Oxidized LDL is LDL cholesterol (the “bad” cholesterol) that has been modified by oxidation. Oxidized LDL triggers inflammation leading to the formation of plaque in the arteries, also known as atherosclerosis. Oxidized LDL may also play a role in increasing the amount of triglycerides the body produces, as well as increasing the amount of fat deposited by the body. In turn, fat tissue can enhance the oxidation of LDL, creating a vicious cycle.

Oxidized phospholipids are found on all apoB-containing lipoproteins, namely, LDL, VLDL, and especially Lp(a). When taken up by the artery wall, oxidized lipoproteins accelerate atherosclerosis, thereby, increasing the risk of myocardial infarctions, strokes, and calcific aortic valve stenosis. Oxidized phospholipids are highly pro-inflammatory and contribute to many diseases of aging.

Clinicians can use OxPL-apoB levels to reclassify patients into higher or lower risk categories allowing better personalized care.

Optimal: <2.0 nM/L

Borderline: 2.0-3.0 nM/L

Increased Risk: >3.0 nM/L

Phenols, including phenol and p-cresol, are aromatic compounds that result from the microbial fermentation of aromatic amino acids, such as tryptophan and tyrosine. These compounds are cytotoxic and may cause damage to the gut, skin, vascular system, kidneys, and more.

Tyrosine tends to be metabolized to phenol by Escherichia coli, Proteus spp., and Streptococcus faecalis, whereas it tends to be metabolized to p-cresol by strictly anaerobic gut bacteria such as Bacteroides fragilis, Fusobacterium spp., and Clostridium spp.

Tryptophan is abundant in foods such as cheese, poultry, red meat, egg whites, and seeds; and therefore, these foods can increase phenol production in the gut. Similarly, tyrosine is also present in protein-rich foods including beef, pork, chicken, fish, chicken, tofu, milk, cheese, beans, seeds, nuts, and whole grains. When paired with a diet low in fermentable fibers, these foods have the potential to dramatically increase phenol and p-cresol production, as gut microbes are forced to use amino acids for energy. Increasing gut acidity through the intake of resistant starches, galactooligosaccharides, and fructooligosaccharides may reduce the production of these toxic metabolites.

P-Ethanolamine, Plasma is short for Phosphoethanolamine (PEA). Phosphoethanolamine (PEA) is a marker measured in the plasma as part of an Amino Acid Profile, Quantitative (Qn) panel. This compound is a derivative of the amino acid serine and plays a critical role in the biosynthesis of phospholipids, which are essential components of cell membranes. In the body, PEA serves as a precursor to phosphatidylethanolamine, one of the most abundant phospholipids in cell membranes, and is involved in various cellular processes, including membrane signaling and repair. Elevated levels of phosphoethanolamine in the plasma can indicate metabolic disruptions or inherited metabolic disorders such as phosphoethanolaminuria, where there is an abnormal accumulation of PEA due to enzyme deficiencies.

P-Ethanolamine stands for Phosphoethanolamine. Phosphoethanolamine is a compound involved in the metabolism of phospholipids, which are essential components of cell membranes. Elevated levels of phosphoethanolamine in urine can indicate metabolic disorders or conditions related to phospholipid metabolism. For instance, abnormal levels may be associated with certain types of metabolic diseases, vitamin B6 deficiency, or issues with kidney function. Monitoring phosphoethanolamine levels can help healthcare providers diagnose these conditions, assess the effectiveness of treatments, and understand more about a patient's metabolic health. It's an important marker because it provides information that can lead to early detection and management of metabolic abnormalities, ultimately contributing to better health outcomes.

The presence of organic compounds such as p-Hydroxybenzoate in the urine may point towards significant dysbiosis (=impaired microbiota).

Associated with small intestinal bacteria overgrowth (SIBO) due to its production by C. di cile, C. stricklandii, C. lituseburense, C. subterminale, C. putrefaciens, and C. propionicum.

Associated with small intestinal bacteria overgrowth (SIBO) due to its production by C. di cile, C. stricklandii, C. lituseburense, C. subterminale, C. putrefaciens, and C. propionicum.

p-hydroxyphenyllactate is a marker of cell turnover. It is also a metabolite in tyrosine degradation and may be useful for studying disorders of tyrosine metabolism.

p-tau181 (phosphorylated tau at threonine 181) is a biomarker that reflects Alzheimer’s-type brain changes involving amyloid plaques and tau buildup. Measured in cerebrospinal fluid (CSF) or blood, it helps distinguish Alzheimer’s disease (AD) from other dementias, with blood testing offering a less invasive option. Higher levels increase the likelihood of AD-related pathology, while lower levels make it less likely, though results must always be interpreted within the lab-specific reference range and alongside clinical evaluation, cognitive testing, and sometimes confirmatory imaging or CSF studies. Because ranges differ across labs and borderline (“gray zone”) results are possible, p-tau181 is most useful when combined with other markers such as the Aβ42/40 ratio or p-tau217, and it serves best as part of a full workup to guide diagnosis, treatment planning, and follow-up.

p-tau217 is a phosphorylated form of tau (at threonine 217) measured in blood or CSF that reflects Alzheimer’s-type biology—particularly amyloid plaque and tau changes—and often outperforms older phospho-tau markers like p-tau181 for identifying AD pathology. For patients with new or progressive memory concerns, p-tau217 can provide earlier, less-invasive insight, help triage who should proceed to confirmatory testing (amyloid PET or CSF), clarify mixed presentations, and inform treatment discussions. Interpretation is assay-specific: rely on the reference range and cutoffs shown on your report (methods are not interchangeable). Higher values—or a high p-tau217/Aβ42 ratio—raise the likelihood of AD pathology; lower values reduce it; and “gray-zone” results may warrant repeat testing or confirmation. Results can be influenced by assay platform, clinical context (e.g., intercurrent illness, comorbidities), and preanalytical handling, so they should never be used in isolation. Pair p-tau217 with related biomarkers (Aβ42 ± Aβ40, p-tau217/Aβ42 ratio, p-tau181/p-tau231, NfL) plus clinical assessment to reach a confident conclusion.

The P/E2 ratio describes the relationship between progesterone and estradiol levels, and is used clinically to ascertain dominance of one hormone compared to the other.

When it comes to diagnosing Lyme disease, a condition caused by the Borrelia burgdorferi bacteria, healthcare providers often rely on a combination of clinical evaluation, patient symptoms, and specific laboratory tests. One of the components sometimes found on a Borrelia test panel is the P100 biomarker. Understanding what this biomarker signifies and how it fits into Lyme disease diagnostics can shed light on the often-complex process of diagnosing this tick-borne illness.

What is the P100 Biomarker?

P100 is a protein antigen found in the Borrelia burgdorferi bacterium. This protein, along with others like P41, OspC, and others, is used to detect the presence of an immune response to Lyme disease. The P100 antigen, sometimes referred to as the 100 kDa protein, gets its name from its molecular weight. This protein becomes relevant in Lyme disease testing because it is associated with the immune response to the infection; when the immune system encounters Borrelia burgdorferi, it generates antibodies that specifically target bacterial antigens, including P100. Detecting antibodies against P100 can provide insight into a patient’s exposure to the Lyme-causing bacteria.