411. doi:10.1097/HCO.0000000000000740. PMID 32412961.
55. ↑ Howard, Barbara V.; Robbins, David C.; Sievers, Maurice L.; Lee, Elisa T.; Rhoades, Dorothy; Devereux, Richard B.; Cowan, Linda D.; Gray, R. Stuart et al. (March 2000). "LDL Cholesterol as a Strong Predictor of Coronary Heart Disease in Diabetic Individuals With Insulin Resistance and Low LDL: The Strong Heart Study". Arteriosclerosis, Thrombosis, and Vascular Biology 20 (3): 830–835. doi:10.1161/01.atv.20.3.830. PMID 10712410.
56. ↑ Wang, Y Richard; G Caleb Alexander; David O Meltzer (December 2005). "Lack of Effect of Guideline Changes on LDL Cholesterol Reporting and Control for Diabetes Visits in the U.S., 1995–2004". Diabetes Care 28 (12): 2942–2944. doi:10.2337/diacare.28.12.2942. PMID 16306559.
57. ↑ Peter P. Toth; Michael Grabner; Rajeshwari S. Punekar; Ralph A. Quimbo; Mark J. Cziraky; Terry A. Jacobson (August 2014). "Cardiovascular risk in patients achieving low-density lipoprotein cholesterol and particle targets". Atherosclerosis 235 (2): 585–591. doi:10.1016/j.atherosclerosis.2014.05.914. PMID 24956532.
58. ↑ Krauss RM (August 2010). "Lipoprotein subfractions and cardiovascular disease risk". Current Opinion in Lipidology 21 (4): 305–11. doi:10.1097/MOL.0b013e32833b7756. PMID 20531184.
59. ↑ Brunzell, John D.; Davidson, Michael; Furberg, Curt D.; Goldberg, Ronald B.; Howard, Barbara V.; Stein, James H.; Witztum, Joseph L. (15 April 2008). "Lipoprotein Management in Patients With Cardiometabolic Risk". J Am Coll Cardiol 51 (15): 1512–1524. doi:10.1016/j.jacc.2008.02.034. PMID 18402913.
60. ↑ "Google". https://www.google.com/#q=Vantera+Analyzer.
61. ↑ "MESA - Multi-Ethnic Study of Atherosclerosis". https://www.mesa-nhlbi.org/.
62. ↑ Sniderman, A. D.; Thanassoulis, G.; Glavinovic, T.; Navar, A. M.; Pencina, M.; Catapano, A.; Ference, B. A. (1 Dec 2019). "Apolipoprotein B Particles and Cardiovascular Disease: A Narrative Review". JAMA Cardiology 4 (12): 1287–1295. doi:10.1001/jamacardio.2019.3780. PMID 31642874.
63. ↑ "Management of Blood Cholesterol in Adults: Systematic Evidence Review from the Cholesterol Expert Panel | National Heart, Lung, and Blood Institute (NHLBI)". https://www.nhlbi.nih.gov/health-topics/management-blood-cholesterol-in-adults.
64. ↑ "Archived copy". https://www.acli.com/Events/Documents/Tue22812 - Lipidology - Pamela Morris.pdf.
65. ↑ 65.0 65.1 65.2 65.3 65.4 65.5 65.6 Cite error: Invalid `<ref>` tag; no text was provided for refs named `BBDstatins`
66. ↑ 66.0 66.1 "The discovery and development of HMG-CoA reductase inhibitors". Journal of Lipid Research 33 (11): 1569–1582. November 1992. doi:10.1016/S0022-2275(20)41379-3. PMID 1464741.
67. ↑ "Laboratory Procedure Manual; Total Cholesterol, HDL-Cholesterol, Triglycerides, and LDL-Cholesterol; Serum; Hitachi 704". https://www.cdc.gov/nchs/data/nhanes/nhanes_03_04/l13_c_met_lipids.pdf.
68. ↑ Sajja, A; Park, J; Sathiyakumar, V; Varghese, B; Pallazola, VA; Marvel, FA; Kulkarni, K; Muthukumar, A et al. (1 October 2021). "Comparison of Methods to Estimate Low-Density Lipoprotein Cholesterol in Patients With High Triglyceride Levels.". JAMA Network Open 4 (10): e2128817. doi:10.1001/jamanetworkopen.2021.28817. PMID 34709388.
69. ↑ McNamara, JR; Small, DM; Li, Z; Schaefer, EJ (September 1996). "Differences in LDL subspecies involve alterations in lipid composition and conformational changes in apolipoprotein B.". Journal of Lipid Research 37 (9): 1924–35. doi:10.1016/S0022-2275(20)37557-X. PMID 8895058.
70. ↑ "Management of Blood Cholesterol". JAMA 321 (8): 800–801. February 2019. doi:10.1001/jama.2019.0015. PMID 30715135.
71. ↑ Research, Center for Drug Evaluation and. "Drug Safety Information for Healthcare Professionals - Follow-up to the January 25, 2008 Early Communication about an Ongoing Data Review for Ezetimibe/Simvastatin (marketed as Vytorin), Ezetimibe (marketed as Zetia), and Simvastatin (marketed as Zocor)". https://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/DrugSafetyInformationforHeathcareProfessionals/ucm079524.htm.
72. ↑ "Niacin therapy in atherosclerosis". Current Opinion in Lipidology 15 (6): 659–65. December 2004. doi:10.1097/00041433-200412000-00006. PMID 15529025.
73. ↑ "Nicotinic acid receptor subtypes and their ligands". Medicinal Research Reviews 27 (3): 417–33. May 2007. doi:10.1002/med.20102. PMID 17238156.
74. ↑ "WHO cooperative trial on primary prevention of ischemic heart disease with clofibrate to lower serum cholesterol: final mortality follow-up. Report of the Committee of Principal Investigators". Lancet 2 (8403): 600–4. September 1984. doi:10.1016/s0140-6736(84)90595-6. PMID 6147641.
75. ↑ "TRILIPIX (fenofibric acid)". https://www.rxabbvie.com/pdf/trilipix_pi.pdf.
76. ↑ "Did we abandon probucol too soon?". Current Opinion in Lipidology 26 (4): 304–16. August 2015. doi:10.1097/MOL.0000000000000199. PMID 26125504.
77. ↑ Song, B.L.; DeBose-Boyd, R.A. (2006). "Insig-Dependent Ubiquitination and Degradation of 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Stimulated by Delta- and Gamma-Tocotrienols". J. Biol. Chem. 281 (35): 25054–25601. doi:10.1074/jbc.M605575200. PMID 16831864.
78. ↑ European Food Safety Authority, Journal (2010). "Scientific opinion on the substantiation of health claims related to plant sterols and plant stanols and maintenance of normal blood cholesterol concentrations". http://www.efsa.europa.eu/en/efsajournal/pub/1813.
79. ↑ Trautwein, Elke; Vermeer, Mario; Hiemstra, Harry; Ras, Rouyanne (7 September 2018). "LDL-Cholesterol Lowering of Plant Sterols and Stanols—Which Factors Influence Their Efficacy?". Nutrients (MDPI AG) 10 (9): 1262. doi:10.3390/nu10091262. PMID 30205492.
80. ↑ Cabral, Carlos Eduardo; Klein, Márcia Regina Simas Torres (2017). "Phytosterols in the Treatment of Hypercholesterolemia and Prevention of Cardiovascular Diseases". Arquivos Brasileiros de Cardiologia (Sociedade Brasileira de Cardiologia) 109 (5): 475–482. doi:10.5935/abc.20170158. PMID 29267628.
81. ↑ Demonty, I.; Ras, R.T.; van der Knaap, H.C.; Duchateau, G.S.; Meijer, L.; Zock, P.L.; Geleijnse, J.M.; Trautwein, E.A. (Feb 2009). "Continuous dose-response relationship of the LDL-cholesterol-lowering effect of phytosterol intake.". The Journal of Nutrition 139 (2): 271–84. doi:10.3945/jn.108.095125. PMID 19091798.
82. ↑ "Cholesterol Diet: How Nutrition & Foods Impact Levels" (in en). https://my.clevelandclinic.org/health/articles/16867-cholesterol--nutrition-tlc.
83. ↑ "Saturated Fat" (in en). https://www.heart.org/en/healthy-living/healthy-eating/eat-smart/fats/saturated-fats.
84. ↑ "Half the world now following doctors' orders on cutting trans fats: WHO". 24 June 2024. https://news.un.org/en/story/2024/06/1151386.
85. ↑ Turpeinen, A.; Merimaa, P. (2011). "Functional fats and spreads". Functional Foods. pp. 383–400. doi:10.1533/9780857092557.3.383. ISBN 978-1-84569-690-0. "In addition to hydrogenated oils, dairy products are a dietary source of trans fatty acids. Ruminant fat contains on average 1–3% trans fatty acids, which originate from the action of ruminant bacteria on feed unsaturated fatty acids."
86. ↑ Delgado, Graciela E.; Kleber, Marcus E. (2019). "Trans Fatty Acids and Mortality". The Molecular Nutrition of Fats. pp. 335–345. doi:10.1016/B978-0-12-811297-7.00026-3. ISBN 978-0-12-811297-7. "Milk, dairy products, and meat from ruminants contain ∼2%–10% trans fatty acids"
87. ↑ Schoeneck, Malin; Iggman, David (May 2021). "The effects of foods on LDL cholesterol levels: A systematic review of the accumulated evidence from systematic reviews and meta-analyses of randomized controlled trials". Nutrition, Metabolism and Cardiovascular Diseases 31 (5): 1325–1338. doi:10.1016/j.numecd.2020.12.032. PMID 33762150.
88. ↑ "Non-soy legume consumption lowers cholesterol levels: a meta-analysis of randomized controlled trials". Nutr Metab Cardiovasc Dis 21 (2): 94–103. 2009. doi:10.1016/j.numecd.2009.08.012. PMID 19939654.
89. ↑ "Effect of dietary pulse intake on established therapeutic lipid targets for cardiovascular risk reduction: a systematic review and meta-analysis of randomized controlled trials". Canadian Medical Association Journal 186 (8): E252-62. 2014. doi:10.1503/cmaj.131727. PMID 24710915.

## Further reading

* "The LDL Cumulative Exposure Hypothesis: Evidence and Practical Applications". Nature Reviews Cardiology 21 (10): 701–716. 2024. doi:10.1038/s41569-024-01039-5. PMID 38969749. https://www.nature.com/articles/s41569-024-01039-5.
* "Optimal low-density lipoprotein is 50 to 70 mg/dL: lower is better and physiologically normal". Journal of the American College of Cardiology 43 (11): 2142–6. June 2004. doi:10.1016/j.jacc.2004.03.046. PMID 15172426.

## External links

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