The standard lipoprotein profile

Discuss the individual tests performed in a standard lipoprotein profile. 

A standard serum “lipid panel” includes: total cholesterol, High-density lipoprotein cholesterol (HDLC), Low-density lipoprotein cholesterol (LDL-C), Triglycerides.

Cholesterol is a steroid. A steroid is a 4-ringed carbon organic compound that varies depending on
the attached functional group and by the oxidation state of the rings. Steroids are found as
stabilizing structures in cells, cholesterol, or as hormones (e.g., estradiol, testosterone,
progesterone). Cholesterol can be synthesized by all animal cells for cell structure integrity (93%)
and circulating in blood (7%) as a precursor for steroid hormones, bile acid and vitamin D.
Cholesterol circulates in blood as part of a lipoprotein complex which contains a protein,
cholesterol, triglyceride, and phospholipid molecule. The lipoprotein complex can be classified by
density into HDL, LDL, and very-low density lipoproteins (VLDL).

Triglycerides (TG) are the main components of body and vegetable fat and are made up of a
glycerol and 3 fatty acids (thus TRI-fatty-acid + Glycerol shortens to Triglycerides). There are
saturated and unsaturated types of TG. Saturated TG are saturated with hydrogen, which means
all available places on the carbon structures are occupied. Unsaturated TG have double bonds
between carbon atoms. Functionally we see saturated TG solid a room temperature (e.g. Butter)
and we see unsaturated TG liquid at room temperature (e.g., vegetable oil). Since humans live at
~98 degrees F, saturated TG can be used as they are liquid at this higher temperature. Fish
however, or plants that grow in northern latitudes need liquid fats at colder temperatures and so we
find mostly unsaturated TG in these organisms. With more double bonds, unsaturated TG are more
prone to oxidation – “oil oxidation is an undesirable series of chemical reactions involving oxygen
that degrades the quality of an oil” (4).

Lipoproteins carry hydrophobic molecules in serum and consist of a single layered membrane of
phospholipids with the hydrophilic portions (the phosphate head) facing outwards and the
hydrophobic portion (the fatty acid tails) facing inward. Apolipoproteins are embedded in this
membrane of phospholipids to stabilize the structure and provide different functions. The various
lipoproteins consist of plasma lipoprotein particles classified as HDL, LDL, IDl, VLDL, ULDL
(chylomicrons). Other lipoproteins include the transmembrane proteins of mitochondria.
HDL is often called "good cholesterol" because it removes excess cholesterol and carries it to the
liver for removal. LDL is often called "bad cholesterol" because it deposits excess cholesterol in
walls of blood vessels, which can contribute to atherosclerosis.

LDL particles package fatty acids for delivery around body via serum. Each LDL particle contains a
single apolipoprotein B-100 (Apo B 100) molecule, and contains a hydrophobic core containing
cholesterol molecules and TG. LDL particles are ~25 nm in size and have a 3 million Dalton mass.
LDL size can vary substantially and with new technology (NMR spectroscopy), much smaller dense
LDL particles identified. More small dense LDL particles appears to equate to higher risks for
atherosclerosis than more larger and less dense LDL forms, possibly due to small forms able to
penetrate vascular endothelium more readily. LDL reported on blood tests (LDL-C) is based on a
calculation (the Friedewald equation) in which Total Cholesterol less HDL and TG gives an estimate
of LDL.

From the National Cholesterol Education Program, 2001, elevate risk of heart disease occurs when
TC more than 240 mg/dL. Likewise, LDL levels exceeding 100 have higher risks, especially high
over 160 mg/dL. Higher HDL in this scheme confers less risk at more than 60 mg/dL.
Growing evidence indicates that LDL levels may not correlate so strongly with heart disease
however. In a 1997 prospective Quebec Cardiovascular Study, 2013 healthy men were followed,
and it was found that of the 114 that developed ischemic heart disease that total LDL levels had
virtually no impact, although small LDL particles were associated with increased risk. (3)
Many lipid studies seem to be association studies and as such difficult to prove causation. Other
association studies show that Bacteroidetes bacteria are associated with atherosclerosis, so
perhaps diet that limits endotoxin production is of primary importance in preventing ischemic heart
disease. (4) The endotoxin theory of atherosclerosis has been described. (5,6) Additionally, nitric
oxide, often said to be a beneficial compound, may not be benign and seems to be induced by
endotoxin.

Sources:
1/Nutritional Assessment

2/Moseby’s

3/Enig, Mary. Know Your Fats

4/Oxidation of food grade oils – www.plantandfood.com (http://www.plantandfood.com) . Good
summary on oxidation.

3/Lamarche, B., Tchernof, A., Moorjani, S., Cantin, B., Dagenais, G.R., Lupien, P.J., Despres, J.-P.,
1997. Small, Dense Low-Density Lipoprotein Particles as a Predictor of the Risk of Ischemic Heart
Disease in Men: Prospective Results From the Quebec Cardiovascular Study. Circulation 95, 69–
75. https://doi.org/10.1161/01.CIR.95.1.69 (https://doi.org/10.1161/01.CIR.95.1.69)

4/Nemati, R., Dietz, C., Anstadt, E.J., Cervantes, J., Liu, Y., Dewhirst, F.E., Clark, R.B., Finegold,
S., Gallagher, J.J., Smith, M.B., Yao, X., Nichols, F.C., 2017. Deposition and hydrolysis of serine
dipeptide lipids of Bacteroidetes bacteria in human arteries: relationship to atherosclerosis. Journal
of Lipid Research 58, 1999–2007. https://doi.org/10.1194/jlr.M077792
(https://doi.org/10.1194/jlr.M077792)

5/Got a Bad Ticker? Bacterial Fats Could be the Blame. GEN News Highlights. 11/2/207.
https://www.genengnews.com/gen-news-highlights/got-a-bad-ticker-bacterial-fats-could-beto-
blame/81255124 (https://www.genengnews.com/gen-news-highlights/got-a-bad-ticker-bacterialfats-
could-be-to-blame/81255124)

6/Anikhovskaia, I.A., Kubatiev, A.A., Iakovlev, M.I., 2015. [Endotoxin theory of atherosclerosis].
Fiziol Cheloveka 41, 106–116.

7/Konev, I.V., Lazebnik, L.B., 2011. [Endotoxin (LPS) in the pathogenesis of atherosclerosis]. Eksp
Klin Gastroenterol 15–26.

8/McCann, S.M., Licinio, J., Wong, M.L., Yu, W.H., Karanth, S., Rettorri, V., 1998. The nitric oxide
hypothesis of aging. Exp. Gerontol. 33, 813–826.

9/McCANN, S.M., 2005. The Nitric Oxide Theory of Aging Revisited. Annals of the New York
Academy of Sciences 1057, 64–84. https://doi.org/10.1196/annals.1356.064
(https://doi.org/10.1196/annals.1356.064)
(http