Top Lab Tests That Reveal Hidden Cancer Risks: A Functional Medicine Guide to Terrain-Based Healing

From Glucose and Ketones to Genetics and Toxins—Why Testing Beats Guessing in Cancer Prevention and Metabolic Therapy

Written and researched by Keith Bishop, Clinical Nutritionist, Cancer Coach, Retired Pharmacist, and founder of Prevail Over Cancer

What if the most dangerous cancer risks aren’t visible on a scan or felt in the body—but quietly building in your blood, urine, and genes?

In cancer care, guessing is gambling. Symptoms can be vague, and even “clean” imaging doesn’t mean the terrain is safe. That’s why lab testing isn’t just helpful—it’s essential. From glucose and ketones to hormone metabolites and heavy metals, these biomarkers reveal the biochemical landscape cancer cells exploit—and the ones we can disrupt.

Whether you're navigating active treatment, remission, or prevention, here’s a breakdown of the tests I recommend most often for clients—and why they matter.

The following tests are part of what I help clients with and are not a comprehensive list. It is essential to work with your healthcare team to assess these items and create a plan and tactics to enhance cancer outcomes.

🔴 Blood Glucose & HbA1c: Cancer’s Favorite Fuel

Cancer cells thrive on glucose via the Warburg effect. Elevated blood sugar and insulin levels are linked to increased cancer incidence, faster progression, and poorer outcomes.

Blood glucose and hemoglobin A1C (HbA1c) are foundational markers in assessing cancer risk and metabolic terrain. Elevated fasting glucose levels can fuel cancer cell proliferation via the Warburg effect, where tumors preferentially metabolize glucose even in the presence of oxygen. Chronic hyperglycemia also promotes insulin resistance, systemic inflammation, and oxidative stress—all of which contribute to tumor initiation and progression. A1C reflects average blood glucose over the past 2–3 months and is a more stable indicator of glycemic control than a single glucose reading. Studies show that even modest elevations in A1C (≥5.7%) are associated with increased risk of colorectal, breast, and pancreatic cancers—even in non-diabetic individuals. Monitoring both fasting glucose and A1C allows clinicians to detect hidden metabolic dysfunction, personalize dietary strategies (such as ketogenic therapy), and reduce the biochemical fuel that cancer cells exploit. In cancer care, these markers aren’t just for diabetes—they’re metabolic red flags
📖 MDPI: Hyperglycemia and Cancer Progression
📖 BMC Public Health: Glucose & Mortality in Cancer Survivors

Test Sources:

• Keto Mojo finger stick: Amazon link - https://amzn.to/4leF3xX
• Laboratory blood test: https://www.ultalabtests.com/partners/prevailovercancer/test/hemoglobin-a1c-test

🟡 Ketone Bodies: Fueling the Anti-Cancer Terrain

Ketones like β-hydroxybutyrate suppress inflammation and oxidative stress while depriving cancer cells of glucose. Monitoring ketones helps personalize ketogenic protocols and track metabolic shifts.

Ketone bodies—primarily β-hydroxybutyrate (BHB), acetoacetate, and acetone—are more than just alternative fuel sources during carbohydrate restriction. In cancer care, they play a strategic role in shifting the metabolic terrain away from glycolysis and toward oxidative metabolism. Produced in the liver during fasting, ketogenic diets, or caloric restriction, ketones bypass the glucose-dependent pathways that many cancer cells rely on for survival and proliferation. β-hydroxybutyrate, in particular, has been shown to suppress histone deacetylases (HDACs), reduce oxidative stress, and modulate inflammatory signaling—creating an environment less conducive to tumor growth. Unlike glucose, ketones do not stimulate insulin or IGF-1, both of which are known to promote cancer cell proliferation and angiogenesis. Monitoring blood ketone levels allows clinicians to confirm therapeutic ketosis and personalize dietary protocols for patients using metabolic therapy. In essence, ketone bodies are not just passive byproducts—they are active metabolic regulators with anti-cancer potential.
📖 Biomedicines: Ketone Bodies in Cancer Metabolism
📖 BMC Medicine: Ketogenic Therapy in Glioblastoma

Test Source: Amazon Link https://amzn.to/4leF3xX

⚖️ Zinc & Copper: The Ratio That Reveals Risk

Zinc supports DNA repair and immune function. Excess copper promotes angiogenesis and tumor growth. The zinc/copper ratio is a powerful predictor of cancer risk and inflammatory burden.

Zinc and copper are essential trace minerals with profound implications for cancer biology, immune regulation, and oxidative stress. Zinc plays a critical role in DNA synthesis, cellular repair, and immune surveillance—functions that are especially vital in cancer prevention and recovery. It’s a cofactor for over 300 enzymes and supports apoptosis, antioxidant defense, and T-cell activity. Copper, while also essential, has a more complex relationship with cancer. It’s required for angiogenesis, mitochondrial respiration, and connective tissue integrity. Still, elevated copper levels have been linked to tumor growth and metastasis due to its role in promoting new blood vessel formation. The zinc-to-copper ratio (Zn/Cu) is a clinically relevant marker: a low ratio (often due to excess copper or zinc deficiency) is associated with increased inflammation, oxidative stress, and poorer outcomes in cancers such as colorectal, breast, and lymphoma. Functional medicine practitioners often use this ratio to assess immune balance and guide supplementation. Significantly, high-dose zinc supplementation without adequate copper can induce copper deficiency, impairing cardiovascular and neurological function. Maintaining a balanced Zn/Cu ratio is not just about avoiding deficiency—it’s about optimizing the biochemical terrain to resist cancer progression and support immune resilience.
📖 Oxford Academic: Copper/Zinc Ratio & Colorectal Cancer
📖 MDPI Antioxidants: Zn/Cu Ratio in BRCA1 Carriers
📖 Rupa Health: Zinc/Copper Ratio in Functional Medicine

Test Source: https://labs.rupahealth.com/store/storefront_64e2oDG?storefrontProduct=strprod_MQ5vAlM

☠️ Heavy Metals: Silent Saboteurs of Cellular Health

Mercury, arsenic, cadmium, and lead disrupt mitochondrial function, impair detox pathways, and increase cancer risk—even at low levels.

Heavy metals such as mercury, arsenic, cadmium, and lead are environmental toxins with profound implications for cancer risk, cellular dysfunction, and immune suppression. These metals are classified as carcinogens by agencies like the International Agency for Research on Cancer (IARC) due to their ability to disrupt DNA repair, promote oxidative stress, and interfere with mitochondrial function. Chronic exposure—even at low levels—can impair detoxification pathways, alter gene expression, and create a pro-inflammatory terrain that favors tumor initiation and progression. Mercury, for example, accumulates in neural and renal tissues, impairing glutathione activity and increasing lipid peroxidation. Arsenic has been linked to skin, bladder, and lung cancers through its epigenetic effects and interference with DNA methylation. Cadmium mimics estrogen and has been implicated in breast and prostate cancers, while lead disrupts calcium signaling and immune cell function. These metals often enter the body through contaminated food, water, air, or consumer products, and their bioaccumulation can go undetected for years. Testing blood, urine, or hair levels of heavy metals is essential for identifying hidden toxic burdens and guiding chelation, nutritional support, and lifestyle interventions. In cancer care, assessing heavy metal exposure isn’t optional—it’s foundational.
📖 Frontiers in Pharmacology: Toxic Mechanisms of Heavy Metals
📖 BMC Public Health: Metals & Cancer Risk Review

Test Source: https://labs.rupahealth.com/store/storefront_64e2oDG?storefrontProduct=strprod_MQ5vAlM

🧪 Iodine: The Forgotten Anti-Cancer Mineral

Iodine supports cellular differentiation and immune activation. Deficiency has been linked to breast, thyroid, and gastric cancers.

Iodine is a critical micronutrient with far-reaching implications for cancer prevention, immune regulation, and hormonal balance. Most commonly known for its role in thyroid hormone synthesis, iodine supports the production of thyroxine (T4) and triiodothyronine (T3), which regulate metabolism, cellular differentiation, and mitochondrial activity. In cancer biology, iodine’s influence extends beyond the thyroid. It has been shown to induce apoptosis in breast and prostate cancer cells, modulate estrogen receptor expression, and act as an antioxidant in glandular tissues. Iodine deficiency—still prevalent in specific populations despite iodized salt—can lead to hypothyroidism, impaired detoxification, and increased susceptibility to hormone-sensitive cancers. Additionally, iodine helps displace toxic halogens like bromine and fluoride, which may interfere with cellular signaling and immune resilience. Testing iodine status via serum or urinary iodine can reveal hidden deficiencies, especially in individuals avoiding dairy, seafood, or iodized salt. For cancer patients and those at high risk, optimizing iodine levels is not just about thyroid health—it’s about restoring a biochemical terrain that resists tumor growth and supports hormonal harmony.
📖 Prevail Over Cancer: Iodine and Cancer Review
📖 MDPI Nutrients: Iodine & BRCA1 Cancer Risk

Test Source: https://labs.rupahealth.com/store/storefront_64e2oDG?storefrontProduct=strprod_MQ5vAlM

Screening Iodine Paint Guide: https://www.prevailovercancer.com/learning-center

🧬 Selenium: Antioxidant Armor Against Tumor Growth

Selenium is a cofactor for glutathione peroxidase and other antioxidant enzymes. Deficiency increases oxidative stress and DNA damage—key drivers of carcinogenesis.

Selenium is a trace mineral with powerful antioxidant, immunomodulatory, and anti-carcinogenic properties. It plays a central role in the function of selenoproteins, particularly glutathione peroxidase and thioredoxin reductase—enzymes that protect cells from oxidative damage and maintain redox balance. In cancer biology, selenium’s influence is multifaceted: it helps prevent DNA mutations, supports apoptosis of damaged cells, and modulates inflammatory cytokines that can promote tumor growth. Epidemiological studies have linked low selenium levels to increased risk of cancers, including prostate, breast, colorectal, and lung. Notably, selenium status may also affect cancer prognosis and response to treatment, especially in patients undergoing chemotherapy or radiation, where oxidative stress is heightened. However, selenium’s therapeutic window is narrow—both deficiency and excess can be harmful. Testing serum selenium levels allows clinicians to personalize supplementation and avoid toxicity, particularly in individuals with impaired methylation or heavy metal burden. In functional oncology, selenium is not just a micronutrient—it’s a molecular shield against carcinogenesis.
📖 BMC Cancer: Selenium & Cancer Risk
📖 Frontiers in Oncology: Selenium in Cancer Management

Test Source: https://labs.rupahealth.com/store/storefront_64e2oDG?storefrontProduct=strprod_MQ5vAlM

🧪 Urine & Saliva pH: Terrain Matters

An acidic internal environment may promote cancer cell survival and invasiveness. Urine pH has been associated with poor prognosis in bladder cancer and may reflect systemic metabolic stress.

Urine and saliva pH are simple yet insightful markers of systemic acid-base balance, terrain integrity, and metabolic stress—especially relevant in cancer care. While blood pH is tightly regulated, urine and saliva offer dynamic windows into how the body is buffering acids and managing cellular waste. Urine pH, typically measured first thing in the morning, reflects renal excretion of metabolic acids. A persistently low urine pH (below 6.0) may indicate high dietary acid load, poor mineral buffering, or excessive oxidative stress—all of which can promote inflammation and impair immune function. In cancer patients, acidic urine has been associated with poorer prognosis in bladder and prostate cancers due to its correlation with systemic acidosis and tumor-promoting conditions. Saliva pH, on the other hand, reflects the buffering capacity of alkaline minerals and the influence of sympathetic nervous system activity. A low saliva pH may signal adrenal stress, poor digestion, or mineral depletion—factors that compromise immune resilience and cellular repair. Ideally, first-morning saliva pH should range from 7.0 to 7.4, while second-morning urine pH should fall between 6.5 and 7.5, indicating balanced terrain and effective acid elimination. Regular monitoring of these values can guide dietary adjustments, hydration strategies, and mineral support to restore a biochemical environment less conducive to cancer cell survival.
📖 Frontiers in Oncology: Acidic Urine & Bladder Cancer Prognosis
📖 AACR: Urine pH & Bladder Cancer Risk

Downloadable Test Guide: https://www.prevailovercancer.com/learning-center

Lymphocyte-to-monocyte ratio (LMR) & Neutrophil-to-lymphocyte ratio (NLR)

In a standard complete blood count (CBC), the ratios between lymphocytes, monocytes, and neutrophils offer powerful insights into immune status and cancer-related inflammation. The lymphocyte-to-monocyte ratio (LMR) is emerging as a prognostic marker in several cancers, including lymphoma, colorectal, and breast cancer. A low LMR often reflects immune suppression and tumor-promoting inflammation. Similarly, the neutrophil-to-lymphocyte ratio (NLR) is a well-established indicator of systemic inflammation and poor prognosis in solid tumors. Elevated NLR suggests a shift toward innate immune dominance and reduced adaptive surveillance—conditions that favor tumor progression. These ratios are simple to calculate but clinically profound, helping guide decisions around immunotherapy, metabolic support, and anti-inflammatory strategies.
📖 Journal of Translational Medicine: NLR and LMR in Cancer Prognosis
📖 Frontiers in Oncology: Immune Ratios and Cancer Outcomes

Test Source: https://www.ultalabtests.com/partners/prevailovercancer/testing/search

🧬 MyRisk Genetics: Precision Risk Stratification

This test evaluates 48 genes linked to hereditary cancer risk. It includes a polygenic risk score (PRS) that improves prediction accuracy for breast, ovarian, and other cancers—especially in BRCA carriers.

The MyRisk® Hereditary Cancer Test goes far beyond identifying genetic mutations—it offers a blueprint for proactive, terrain-targeted cancer care. By analyzing 48 genes linked to hereditary cancer syndromes (including BRCA1/2, CHEK2, ATM, PTEN, and more), MyRisk reveals vulnerabilities in DNA repair, hormone metabolism, detoxification, and immune surveillance. But the real power lies in what you do with that information. A positive or elevated risk score isn’t a sentence—it’s a signal to intervene. For example, BRCA mutations may call for increased intake of cruciferous vegetables and sulforaphane-rich compounds to support estrogen detoxification and DNA repair. CHEK2 or ATM variants may benefit from mitochondrial support via CoQ10, PQQ, and NAD+ precursors. PTEN-related risks can be modulated with anti-inflammatory protocols, intermittent fasting, and insulin-sensitizing nutrients like berberine or myo-inositol. Even in the absence of a mutation, polygenic risk scores (PRS) can guide lifestyle changes—such as reducing alcohol, increasing fiber, and optimizing sleep—to lower epigenetic activation of cancer-promoting pathways.

Beyond food and supplements, MyRisk results can inform the use of repurposed medications like metformin (for insulin regulation), low-dose naltrexone (for immune modulation), or statins (for anti-angiogenic effects in certain cancers). They can also guide decisions around screening frequency, bioidentical hormone use, and detox protocols—especially in individuals with impaired methylation or glutathione pathways. In short, MyRisk transforms genetic insight into an actionable strategy. It empowers clinicians and patients to reshape the terrain—making the body less hospitable to cancer and more resilient to recurrence.
📖 Myriad Genetics: RiskScore Clinical Validation

Test Source: https://www.jscreen.org/product/hereditary-cancer-screen

🧬 MTHFR: Methylation, Detox, and DNA Repair

MTHFR polymorphisms affect folate metabolism, methylation, and homocysteine levels. These influence DNA synthesis, repair, and epigenetic regulation—critical in cancer development.

The MTHFR gene (methylenetetrahydrofolate reductase) plays a central role in methylation—a biochemical process essential for DNA repair, detoxification, neurotransmitter synthesis, and immune regulation. MTHFR converts folate into its active form, 5-MTHF, which fuels the methylation cycle and supports the production of glutathione, the body’s master antioxidant. Variants such as C677T and A1298C can impair this conversion, leading to elevated homocysteine, reduced DNA stability, and compromised detox capacity—all of which increase cancer susceptibility. Research shows that MTHFR polymorphisms are associated with higher risk for breast, colorectal, and ovarian cancers, particularly in populations with poor folate status or high toxic burden.

But the real value of MTHFR testing lies in how it informs terrain-based interventions. Individuals with MTHFR mutations may benefit from methylated B vitamins (like methylfolate and methylcobalamin), glutathione precursors (such as NAC and glycine), and detox-supportive nutrients (like magnesium, zinc, and selenium). Diets rich in leafy greens, cruciferous vegetables, and sulfur-containing foods can further support methylation and antioxidant defense. Lifestyle strategies—such as stress reduction, sleep optimization, and minimizing alcohol—also help preserve methylation integrity. In some cases, repurposed medications like low-dose naltrexone or metformin may be considered to modulate immune and metabolic pathways affected by methylation dysfunction.

Significantly, MTHFR status can influence how patients respond to chemotherapy, radiation, and immunotherapy. A 2023 study found that MTHFR expression correlates with immune checkpoint response, tumor microenvironment heterogeneity, and infiltration of key immune cells across 44 cancer types. This makes MTHFR not just a genetic marker—but a strategic lever for reshaping the terrain to prevent, suppress, or reverse cancer progression.
📖 PLOS One: MTHFR & Colorectal Cancer Risk
📖 Springer Discover Oncology: MTHFR as Cancer Biomarker

Test Sources:

• https://labs.rupahealth.com/store/storefront_64e2oDG?storefrontProduct=strprod_MQa9aqM
• https://labs.rupahealth.com/store/storefront_64e2oDG?storefrontProduct=strprod_M4J9JWO

☣️ Glyphosate: A Carcinogen in Your Pantry?

Glyphosate, a widely used herbicide, has been classified as “probably carcinogenic” by the IARC. It’s linked to non-Hodgkin lymphoma and may disrupt gut microbiota, endocrine function, and immune signaling.

Classified by the World Health Organization’s International Agency for Research on Cancer (IARC) as a probable human carcinogen, glyphosate has been linked to non-Hodgkin lymphoma, leukemia, liver, kidney, and endocrine-related cancers. Mechanistically, glyphosate interferes with mitochondrial respiration, impairs glycine metabolism, chelates essential minerals like manganese and zinc, and promotes oxidative stress and DNA damage. It also alters the gut microbiome and inhibits cytochrome P450 enzymes, weakening detoxification and immune surveillance. A 2025 long-term animal study revealed that glyphosate exposure—even at regulatory thresholds—induced malignant tumors and early-life leukemia, raising serious concerns about cumulative dietary exposure. For terrain-based cancer care, testing glyphosate levels via urine can uncover hidden toxic burdens and guide interventions such as organic dietary shifts, glutathione support, microbiome restoration, and targeted detox protocols. Glyphosate isn’t just a pesticide—it’s a metabolic disruptor that reshapes the terrain in ways that favor cancer cell survival. In terrain-based cancer care, glyphosate isn’t just a pesticide; it’s a metabolic saboteur. Identifying and reducing exposure is a critical step in restoring cellular integrity, immune resilience, and anti-cancer defense.
📖 JNCI: Glyphosate & Cancer Incidence
📖 Environmental Health: Glyphosate Carcinogenicity Study

Test Source: https://labs.rupahealth.com/store/storefront_64e2oDG?storefrontProduct=strprod_Mabo517

🧪 DUTCH Complete: Hormone Metabolites

The DUTCH Complete Hormone Test is a powerful tool for assessing cancer-related terrain through the lens of hormone metabolism, detoxification, and adrenal function. Unlike standard serum hormone tests, DUTCH uses dried urine samples to measure not only sex hormones—like estrogen, progesterone, and testosterone—but also their metabolites, which reveal how the body processes and clears these hormones. This is critical in cancer prevention, especially for hormone-sensitive cancers such as breast, ovarian, and prostate. For example, elevated levels of 4-hydroxyestrone and 16-OH estrone are associated with increased DNA damage and tumor promotion, while 2-hydroxyestrone and 2-methoxyestrone are considered protective. DUTCH also evaluates phase I and phase II estrogen detox pathways, including hydroxylation and methylation, helping clinicians identify whether estrogen is being metabolized safely or dangerously. Additionally, it measures cortisol patterns, DHEA, melatonin, and organic acids—offering insight into stress load, immune suppression, and mitochondrial function. This comprehensive profile allows for terrain-based interventions using food, supplements, lifestyle changes, and even repurposed medications to rebalance hormones, reduce cancer risk, and support long-term resilience.
📖 Understanding DUTCH Test: Hormones, Metabolites & Biomarkers
📖 Journal of Clinical & Translational Endocrinology: DUTCH Validation

Test Source: https://labs.rupahealth.com/store/storefront_64e2oDG?storefrontProduct=strprod_xvyovgO

🔥 Cortisol: Stress Fuels Cancer

Chronic cortisol elevation suppresses immune surveillance, promotes inflammation, and accelerates tumor progression. Flattened diurnal cortisol curves are associated with poorer outcomes in multiple cancer types.

Cortisol, the body’s primary stress hormone, plays a pivotal role in cancer biology through its impact on immune surveillance, inflammation, and hormonal balance. Secreted by the adrenal glands in response to physical or emotional stress, cortisol helps regulate metabolism, blood pressure, and circadian rhythm. However, when cortisol levels remain chronically elevated—as seen in persistent psychological stress or disrupted sleep cycles—it can suppress natural killer (NK) cell activity, impair T-cell function, and weaken the immune system’s ability to detect and destroy emerging cancer cells. High cortisol also fuels systemic inflammation and insulin resistance, creating a biochemical terrain that supports tumor growth, angiogenesis, and metastasis. Moreover, flattened or reversed diurnal cortisol curves have been associated with poorer outcomes in breast, prostate, and colorectal cancers. Testing cortisol patterns through saliva or urine—especially via the DUTCH Complete test—can reveal hidden stress burdens and guide terrain-based interventions such as adaptogenic herbs, breathwork, sleep optimization, and targeted supplementation. In cancer care, cortisol isn’t just a stress marker, it’s a metabolic signal that can either suppress or support the body’s anti-cancer defenses.

📖 Nature: Cortisol & Endometrial Cancer Risk
📖 Frontiers in Endocrinology: Cortisol & Cancer Prognosis

Test Sources:

• https://labs.rupahealth.com/store/storefront_64e2oDG?storefrontProduct=strprod_O1Ddo07
• https://labs.rupahealth.com/store/storefront_64e2oDG?storefrontProduct=strprod_OpDo9YO

🧪 LDH: A Metabolic Marker of Tumor Aggression and Immune Evasion

Lactate dehydrogenase (LDH) is a key enzyme in glycolysis that catalyzes the conversion of pyruvate to lactate, a process hijacked by cancer cells to fuel rapid growth—even in the presence of oxygen, known as the Warburg effect. Elevated serum LDH levels are consistently associated with poor prognosis across multiple cancer types, including melanoma, breast, and lung cancers. LDH not only reflects tumor burden but also correlates with increased metabolic activity, invasiveness, and immunosuppression within the tumor microenvironment. A 2022 review in Nature Reviews Clinical Oncology highlights LDH’s role in activating oncogenic signaling pathways and modulating immune escape mechanisms, making it a potential therapeutic target. Additionally, a 2025 cohort study published in BMC Cancer found a U-shaped association between LDH levels and all-cause mortality in cancer patients, with both low and high extremes linked to worse outcomes—underscoring the importance of maintaining LDH within an optimal range. Monitoring LDH can guide terrain-based interventions, track treatment response, and identify patients at higher risk for aggressive disease.

📖 Nature Reviews: LDH’s Role in Cancer Metabolism and Immunity
📖 BMC Cancer: LDH and Mortality Risk in Cancer Patients

Test Source: https://www.ultalabtests.com/partners/prevailovercancer/test/lactate-dehydrogenase-test

☀️ Vitamin D3 and K2: Synergistic Allies in Cancer Terrain Optimization

Vitamin D3 (cholecalciferol) and Vitamin K2 (menaquinone) are more than bone-health nutrients—they’re potent modulators of cancer-related terrain. Vitamin D3 influences over 1,000 genes, regulating cell growth, immune surveillance, and inflammation. Low serum levels of 25-hydroxyvitamin D have been linked to increased risk and poorer outcomes in breast, colorectal, prostate, and pancreatic cancers. Meanwhile, Vitamin K2 activates matrix Gla protein (MGP) and osteocalcin, which not only support calcium metabolism but also inhibit vascular calcification and tumor angiogenesis. Emerging research suggests that K2 may enhance the anti-proliferative effects of D3, reduce oxidative stress, and improve mitochondrial function—making their combination a strategic intervention in terrain-based cancer care. A 2024 NHS evidence review concluded that both vitamins hold promise in oncology, with D3 showing robust support for symptom management and K2 offering tumor-specific benefits. Additionally, a randomized trial published in JAMA Network Open found that daily supplementation with 2,000 IU of D3 reduced the incidence of advanced cancers in individuals with normal BMI. Together, D3 and K2 form a synergistic duo that helps reshape the biochemical environment to resist cancer progression and support immune resilience.

Effect of Vitamin D3 Supplements on the Development of Advanced Cancer

K2 Inhibits Cancer Cell Proliferation

Test Source: https://www.ultalabtests.com/partners/prevailovercancer/test/vitamin-d-k-test-panel  

🧠 The Takeaway: Data Drives Our Cancer Decisions

Cancer isn’t random; it is biochemical. These tests don’t just inform—they empower. They help us personalize nutrition, detoxification, supplementation, and lifestyle protocols with precision. Whether you're a clinician, patient, or advocate, remember:

Symptoms are signals. Labs are maps.
Let’s stop guessing—and start assessing.