MY RESULTS
MICROBIOME TESTING
The gut is the foundation of health. It is home to trillions of bacteria, fungi, and other microorganisms, which have an influence on how much we absorb nutrients, how strong our immune system is, and our overall well-being. It is apparent through numerous research that an imbalanced gut microbiome can promote the onset of chronic diseases. The foods we choose to put in our bodies feed our gut microbiome, thus serving as a reflection of our nutritional choices. Evaluating markers of digestion and absorption is essential in discovering whether the gut can properly break down the nutrients in the foods we eat. The gut microbiome also holds biomarkers that reflect the body's inflammatory status and can reveal whether the gut lining is compromised, also known as leaky gut. Leaky gut has been associated with cardiovascular disease, insulin resistance, food allergies and more. Understanding the status of our microbiome allows us to gain insight into our overall health status.
LAB: GENOVA DIAGNOSTICS GI MAP
BIOMARKER | RESULTS | REFERENCE RANGE |
---|---|---|
MALDIGESTION | OPTIMAL | 0 |
INFLAMMATION | OPTIMAL | 0 |
DYSBIOSIS | OPTIMAL | 2 |
METABOLIC IMBALANCE | OPTIMAL | 0 |
INFECTION | OPTIMAL | 0 |
INFLAMMATION-ASSOCIATED DYSBIOSIS | OPTIMAL | 38 |
TRIGLYCERIDES | OPTIMAL | 0.6 |
CHOLESTEROL | OPTIMAL | 1.3 |
CALPROTECTIN | OPTIMAL | <11 |
SECRETORY IGA | OPTIMAL | <150 |
TOTAL SCFA | OPTIMAL | 44.0 |
TOTAL TOXIN TESTING
TEST: VIBRANT WELLNESS
BECOME A MEMBER TO SEE THE FULL BREAKDOWN OF WHY THESE TOXINS MATTER, HOW THEY IMPACT HEALTH + MY PROTOCOL FOR THE BEST TOTAL TOXIN BURDEN WE HAVE EVER SEEN.
Important note * I do have a FEW toxins in this test, it is essentially impossible to have zero toxins at this point in time. I also live in LA, which makes it 10x more difficult. This is a major reason my husband and I plan to build a home in nature away from toxins in the near future.
MYCOTOXINS/MOLD
The link between mold exposure and chronic illness, often referred to as "mold-related illness" or "mold toxicity," has been a subject of growing interest and research in recent years. Mold, particularly certain species of fungi such as Stachybotrys, Aspergillus, Penicillium, and Alternaria, can release mycotoxins and volatile organic compounds (VOCs) that can have harmful effects on human health.
Respiratory Symptoms: Mold exposure can lead to a range of respiratory symptoms, including coughing, wheezing, throat irritation, nasal congestion, and exacerbation of asthma symptoms. These symptoms are particularly common in individuals with allergies or pre-existing respiratory conditions.
Mendell, M. J., et al. (2011). "Respiratory and Allergic Health Effects of Dampness, Mold, and Dampness-Related Agents: A Review of the Epidemiologic Evidence." Environmental Health Perspectives, 119(6), 748-756.
Fisk, W. J., & Eliseeva, E. A. (2010). "Association of residential dampness and mold with respiratory tract infections and bronchitis: a meta-analysis." Environmental Health, 9, 72.
Neurological Symptoms: Some studies suggest a potential association between mold exposure and neurological symptoms such as headaches, dizziness, fatigue, difficulty concentrating, memory problems, and mood disturbances. However, the exact mechanisms underlying these symptoms are still being investigated.
Shoemaker, R. C., et al. (2018). "Innate immune response activation in the central nervous system following exposure to Mold and Mycotoxins." Toxins, 10(11), 412.
Kilburn, K. H., et al. (2009). "Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals." Toxicology and Industrial Health, 25(9-10), 681-692.
Immune System Effects: Mold exposure can also affect the immune system, leading to increased susceptibility to infections, chronic inflammation, and autoimmune reactions in some individuals. Chronic exposure to mold and mycotoxins may dysregulate immune function and contribute to the development or exacerbation of autoimmune diseases.
Gray, M. R., et al. (2009). "Mixed mold mycotoxicosis: Immunological changes in humans following exposure in water-damaged buildings." Archives of Environmental Health, 58(7), 410-420.
Vesper, S. J., et al. (2009). "Association of Environmental Mold and Mycotoxin Exposure with Adult Asthma." Environmental Science & Technology, 43(15), 5970-5975.
Chronic Fatigue Syndrome (CFS) and Fibromyalgia: There is ongoing research exploring the potential link between mold exposure and conditions such as chronic fatigue syndrome (CFS) and fibromyalgia. While the exact relationship is not fully understood, some individuals with these conditions report improvement in symptoms after reducing exposure to mold and mycotoxins.
Brewer, J. H., et al. (2013). "A chronic illness characterized by fatigue, neurologic and immunologic disorders, and active human herpesvirus type 6 infection." Biomedicine & Pharmacotherapy, 67(2), 91-97.
Kilburn, K. H., & Thrasher, J. D. (2012). "Mold Mycotoxins and Neurotoxicity: Does Ochratoxin A Cause Multiple Sclerosis?" Toxins, 4(11), 1285-1295.
Other Health Effects: Mold exposure has been associated with a variety of other health effects, including skin rashes, gastrointestinal symptoms, and cardiovascular problems. However, more research is needed to better understand these associations and the mechanisms involved.
Thrasher, J. D., & Gray, M. R. (2004). "Kilburn K H. An open study of the treatment of pulmonary and nasal fungal colonization with a naturopathic agent." Clinical Environmental Medicine, 11(4), 167-171.
Horner, W. E., et al. (2006). "Antigenic and allergenic properties of aerosolized Penicillium spores." Clinical & Experimental Allergy, 36(6), 845-852.
BIOMARKER | RESULT | REFERENCE RANGE |
---|---|---|
URINE CREATININE | OPTIMAL | 2.11 |
AFLATOXIN B1 (AFB1) | OPTIMAL | 0.52 |
AFLATOXIN G1 | OPTIMAL | 0.8 |
AFLATOXIN M1 | OPTIMAL | 1.14 |
AFLATOXIN G2 | OPTIMAL | 0.5 |
AFLATOXIN B2 (AFB2) | OPTIMAL | 0.3 |
CHAETOGLOBOSIN A (CHA) | OPTIMAL | 17.56 |
DIHYDROCODEINONE | OPTIMAL | 8.13 |
FUMONISINS B1 | OPTIMAL | 0.99 |
FUMONISINS B2 | OPTIMAL | 0.43 |
FUMONISINS B3 | OPTIMAL | 0.17 |
GLIOTOXIN | OPTIMAL | 54.4 |
MYCOPHENOLIC ACID | OPTIMAL | 0.69 |
OCHRATOXIN A (OTA) | OPTIMAL | <0.05 |
PATULIN | OPTIMAL | 0.98 |
STERIGMATOCYSTIN (STC) | OPTIMAL | <0.05 |
ZEARALENONE (ZEN) | OPTIMAL | 0.2 |
DEOXYNIVALENOL (DON) | OPTIMAL | 22.91 |
DIACETOXYSCIRPENOL (DAS) | OPTIMAL | 2.04 |
NIVALENOL (NIV) | OPTIMAL | 1.57 |
RORIDIN A | OPTIMAL | 3.78 |
RORIDIN E | OPTIMAL | <0.05 |
RORIDIN L2 | OPTIMAL | 1.93 |
SATRATOXIN G | OPTIMAL | <0.05 |
SATRATOXIN H | OPTIMAL | 0.07 |
T-2 TOXIN | OPTIMAL | 0.08 |
VERRUCARIN A | OPTIMAL | <0.05 |
VERRUCARIN J | OPTIMAL | 2.12 |
HEAVY METALS
There is substantial scientific evidence linking heavy metals to neurodegenerative diseases. Heavy metals such as lead, mercury, cadmium, aluminum, and manganese are known to accumulate in the body, particularly in the brain, and can exert toxic effects on the nervous system. Here are some key points regarding this link:
Lead: Lead exposure has been associated with cognitive impairment, behavioral problems, and neurodevelopmental disorders in children. Chronic exposure to lead in adults has been linked to neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.
Needleman, H. L., et al. (1979). "The Long-term Effects of Exposure to Low Doses of Lead in Childhood - an 11-Year Followup Report." New England Journal of Medicine, 302(12), 686-691.
Weiss, B. (2000). " Vulnerability of children and the developing brain to neurotoxic hazards." Environmental Health Perspectives, 108(Suppl 3), 375-381.
Mercury: Mercury exposure, especially methylmercury found in contaminated seafood, has been linked to impairments in cognitive function, memory, and motor skills. Studies suggest that mercury exposure may contribute to the development of neurodegenerative diseases like Alzheimer's and Parkinson's.
Grandjean, P., & Landrigan, P. J. (2006). "Developmental neurotoxicity of industrial chemicals." The Lancet, 368(9553), 2167-2178.
Counter, S. A., & Buchanan, L. H. (2004). "Mercury exposure in children: a review." Toxicology and Applied Pharmacology, 198(2), 209-230.
Cadmium: Cadmium exposure has been associated with neurotoxic effects, including cognitive deficits and motor dysfunction. Accumulation of cadmium in the brain has been observed in neurodegenerative diseases such as Parkinson's disease.
Tjalve, H., & Henriksson, J. (1999). "Uptake of metals in the brain via olfactory pathways." NeuroToxicology, 20(2-3), 181-195.
Satarug, S., et al. (2010). "Cadmium and its health risks from food consumption: Evidence from a population-based prospective cohort study." Chemosphere, 78(6), 639-646.
Aluminum: Aluminum exposure has been implicated in the development of neurodegenerative diseases, particularly Alzheimer's disease. Aluminum can accumulate in the brain and contribute to the formation of amyloid plaques, which are characteristic of Alzheimer's pathology.
Exley, C. (2014). "Why industry propaganda and political interference cannot disguise the inevitable role played by human exposure to aluminum in neurodegenerative diseases, including Alzheimer's disease." Frontiers in Neurology, 5, 212.
Bondy, S. C. (2016). "The neurotoxicity of environmental aluminum is still an issue." NeuroToxicology, 52, 222-224
Manganese: Manganese is an essential nutrient, but excessive exposure to manganese, particularly through occupational settings or environmental pollution, can lead to neurotoxicity. Manganese exposure has been linked to Parkinsonism and other neurodegenerative disorders.
Aschner, J. L., & Aschner, M. (2005). "Nutritional aspects of manganese homeostasis." Molecular Aspects of Medicine, 26(4-5), 353-362.
Racette, B. A., et al. (2001). "Manganese intoxication and chronic liver failure." Annals of Neurology, 50(6), 714-716.
These studies represent a fraction of the extensive research conducted on the relationship between heavy metals and neurodegenerative diseases. They provide evidence of the neurotoxic effects of heavy metals and their potential contribution to the development and progression of neurodegenerative disorders.The mechanisms by which heavy metals contribute to neurodegenerative diseases are not fully understood but may involve oxidative stress, inflammation, mitochondrial dysfunction, and the disruption of essential cellular processes. Additionally, heavy metals may exacerbate existing genetic predispositions or other environmental factors contributing to neurodegeneration.
Reducing exposure to heavy metals through environmental regulations, occupational safety measures, and dietary choices can help mitigate the risk of neurodegenerative diseases associated with heavy metal toxicity. Additionally, further research into the mechanisms underlying heavy metal neurotoxicity is essential for developing targeted prevention and treatment strategies for neurodegenerative diseases.
ENVIRONMENTAL TOXINS
Environmental toxins have been implicated in various aspects of reproductive health, including infertility. Exposure to certain chemicals, pollutants, and environmental toxins can disrupt reproductive processes in both men and women, leading to difficulties in conceiving. Here are some key points regarding the link between environmental toxins and infertility:
Endocrine Disruption: Many environmental toxins are known as endocrine disruptors, meaning they interfere with the body's hormonal system. These substances can mimic or block hormones, leading to hormonal imbalances that affect reproductive function.
Gore, A. C., et al. (2015). "EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals." Endocrine Reviews, 36(6), E1-E150.
Diamanti-Kandarakis, E., et al. (2009). "Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement." Endocrine Reviews, 30(4), 293-342.
Impact on Sperm Quality: Exposure to environmental toxins has been associated with reduced sperm quality, including decreased sperm count, motility, and morphology. Common toxins such as heavy metals, pesticides, and industrial chemicals can accumulate in the body and adversely affect sperm production and function.
Sengupta, P., et al. (2018). "Environmental and occupational exposure of metals and male reproductive infertility." Environmental Science and Pollution Research International, 25(20), 19986-20007.
Radwan, M., et al. (2016). "Exposure to environmental pollutants and lifestyle factors related to oxidative stress and semen quality in men." Environmental Research, 150, 191-198.
Ovulatory Dysfunction: Environmental toxins can disrupt ovulation in women, leading to irregular menstrual cycles and anovulation (lack of ovulation). Chemicals such as polychlorinated biphenyls (PCBs), dioxins, and phthalates have been linked to ovulatory dysfunction and reduced fertility in women.
Buck Louis, G. M., et al. (2011). "Persistent Lipophilic Environmental Chemicals and Endometriosis: The ENDO Study." Environmental Health Perspectives, 119(6), 81-87.
Zhou, W., & Fang, F. (2014). "Endocrine disrupting chemicals in indoor and outdoor air: a review of recent studies." Frontiers in Environmental Science & Engineering, 8(2), 24-33.
Reproductive Disorders: Exposure to environmental toxins has been linked to various reproductive disorders, including polycystic ovary syndrome (PCOS), endometriosis, and uterine fibroids. These conditions can affect fertility by disrupting normal reproductive function.
Louis, G. M., et al. (2016). "Persistent environmental pollutants and couple fecundity: The LIFE study." Environmental Health Perspectives, 124(6), 799-806.
Duty, S. M., et al. (2003). "The relationship between environmental exposures to phthalates and DNA damage in human sperm using the neutral comet assay." Environmental Health Perspectives, 111(9), 1164-1169.
Pregnancy Complications: Environmental toxins can increase the risk of pregnancy complications, such as miscarriage, preterm birth, and low birth weight. Exposure to pollutants such as air pollution, heavy metals, and pesticides during pregnancy can adversely affect fetal development and pregnancy outcomes.
Shah, P. S., et al. (2011). "Air pollution and birth outcomes: a systematic review." Environment International, 37(2), 498-516.
Ferguson, K. K., et al. (2014). "Environmental phthalate exposure and preterm birth." JAMA Pediatrics, 168(1), 61-67.
Epigenetic Effects: Environmental toxins can induce epigenetic changes, altering gene expression patterns without changing the underlying DNA sequence. These epigenetic changes can be inherited and may affect fertility and reproductive health in future generations.
Joubert, B. R., et al. (2016). "DNA Methylation in Newborns and Maternal Smoking in Pregnancy: Genome-wide Consortium Meta-analysis." American Journal of Human Genetics, 98(4), 680-696.
Soubry, A., et al. (2016). "DNA Methylation Patterns in Newborns Exposed to Low Levels of Arsenic in Utero: An Epigenome-Wide Study." Environmental Health Perspectives, 124(10), 1299-1306.
Cumulative Effects: The effects of environmental toxins on fertility are often cumulative, with long-term exposure leading to greater reproductive health risks. Additionally, individuals may be exposed to multiple toxins simultaneously, further increasing the risk of adverse effects on fertility.
Research has shown a link between environmental toxins and autoimmune diseases, where exposure to certain environmental factors can trigger or exacerbate autoimmune responses in susceptible individuals. Here's how environmental toxins can be linked to autoimmune diseases:
Endocrine Disruption: Many environmental toxins are known to disrupt the endocrine system, which regulates the body's hormones. Disruption of hormone signaling pathways can lead to dysregulation of the immune system and contribute to the development of autoimmune diseases.
Goldman, L. R. (2000). "Chemicals and pediatric cancer." Environmental Health Perspectives, 108(Suppl 1), 133-142.
Cooper, G. S., et al. (1999). "Occupational and environmental associations with SLE." Environmental Health Perspectives, 107(Suppl 5), 679-686.
Immune Dysregulation: Exposure to environmental toxins can dysregulate the immune system, leading to inappropriate immune responses and the production of autoantibodies, which mistakenly target the body's own tissues. This immune dysregulation can contribute to the development or exacerbation of autoimmune diseases.
Parks, C. G., et al. (2017). "Exposure to trichloroethylene and tetrachloroethylene and risk of systemic lupus erythematosus in polyautoimmunity." Arthritis Care & Research, 69(5), 763-769.
Sorahan, T. (2000). "Occupation and occupational exposure to potential endocrine-disrupting chemicals in Britain." Occupational Medicine, 50(4), 243-250.
Molecular Mimicry: Some environmental toxins may resemble molecules found in the body's own tissues. When the immune system mounts a response against these toxins, it may also inadvertently attack similar-looking self-antigens, leading to autoimmune reactions.
Pollard, K. M., & Hultman, P. (2009). "Toxicology of autoimmune diseases." Chemical Research in Toxicology, 23(3), 455-466.
Dwyer, J. H., et al. (1998). "Dietary fat and the development of type 1 diabetes." Nutrition Reviews, 56(1 Pt 1), S19-S23.
Epigenetic Modifications: Environmental toxins can induce epigenetic changes, altering gene expression patterns without changing the underlying DNA sequence. These epigenetic modifications can influence immune function and increase susceptibility to autoimmune diseases.
Schübeler, D. (2015). "Function and information content of DNA methylation." Nature, 517(7534), 321-326.
Aranda, A., et al. (2012). "Epigenetic regulation of the immune response in health and disease." Tissue Antigens, 80(4), 305-317.
Microbiome Disruption: Environmental toxins can disrupt the composition and function of the gut microbiome, which plays a crucial role in immune regulation. Dysbiosis of the gut microbiota can contribute to autoimmune diseases by altering immune responses and increasing intestinal permeability.
Vojdani, A., & Vojdani, E. (2015). "Role of Th17 in the pathogenesis of autoimmune diseases." Immunologic Research, 61(1-2), 137-142.
Berer, K., et al. (2017). "Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination." Nature, 479(7374), 538-541.
Oxidative Stress and Inflammation: Many environmental toxins induce oxidative stress and inflammation in the body, which are known to contribute to the pathogenesis of autoimmune diseases. Chronic exposure to toxins can exacerbate inflammatory processes and promote autoimmune responses.
Maeda, A., et al. (2019). "Inflammatory processes triggered by pathogenic Brucella abortus and Brucella melitensis infections." Frontiers in Microbiology, 10, 1451.
Wu, C. C., & Eiserich, J. P. (2006). "Proteomic profiling of acetaminophen-induced protein tyrosine nitration in rat liver: mass spectrometric detection of acetaminophen and 3-nitrotyrosine-modified liver proteins." Chemical Research in Toxicology, 19(7), 874-886.
Genetic Susceptibility: Genetic factors play a significant role in determining an individual's susceptibility to autoimmune diseases. Environmental toxins can interact with genetic predispositions to increase the risk of developing autoimmune diseases.
Sawcer, S., et al. (2011). "Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis." Nature, 476(7359), 214-219.
Eyre, S., et al. (2012). "High-density genetic mapping identifies new susceptibility loci for rheumatoid arthritis." Nature Genetics, 44(12), 1336-1340.
Some examples of environmental toxins that have been implicated in autoimmune diseases include heavy metals (such as mercury, lead, and arsenic), air pollutants, industrial chemicals (such as bisphenol A and phthalates), pesticides, and certain medications.
Overall, reducing exposure to environmental toxins through lifestyle modifications, environmental regulations, and public health interventions is important for protecting reproductive health and reducing the risk of infertility and other reproductive disorders along with reducing your risk of triggering autoimmune.
FITNESS
BODY COMPOSITION SCANNER RESULTS:
BIOMARKER | RESULTS |
---|---|
WEIGHT | 127.4 |
HEIGHT | 5FT 8 IN |
WAIST CIRCUMFERENCE | 24 IN |
BMI | 19.4 |
SKELETAL MUSCLE MASS | 46.1 LBS (36.2%) |
SKELETAL MUSCLE MASS INDEX BY MRI | 7.0 |
FAT MASS PERCENTAGE | 19.1% |
PHASE ANGLE | 82 PERCENTILE |
VISCERAL ADIPOSE TISSUE | - 0.3 LITERS |
TOTAL BODY WATER Total Body Water (TBW) is divided into Extracellular (ECW) and Intracellular Water (ICW). |
34.0 LITERS |
ECW | 14.4 LITERS |
CARDIOVASCULAR HEALTH
HEART HEALTH CLEERY SOFT PLAQUE ANALYSIS
Coronary artery disease occurs when atherosclerosis (plaque) builds up in the blood vessel wall, and causes one or more coronary arteries to narrow, a typically silent process that occurs over decades.
• Plaques that cause heart attacks are paradoxically associated with only MILD narrowing (i.e., stenosis) of the heart artery at the time of evaluation. The riskiest plaques are soft, filled with cholesterol, and are the most likely to rupture and cause a clot – which is the actual mechanism of a heart attack (or stroke!).
• This artificial intelligence (AI)-enhanced phenotypic mapping applied to my cardiac CT angiogram uses advanced deep learning frameworks to help quantify and characterize the riskiest SOFT, cholesterol-rich plaque in a way not possible before.
• The AI algorithm finds information in the pixels of the CT scan images not easily appreciated by the naked eye of even a trained radiologist or cardiologist.
• Then, the system evaluates each of the coronary arteries and their branches with a sub-millimeter resolution with 360-degree precision.
• Lastly, the data is integrated and several scores are provided which depict the volume of each type of plaque in each coronary artery.
• The most concerning type of plaque is the soft "non-calcified plaque.
• The goal is to have less than a total of 200 cubic millimeters throughout your heart artery system.
• The "remodeling index" (RMI) is a marker of how quickly plaque is accumulating in a particular spot.
• Our goal is to keep RMI less than 1.1
BIOMARKER |
TOTAL PLAQUE VOLUME |
LOW DENSITY NON-CALCIFIED PLAQUE |
TOTAL NON-CALCIFIED PLAQUE |
TOTAL CALCIFIED PLAQUE VOLUME | PERCENT ATHEROMA VOLUME |
---|---|---|---|---|---|
LM + LAD | 2.3 | 0 | 2.3 | 0 | 0.5 |
RCA | 1.1 | 0 | 1.1 | 0 | 0.2 |
Cx | 1.1 | 0 | 1.1 | 0 | 0.3 |
Total | 4.5 | 0 | 4.5 | 0 | 0.3 |
CARDIOVASCULAR RESULTS:
CORONARY CALCIFICATION | RESULT | |
---|---|---|
LEFT MAIN CORONARY ARTERY | OPTIMAL | 0 |
LEFT ANTERIOR DESCENDING CORONARY ARTERY | OPTIMAL | 0 |
LEFT CIRCUMFLEX CORONARY ARTERY | OPTIMAL | 0 |
RIGHT CORONARY ARTERY | OPTIMAL | 0 |
POSTERIOR DESCENDING ARTERY | OPTIMAL | 0 |
TOTAL CORONARY ARTERY CALCIUM SCORE | OPTIMAL | 0 |
RCA TOTAL PAQUE VOLUME | OPTIMAL | 1.1MM3 |
BLOOD GLUCOSE MONITORING
(ROUTINE MEASUREMENT)
BIOMARKER | RESULT | |
---|---|---|
LEVELS CGM | OPTIMAL | 83-107MG/DL |
CANCER SCREENING
(LIQUID BIOPSY) - ROUTINE MEASUREMENTS
BIOMARKER | RESULT | |
---|---|---|
GRAIL | OPTIMAL | NO CANCER DETECTED |
BRAIN VOLUME | OPTIMAL |
BONE DENSITY
(ROUTINE MEASUREMENTS - YEARLY)
BIOMARKER | RESULT | REFERENCE RANGE |
---|---|---|
TOTAL SPINE T-SCORE | OPTIMAL | 0.4 |
TOTAL SPINE Z-SCORE | OPTIMAL | 0.4 |
LEFT HIP T-SCORE | OPTIMAL | 0.6 |
LEFT HIP Z-SCORE | OPTIMAL | 0.6 |
BALANCE TRACKER
(ROUTINE MEASUREMENTS, YEARLY)
BIOMARKER | RESULT | REFERENCE RANGE |
---|---|---|
FALL RISK ASSESSMENT | OPTIMAL | LOW |
COP PATH LENGTH | 14 | 94th PERCENTILE |