I have seen countless labs in clinical practice.
I rarely see more than the basic lipid panel (Cholesterol, LDL Cholesterol, Triglycerides, and HDL) for the evaluation of cardiovascular disease.
This is simply inadequate and opens the door to leading to unnecessary cardiac events (stroke, heart attack, etc.)
Remember, although you may have a standard lipid profile, it does not fully protect you from having a cardiac event.
It requires doing a deeper dive into your lipid particles and ApoB
A growing population of advanced and progressive physicians are now ordering the following:
Lipid Panel (Cholesterol, LDL, HDL, VLDL, HDL/Chol Ratio, LDL/HDL Ratio)
Apolipoprotein Assessment (A1/B/+ratio)–216010
Lipoprotein (a)–120188
NMR Lipoprofile-123638 (LDL-C, LDL-P, small LDL-P, Non-HDL-C, HDL-P, HDL-C)
Non-HDL Cholesterol
Lipoprotein-associated Phospholipase A2 (Lp-PLA2) Activity–123283
Myeloperoxidase (MPO)–123006
Oxidized LDL, Plasma–123023
Microalbumin/Creatinine Ratio, Random Urine–140285
F2-Isoprostanes/Creatinine Ratio, Random Urine–820478
C-Reactive Protein (CRP) High Sensitivity (Cardiac)–120766
Uric Acid–001057 (optimal <5.5)
Homocysteine–706994 (optimal= 7)
ADMA/SDMA–821413
Troponin–140150 (optimal-0 – 0.04 ng/mL)
Fibrinogen Activity, Quantitative–001610
Today’s article will focus on the most common reasons for elevated LDL particles and ApoB
Insulin Resistance and Metabolic Syndrome
Insulin resistance and elevated apolipoprotein B (apoB) levels are closely linked. Insulin helps regulate apoB by promoting its degradation in the liver and its clearance from the bloodstream. When insulin resistance occurs, such as in type 2 diabetes, the liver may secrete more apoB and have difficulty clearing it.
Poor Thyroid Function
Hypothyroidism can cause elevated levels of apolipoprotein B (ApoB) and low-density lipoproteins (LDL). ApoB is a component of lipoprotein cholesterols, such as LDL-C and triglyceride (TG). Hypothyroidism can also increase the ratios of ApoB to ApoA-containing lipoprotein cholesterols, such as LDL-C/HDL-C and TG/HDL-C.
Studies show that LDL particle number is higher even in subclinical hypothyroidism (high TSH with normal T4 and T3) and that it will decrease after treatment with thyroid hormone. I like to see TSH between 1 and 2, no higher.
Infections
Another cause of a high cholesterol profile is infections. Multiple studies have shown associations between bacterial infections like Chlamydia pneumoniae and H. pylori.
Helicobacter pylori (H. pylori) infection can disrupt lipid and lipoprotein metabolism, leading to changes in serum lipids. A meta-analysis of cross-sectional studies found that H. pylori infection is associated with:
Low levels: High-density lipoprotein cholesterol (HDL-C), low-density lipoprotein (LDL-C), and total cholesterol (TC)
High levels: Triglycerides (TG)
Epstein-Barr virus (EBV) infection can cause significant changes in lipids in newly infected B-cells, including increased cholesterol levels, fatty acids, phospholipids, and triglycerides. These changes can begin early after infection and remodel B-cells into activated lymphoblasts. EBV infection can also alter serum fatty acid proportions for up to a year after infection
Understanding and managing elevated lipid particle numbers can be done effectively through functional medicine testing and treatment.
Leaky gut
A leaky gut can be linked to elevated lipids or high levels of blood fats like cholesterol and triglycerides. A leaky gut, or intestinal hyperpermeability, can lead to a chronic inflammatory state linked to health conditions like high cholesterol and hyperlipidemia. This can happen when fatty acids impair tight junction function, which can open the leak pathway
If left unaddressed, a leaky gut can lead to a chronic low-grade inflammatory state, which has been linked to the development of various health conditions, including heart disease, diabetes, fatty liver disease, high cholesterol, and hyperlipidemia
Watch the below video on Leaky Gut
https://www.functionalmedicineuniversity.com/public/481.cfm
Omega 3 Deficiency
Please read a recent article on Omega 3 Fatty acids
https://www.functionalmedicineuniversity.com/public/2025.cfm
Genetics
The final cause of elevated LDL-P is genetics. Familial hypercholesterolemia, or FH, involves a gene mutation that codes for the LDL receptor or the gene that codes for apolipoprotein B (ApoB).
However, Heterozygous carriers only have a single copy of the mutated gene, and the other copy functions normally. This is much more common. The prevalence is between 1 in 300 to 1 in 500 people, depending on which study you look at. These heterozygous carriers of FH have total cholesterol levels that often range between 350 and 550 mg/dL and very high LDL particle numbers. They have about three times higher risk of death from heart disease than people without FH if it goes untreated.
Comments and Recommendations
As you can see from the above-listed causes of compromised lipid particles, it is important to have your doctor do their due diligence in adequately evaluating all of the above potential causes to decrease your cardiovascular risk and prevent a cardiac event (stroke, heart attack, etc.).
The above recent lipid particle/ApoB grid is a recent patient who came to see me with a history of cardiovascular disease. As you can see, her lipid particles, including ApoB, were problematic in November of 2023.
My deep dive into her history and appropriate testing identified that she had insulin resistance, elevated LPS (leaky gut), and hypothyroidism.
With a special emphasis on a plant-based/Mediterranean diet and addressing her insulin resistance, leaky gut, and thyroid issues, her lipids improved nicely.
Watch this important video ApoB
https://www.youtube.com/watch?v=wXLvdoZiSUM
References:
https://pubmed.ncbi.nlm.nih.gov/20356594/
https://www.ahajournals.org/doi/full/10.1161/01.atv.17.7.1447
https://www.sciencedirect.com/science/article/pii/S0022227520318782
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3810413/
https://www.atherosclerosis-journal.com/article/S0021-9150(04)00617-3/abstract
https://pubmed.ncbi.nlm.nih.gov/22786447/
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