I published a series of blogs on lipoproteins. A 2022 publication shows that statin use increase a lipoprotein associate with heart disease and early mortality. The specific lipoprotein is Lipoprotein (a) (Lp (a)) aka Lp(a). I have included the past blog that discusses Lp(a) at the end of this new posting.
Here is the additional bad news.
Summary:
Background: Lipoprotein (a) [Lp(a)] is an independent risk factor for coronary artery disease (CAD). Recent studies have indicated that statins tend to increase Lp(a) levels by 10–20%.
Methods: This study included 488 patients with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI). Lp(a) levels were measured at baseline and 1 month after statin therapy. The study endpoints were major adverse cardiovascular events (MACE).
Results: After statin therapy, the mean level of Lp(a) increased by 19.3% from baseline. Lp(a) levels increased in 307 patients (62.9%) with a median elevation of 4.1 mg/dL.
Patients with an increase in Lp(a) were at higher risk for MACE than those without an increase in Lp(a) (p=0.044). Subgroup analyses revealed that a mild-to-moderate increase in Lp(a) was not associated with MACE, whereas
there was a strong correlation between the highest quartile increase in Lp(a) (≥10.1 mg/dL) and MACE (HR=2.29, 95%CI=1.36–3.84, p=0.002).
This correlation was independent of baseline Lp(a) levels but not independent of on-statin Lp(a) levels.
Conclusions: Severe increases in Lp(a) following statin therapy raise the risk of MACE, but a mild-to-moderate increase in Lp(a) may not afect the cardiovascular prognosis of CAD patients.
Even if the baseline Lp(a) levels are low, it is necessary to continue testing for Lp(a) concentration at least once after statin.
From Part 1
If you want to understand the true cause of heart disease and many diseases related to poor vascular health, this is a "must-read."
Here are the highlights.
LEWIS COMMENT: The small particles are the problem - or are they? It's clear they are formed and respond to an "insult," a.k .a. toxicity of some type. What are the toxins, and what is the way to reduce heart disease? THIS IS VERY IMPORTANT...
LOWER YOUR SUGARS - LOWER YOUR HEART DISEASE RISK
LOWER INFECTION - LOWER YOUR HEART DISEASE RISK
LOWER LDL - RAISE YOUR HEART DISEASE RISK.
WHY? THEY ARE THERE RESPONDING TO THESE ROOT-CAUSE PROBLEMS - SUGARS AND INFECTION (AND THESE 2 GO HAND-IN-HAND. THE SMALL PARTICLES ARE NOT THE ROOT CAUSE - SUGARS AND INFECTIONS ARE.
INTRODUCTION
Because lipids (fats), such as cholesterol and triglycerides, are insoluble in water, these lipids must be transported in association with proteins (lipoproteins - LDL, HDL) in the circulation.
To avoid toxicity, large quantities of fatty acids from meals must be transported as triglycerides.
These lipoproteins play a key role in the absorption and transport of dietary lipids by the small intestine, in the transport of lipids from the liver to peripheral tissues, and the transport of lipids from peripheral tissues to the liver and intestine (reverse cholesterol transport).
LEWIS COMMENT: LDL transports fats from the liver - HDL transports fats back to the liver
A secondary function is transporting toxic foreign hydrophobic and amphipathic compounds, such as bacterial toxins, from areas of invasion and infection (1).
LEWIS COMMENT: This is why HDL is so important - it detoxifies your body from what is called LPS.
LEWIS COMMENT: LDL is important because bacterial toxins create cellular damage, and LDL carries fats that repair and build new cell membranes destroyed by the toxins.
For example, lipoproteins bind endotoxin (LPS) from gram-negative bacteria and lipoteichoic acid from gram-positive bacteria, thereby reducing their toxic effects (1). In addition, apolipoprotein L1, associated with HDL particles, has lytic activity against the parasite Trypanosoma brucei brucei and lipoproteins can neutralize viruses (2,3).
LEWIS COMMENT: If you saw testing results on people I work with, you would see that viral burden is prolific, especially in people with chronic fatigue and sleeplessness.
Thus, while this article will focus on the transport properties of lipoproteins, the reader should recognize that lipoproteins may have other important roles.
Here is the definition of the other lipoproteins, some of which are not discussed regarding your health.
Lipoprotein (a) (Lp (a)) (13-16)
Lp (a) is an LDL particle with apolipoprotein (a) attached to Apo B-100 via a disulfide bond. Lp (a) contains Apo (a) and Apo B-100 in a 1:1 molar ratio. The size of Lp(a) particles can vary greatly based on the size of apolipoprotein (a). This particle is pro-atherogenic.
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LEWIS COMMENT: Testing for your lipoproteins is costly compared to obtaining a hs-CRP and triglycerides.
"Elevated lipoprotein(a) [Lp(a)] levels are associated with the risk of coronary artery disease (CAD) and calcific aortic valve stenosis (CAVS). Observational studies revealed that Lp(a) and C-reactive protein (CRP) levels, a biomarker of systemic inflammation, may jointly predict CAD risk."
There is no "may" about it. CRP tells the Lp(a) story at pennies on the dollar. And, the treatment is NOT statins.
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Apolipoproteins have four major functions, including
1) serving a structural role,
2) acting as ligands for lipoprotein receptors,
3) guiding the formation of lipoproteins, and
4) serving as activators or inhibitors of enzymes involved in the metabolism of lipoproteins (Table 3). Apolipoproteins thus play a crucial role in lipoprotein metabolism.
Apolipoprotein A-I (19)
Apo A-I is synthesized in the liver and intestine and is the major structural protein of HDL, accounting for approximately 70% of HDL protein. It also plays a role in the interaction of HDL with ATP-binding cassette protein A1 (ABCA1), ABCG1, and class B, type I scavenger receptor (SR-B1). Apo A-I activates lecithin: cholesterol acyltransferase (LCAT), an enzyme that converts free cholesterol into cholesteryl ester. High levels of Apo A-I are associated with a decreased risk of atherosclerosis.
High levels of that protein are associated with low levels of CRP
Apolipoprotein A-II (20)
Apo A-II is synthesized in the liver and is the second most abundant protein in HDL, accounting for approximately 20% of HDL protein. The role of Apo A-II in lipid metabolism is unclear. Apo A-II is a strong predictor of risk for CVD.
LEWIS COMMENT: Since this is associated with HDL, look at the summary at the top of the page to see what HDL does.
Apolipoprotein A-IV (21)
Apo A-IV is synthesized in the intestine during fat absorption. Apo A-IV is associated with chylomicrons and high-density lipoproteins but is also found in the lipoprotein-free fraction. Its precise role in lipoprotein metabolism remains to be determined, but studies have suggested a role for Apo A-IV in regulating food intake.
Apo A-V is synthesized in the liver and associates with triglyceride-rich lipoproteins. It is an activator of LPL-mediated lipolysis and thereby plays an important role in the metabolism of triglyceride-rich lipoproteins.
Apolipoprotein B-48 (24)
Apo B-48 is synthesized in the intestine and is the major structural protein of chylomicrons and chylomicron remnants.
Apolipoprotein B-100
Apo B-100 is synthesized in the liver and is the major structural component of VLDL, IDL, and LDL. Apo B-100 is a ligand for the LDL receptor and, therefore, plays an important role in the clearance of lipoprotein particles. High levels of Apo B-100 are associated with an increased risk of atherosclerosis.
Apolipoprotein C (26-29)
The C apolipoproteins are synthesized primarily in the liver and freely exchange between lipoprotein particles and, therefore, are found in association with chylomicrons, VLDL, and HDL.
Apolipoprotein E (33)
Apolipoprotein E is synthesized in many tissues, but the liver and intestine are the primary source of circulating Apo E. Apo E3 and E4 are ligands for the LDL receptor while Apo E2 is poorly recognized by the LDL receptor. Patients who are homozygous for Apo E2 can develop familial dysbetalipoproteinemia (30). Apo E4 is associated with an increased risk of Alzheimer’s disease and an increased risk of atherosclerosis.
Apo (a) is synthesized in the liver. High levels of Apo (a) are associated with an increased risk of atherosclerosis. Apo (a) is an inhibitor of fibrinolysis and can also enhance the uptake of lipoproteins by macrophages, both of which could increase the risk of atherosclerosis.
"Increased serum apoA-1 levels may be associated with decreased hs-CRP levels and decreased WBC counts as predictive inflammatory biomarkers of the onset of CAD. In particular, increase in the hs-CRP level and decrease in the apoA-1 level may be useful indices of the risk of CAD."
LEWIS COMMENT: As you can see, CRP is the main marker!
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