To fully understand the process of arteriosclerosis, we must explain the differences between a standard lipid panel and the information that can be obtained from an advanced lipid panel.
Advanced lipid panels are not routinely performed! A standard panel is sufficient to correctly make therapeutic decisions, so advanced panels are only requested when there are diagnostic doubts or a family history of premature cardiovascular disease. However, knowing in detail the advanced measurements that can be performed today will help you better understand the initiation and development of an atheroma plaque.
The number of LDL lipoprotein particles (LDL-P) has a greater correlation with the risk of cardiovascular disease than simply measuring the "load" of transported cholesterol (LDL-C). The amount of cholesterol that an LDL particle can carry is variable.
LDL particles are responsible for the development of atheroma plaque, not the cholesterol they carry!
We find LDL particles with a large amount of attached cholesterol ("large" and "less dense" LDL particles, less atherogenic) and LDL particles with a low amount of attached cholesterol ("small" and "dense" LDL, significantly more atherogenic).
The number of particles is a more accurate predictor of cardiovascular risk than the total amount of LDL cholesterol. Also note that within an LDL particle we find an essential protein to maintain its structure, known as "ApoB 100" (or, in the clinic, simply as ApoB). There is only one ApoB protein for each LDL particle, so ApoB is used in blood tests to estimate the number of LDL particles.
In a standard panel, measuring the amount of total cholesterol bound to LDL (LDL-C) is a pretty good estimate of the number of LDL (LDL-P) particles, since, in most people, they have a distribution intermediate in quantity and density. However, if your standard lipid profile is in doubt, further investigation of the content and amount of circulating particles may be indicated.
It is possible to have high levels of LDL-C, but normal or low levels of ApoB (that is, of the number of particles): this means that most of your LDL particles are "large and dense", with less atherogenic risk.
Also, it is possible to have a high ApoB (many LDL particles!) But a low LDL-C: your particles transport little cholesterol, they are "small and dense": the atherogenic risk is markedly high. This situation is especially predominant if the patient suffers from metabolic syndrome, which is diagnosed based on the presence of 5 criteria: low HDL-C, elevated triglycerides, fasting hyperglycemia, elevated blood pressure and abdominal obesity.
Finally, it should be noted that some LDL particles may also have a protein known as Apo (a) attached, which makes them a particle called "Lp (a)". The structure and function of an LDL particle with Apo (a) is complex, but we emphasize it for two reasons: its relationship with the ApoE gene (people with the ApoE4 variant have a higher number of Lp (a) and ApoB, and therefore , increased risk of cardiovascular disease and Alzheimer); and because the Lp (a) cholesterol particles have a high affinity for oxidized phospholipids, they are more easily retained in the subendothelial space and tend to initiate the inflammatory cascade that gives rise to the atheroma plaque.
Measuring total cholesterol and HDL-C can estimate the amount of LDL particles (LDL lipoproteins).
Measuring apoB provides a very accurate figure for the amount of LDL lipoprotein.
LDL particles may have little bound cholesterol ("small" and "dense"), which increases their atherogenicity and the risk of cardiovascular disease, even with "normal or low" LDL-C levels.
A high number of LDL particles, specifically bound to Apo (a), increases cardiovascular risk. The Lp (a) study is under investigation, but it could become an important tool in doubtful cases of hypercholesterolemia and patients with a family history.
Requesting an advanced lipid panel is not routine, but a correctly informed patient who wants to know their cardiovascular disease risk in greater detail is free to request this type of test.
With Melio you can analyse ApoA and ApoB in their general profiles. If you want to know more, we recommend you visit our "Profile plus" where we will explain this and other markers in detail.
Medical treatment alternatives
There are numerous treatment alternatives to reduce levels of total cholesterol, LDL-C, ApoB, Lp (a) and / or raise HDL-C levels. We will not discuss them in detail in this article, as their prescription will always be at the discretion of your doctor, but it is good to know that:
Niacin lowers ApoB, in addition to Lp (a) and LDL-C. Raise HDL-C.
Statins do not lower Lp (a), but LDL-C cholesterol does, through inhibition of hepatic cholesterol synthesis and elevation of LDL receptors in the liver (whose function is to bind and excrete excess LDL-C in bile ).
A PCSK9 enzyme inhibitor could help you lower Lp (a) levels, as it significantly increases the amount of liver LDL receptors. The PCSK9 enzyme breaks down liver LDL receptors. There are individuals with a genetically “hyper-functional” PCSK9 (greater receptor degradation, less cholesterol elimination), at higher risk of cardiovascular disease from childhood. Likewise, we found individuals with a "hypo-functional" PCSK9 enzyme, which do not effectively degrade LDL receptors and better eliminate excess cholesterol and circulating lipoproteins. An inhibitor drug PCSK9 performs a function similar to that of having a protective genetic variant: they increase the number of LDL receptors and facilitate the excretion of lipoproteins.
Unfortunately, preliminary scientific studies indicate that Lp (a) numbers do not largely respond to changes in your nutrition. However, in some individuals, a high intake of saturated fatty acids increases endogenous cholesterol production (LDL-C increases). In these cases, replacing saturated fat with monounsaturated fats (such as olive oil: hence its known cardioprotective effect as part of a Mediterranean diet), the levels return to normal.
With the recent popularity of the ketogenic (or low carbohydrate) diet, it is advisable to perform a blood test before starting this nutritional strategy: in most people, its positive effects on insulin sensitivity, inflammation and metabolism Lipids are clearly advantageous, but elevations of LDL-C, PCR (inflammation), or triglycerides could be observed in a small subset of genetically predisposed individuals, which should be investigated in more detail. For this, it is important to have a previous analysis and compare the effects of your dietary changes. Your nutritional context is very relevant in the study of cholesterol. Having the appropriate information, both theoretically, as we expose in this article, and at the diagnostic level, through a blood analysis of Melio, will allow you to make better decisions about your lifestyle, nutrition and physical exercise.
NOTICE: This informative article is based on the bibliographic sources cited below and has been reviewed by the Melio Reviewers Committee. All content is valid as of the date of publication, but may not include more recent previews. This blog is presented for informational purposes only and does not constitute the practice of Medicine, Nursing or other professional health services, including the provision of medical advice, and therefore does not constitute a doctor-patient relationship. The use of information or materials linked from this blog are under the responsibility of the user. The content of this blog is not intended as a substitute for medical advice, diagnosis or treatment.
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DiNicolantonio, J. J. and J. H. O’Keefe (2018). Effects of dietary fats on blood lipids: a review of direct comparison trials, Archives of Disease in childhood.
Feingold, K. R. and C. Grunfeld (2019). The effect of inflammation and infection on lipids and lipoproteins. Endotext [Internet], MDText. com, Inc.
Huff, T. and I. Jialal (2018). Physiology, cholesterol. StatPearls [Internet], StatPearls Publishing.
Lee, Y., et al. (2019). "Cholesterol Levels."
Pahwa, R. and I. Jialal (2018). Chronic inflammation. StatPearls [Internet], StatPearls Publishing.
Rocha, V. Z. and R. D. Santos (2018). Cholesterol and inflammation: The lesser the better in atherothrombosis, SAGE Publications Sage UK: London, England.
Shivappa, N. (2019). Diet and Chronic Diseases: Is There a Mediating Effect of Inflammation?, Multidisciplinary Digital Publishing Institute.
Siri-Tarino, P. W. and R. M. J. J. o. l. r. Krauss (2016). "The early years of lipoprotein research: from discovery to clinical application." 57(10): 1771-1777.
Tsimikas, S. J. J. o. t. A. C. o. C. (2017). "A test in context: lipoprotein (a): diagnosis, prognosis, controversies, and emerging therapies." 69(6): 692-711.
Tsoupras, A., et al. (2018). "Inflammation, not cholesterol, is a cause of chronic disease." 10(5): 604.