Epigenetics Tests and Hair Root Tests, what they measure, and why they matter for understanding your health.
1. What is an Epigenetics Test?
The Epigenetics Test
"How fast are you aging?"
While a standard DNA test (like 23andMe) examines your genetic makeup (which remains constant), an epigenetics test assesses your epigenetic profile (which changes constantly based on your lifestyle choices).
What it is: A test (usually saliva or blood) that analyses DNA Methylation.It looks for chemical "tags" (methyl groups) attached to your DNA that turn specific genes "on" or "off."
Simple meaning
An epigenetics test looks at how your genes are being switched ON or OFF by your lifestyle and environment—not by changing the genes themselves, but by controlling how they work.
Think of your DNA as a keyboard.
Epigenetics decides which keys are being pressed.
What it tells you:
Biological Age: You might be 40 years old chronologically (birthdays), but your body might be aging at the rate of a 50-year-old due to stress, diet, or toxins.
Pace of Aging: Are you currently aging faster or slower than the average person?
Disease Risk: It can reveal early warning signs for conditions like cancer, diabetes, or heart disease before they physically manifest.
What does it measure?
Epigenetics tests typically analyse:
DNA methylation patterns (chemical tags on DNA)
Gene expression activity
Biological pathways related to:
Inflammation
Aging
Metabolism
Stress response
Detoxification
Hormone regulation
What influences epigenetics?
Your epigenetic patterns change based on:
Diet & nutrition
Stress & emotional health
Sleep quality
Physical activity
Toxins (pollution, smoking, chemicals)
Trauma and long-term stress
Aging
👉 This means epigenetics is dynamic and reversible, unlike DNA.
Why is an Epigenetics Test important?
It helps you understand:
Why you may develop diseases despite “normal genes”
How lifestyle choices are affecting your health right now
Your biological age vs chronological age
Your risk for:
Diabetes
Heart disease
Cancer
Autoimmune disorders
Neurodegenerative diseases
Most importantly:
It tells you what you can change to improve your health.
Why it’s important: It proves that biology is not destiny.Unlike a genetic test which might say "You have the gene for Alzheimer's," an epigenetic test can show you if your current lifestyle is actively triggering that gene or keeping it dormant. It allows you to measure if your diet or exercise changes are actually working.
2. What is a Hair Root Test?
"What has your body been exposed to?"
It is important to distinguish between the two main types of hair tests: Standard Toxicology (medical/forensic) and Epigenetic Hair Mapping (wellness/nutrition).
Standard Hair Follicle Analysis (Medical/Forensic)
What it is: A lab analyzes the hair shaft and the root to detect substances trapped in the hair protein as it grew.
What it tells you: It provides a timeline (typically 3–6 months) of drug use, heavy metal exposure (like lead or mercury), and mineral imbalances.
Why it’s important: Blood and urine tests only show what is in your system right now (usually the last 24–48 hours). Hair tests show a long-term history.This is vital for identifying chronic exposure to environmental toxins (e.g., mold or lead in water) that might be causing unexplained fatigue or illness.
Simple meaning
A hair root test examines the root of the hair (follicle) to assess long-term mineral, toxin, and metabolic status of the body.
Blood tests show today’s condition.
Hair root tests show what has been happening for months.
Mineral ratios (important for hormone and nerve function)
Cellular metabolism patterns
Oxidative stress indicators
Why hair roots (not just hair strands)?
Hair roots are living tissue
Reflect cellular-level nutrition
Show chronic deficiencies or toxic exposure
Less influenced by daily fluctuations than the blood
Why is a Hair Root Test important?
It helps identify:
Hidden mineral deficiencies
Heavy metal toxicity
Reasons for:
Chronic fatigue
Hair loss
Neuropathy
Poor immunity
Hormonal imbalance
Brain fog
Why treatments or supplements may not be working
This is especially useful in:
Chronic illness
Diabetes complications
Neurological symptoms
Unexplained health issues
What it is: A newer, popular wellness test (often using a "digitizer" to scan hair bulbs). It claims to use bio-resonance to map epigenetic indicators.
What it claims to tell you: It generates a report on nutritional deficiencies (vitamins/minerals), food intolerances, gut health, and environmental sensitivities (EMF, radiation).
3. How Epigenetics Test & Hair Root Test Work Together
Epigenetics Test
Hair Root Test
Shows gene activity
Shows cellular nutrition
Tells why genes are misbehaving
Tells what the cells lack or accumulate
Focuses on regulation
Focuses on materials
Guides lifestyle change
Guides supplementation & detox
🔹 Epigenetics = Control system
🔹 Hair root test = Raw materials & toxins
Together they give a root-cause health map, not just symptoms.
4. Why These Tests Are Especially Valuable Today
Modern diseases are mostly lifestyle-driven, not genetic:
Diabetes
Heart disease
Cancer
Autoimmune disorders
Neurodegeneration
Traditional tests often detect disease after damage is done.
These tests focus on early dysfunction and prevention.
5. Key Takeaway
Epigenetics Test tells you how your lifestyle is controlling your genes
Hair Root Test tells you what your cells have been missing or overloaded with
Metformin (brand names include Glucophage, Fortamet, Glumetza) is the most widely prescribed medication for Type 2 diabetes worldwide. It belongs to a class of drugs called biguanides.
Here is a comprehensive breakdown of what it is, how it works, and what you need to know if you are taking it.
1. Primary Uses
Type 2 Diabetes: It is the first-line medication recommended for lowering blood sugar levels. It is often used alone or in combination with other drugs (like insulin).
Prediabetes (Off-label): Doctors often prescribe it to prevent the progression from prediabetes to full Type 2 diabetes, particularly in people with a high BMI.
Polycystic Ovary Syndrome (PCOS) (Off-label): It helps lower insulin levels and androgen (male hormone) levels, which can help regulate menstrual cycles and improve fertility/ovulation.
Gestational Diabetes: Sometimes used during pregnancy when insulin is not an option or not preferred, though insulin remains the gold standard.
2. How It Works
Metformin does not increase the amount of insulin your body makes (so it rarely causes low blood sugar/hypoglycemia on its own). Instead, it works in three main ways:
Stops the Liver: It reduces the amount of sugar (glucose) your liver produces and releases into your bloodstream.
Boosts Sensitivity: It makes your muscle tissue more sensitive to insulin, allowing your cells to use glucose more effectively.
Reduces Absorption: It slightly decreases the amount of sugar your gut absorbs from the food you eat.
3. Side Effects
Common (The "Metformin Tummy"):
The most common complaints are digestive. These usually happen when you first start the drug and often go away after a few weeks.
Diarrhea
Nausea/Vomiting
Stomach cramps/bloating
Metallic taste in the mouth
Serious (Rare):
Lactic Acidosis: A dangerous buildup of lactic acid in the blood. This is very rare (approx. 1 in 30,000 users) but can be fatal. Symptoms include extreme fatigue, muscle pain, difficulty breathing, and slow heart rate. It is mostly a risk for people with kidney or liver failure.
Vitamin B12 Deficiency: Long-term use can block the absorption of Vitamin B12. Your doctor may monitor your levels periodically.
4. Important Warnings & Contraindications
Kidney Function: Metformin is cleared by the kidneys. If you have severe kidney disease (typically eGFR < 30 mL/min), you cannot take it because it increases the risk of lactic acidosis.
CT Scans/Contrast Dye: If you are having an imaging scan that uses iodinated contrast dye, you may need to stop taking Metformin for 48 hours before and after the procedure to protect your kidneys.
Alcohol: Excessive alcohol intake (acute or chronic) drastically increases the risk of lactic acidosis.
Liver Disease: Used with caution or avoided in severe liver disease.
5. Practical Tips for Success
If you have been prescribed Metformin, these strategies can help minimize side effects:
Take with Food: Always take it in the middle of a meal or immediately after to buffer your stomach.
Start Low, Go Slow: Doctors usually start you on a low dose (e.g., 500mg once daily) and slowly increase it over weeks. Do not rush this titration.
Ask for Extended Release (XR/ER): If the standard "immediate release" tablets give you severe stomach upset, ask your doctor for the Extended Release version. It releases the drug slowly and is generally much gentler on the stomach.
6. Research on Longevity
You may hear Metformin discussed in "biohacking" or anti-aging circles. Some research suggests it might mimic the effects of calorie restriction and activate longevity pathways (like AMPK). However, there is currently no definitive clinical evidence that it extends lifespan in healthy humans, and it is not FDA-approved for anti-aging.
Glomerular Filtration Rate (GFR) is the primary test used to check how well the kidneys are functioning.It measures the amount of blood that passes through the glomeruli—the tiny filters in the kidneys that remove waste—every minute.
GFR is a key measure of how well your kidneys are filtering blood. It estimates how much blood (in millilitres) the kidneys filter per minute to remove waste and excess fluid.
Why GFR is Important
Your kidneys act as the body's filtration system. A high GFR means your kidneys are efficiently clearing waste, while a low GFR indicates that waste products (like creatinine) are building up in your blood because the filters are damaged or sluggish.
Standard Unit:mL/min/1.73m^2 (millilitres per minute per 1.73 square meters of body surface area).
Normal Range: Roughly 90–120mL/min for healthy adults.
In a clinical setting, you will likely see eGFR (estimated GFR) on your lab results rather than a direct measurement.
Measured GFR (mGFR): The "gold standard" involves injecting a substance, such as inulin or Iohexol, into the blood and measuring how quickly the kidneys clear it. This is a complex process and is rarely done outside of research.
Estimated GFR (eGFR): This is a calculated estimate using a mathematical formula. It typically requires:
Understanding how medications affect GFR requires looking at the "pipes" leading into and out of the kidney's filters (the glomeruli).
To keep the filtration rate steady, the kidney needs a certain amount of internal pressure. It maintains this pressure by adjusting two main vessels: the Afferent Arteriole (the "inlet" pipe) and the Efferent Arteriole (the "outlet" pipe).
1. ACE Inhibitors: Opening the "Outlet"
ACE Inhibitors (like Lisinopril or Enalapril) and ARBs (like Losartan) block Angiotensin II, a hormone that normally constricts the outlet pipe (efferent arteriole).
The Effect: These drugs cause the outlet pipe to widen (vasodilation).
Impact on GFR: Because the "exit" is now wide open, the pressure inside the filter drops. This usually causes an initial, small decrease in eGFR (a rise in creatinine).
Why doctors use them anyway: Even though GFR drops slightly at first, lowering that internal pressure protects the filters from long-term wear and tear. It’s like lowering the water pressure in a delicate pipe to prevent it from bursting over time.
2. NSAIDs: Narrowing the "Inlet"
NSAIDs (like Ibuprofen, Naproxen, or Celebrex) block Prostaglandins, which are chemicals that normally keep the inlet pipe (afferent arteriole) open.
The Effect: Without prostaglandins, the inlet pipe narrows (vasoconstriction).
Impact on GFR: Less blood can get into the filter, which reduces the pressure and lowers the GFR.
The Risk: In healthy people, the body can usually compensate. However, if you are dehydrated or already have kidney issues, NSAIDs can "starve" the kidney of blood, leading to a sudden drop in function.
3. The "Triple Whammy"
The most dangerous scenario for GFR occurs when a patient takes three types of medications together:
ACE Inhibitor/ARB: Opens the outlet (lowers pressure).
When all three are used, the kidney loses its ability to regulate its own internal pressure. This can lead to Acute Kidney Injury (AKI) because the GFR plummets dangerously low.
The stream of news about cancer research is constant, and while every step forward is important, the sheer volume can make individual advances feel incremental. We hear about new drugs and promising trials, but it's often hard to distinguish a small step from a giant leap.
This article cuts through the noise to highlight five breakthroughs from 2025 that represent more than just progress—they signal fundamental shifts in how scientists understand and attack cancer. These are not simply better versions of existing treatments; they are based on new, sometimes counter-intuitive, strategies for outsmarting the disease.From completely eliminating problematic proteins instead of just blocking them, to making organ preservation a primary goal of treatment, these concepts offer a glimpse into the future of oncology. They are rewriting the rules of engagement and showing that the next generation of cancer therapy will be defined by a smarter, more strategic approach to biology itself.
1. The New Strategy: Don't Just Block Cancer Proteins—Destroy Them
For decades, the standard approach in targeted cancer therapy has been to find a protein driving a tumor's growth and design a drug to inhibit, or block, its function. A new class of drugs, however, is built on a more decisive strategy: don't just block the protein, get rid of it entirely. This approach, known as targeted protein degradation, is now showing its power in the clinic.
The leading example is Vepdegestrant (ARV-471), a new oral therapy for ER-positive/HER2-negative breast cancer. It is a PROTAC (PROteolysis TArgeting Chimaera), a molecule that not only blocks the estrogen receptor (ER) that fuels these cancers but also targets it for degradation. Instead, it acts as a molecular matchmaker, using the cell’s own machinery to degrade and destroy the receptor. By recruiting the cell's natural disposal system, it marks the ER protein for complete elimination.
This is a powerful way to overcome drug resistance, a major challenge in breast cancer treatment. Many tumors develop mutations in the ESR1 gene, which allows them to resist standard endocrine therapies. The Phase 3 VERITAC-2 trial provided a clear picture of Vepdegestrant’s unique strength. In the overall trial population, the benefit was modest and did not reach statistical significance (median Progression-Free Survival of 3.8 vs 3.6 months). However, in the crucial ESR1-mutant subgroup, where resistance is most common, the results were dramatic. Vepdegestrant achieved a median Progression-Free Survival (PFS) of 5.0 months, more than doubling the 2.1 months seen with the standard-of-care drug fulvestrant (HR 0.58). The Objective Response Rate (ORR) was also more than four times higher, at 18.6% versus 4.0%.
This marks a conceptual leap from merely disrupting a cancer pathway to surgically removing its key components, a strategy designed to preempt resistance before it can begin.
2. A Surprising New Goal: Saving Organs, Not Just Lives
For certain cancers, a successful outcome has long meant removing the affected organ—a life-saving but life-altering necessity. A recent breakthrough in uveal melanoma, a rare cancer of the eye, is challenging that paradigm by showing that it's possible to treat the cancer effectively while preserving the organ and its function.
Patients with primary uveal melanoma often face surgical removal of the eye, a procedure known as enucleation. The new drug Darovasertib, a selective PKC inhibitor, represents a "genuine paradigm shift" by offering a powerful neoadjuvant (pre-surgery) treatment that can shrink tumors enough to make less radical therapies possible.
The results from the Phase 2 OptimUM-09 trial are unprecedented. Across all patients, 83% experienced measurable tumor shrinkage, and 54% achieved shrinkage of 20% or more. This translated directly into organ preservation. Among patients who were originally recommended for enucleation, treatment with Darovasertib preserved the eye in 57% of cases. For patients whose tumors shrank by at least 20%, the eye-preservation rate soared to an incredible 95%.
Even more remarkably, the treatment not only saved the eye but also protected and even improved its function. More than half of all patients in the trial experienced an improvement in their visual acuity during treatment. This redefines what a successful outcome can be, shifting the goal from just survival to include profound quality-of-life improvements. The focus is no longer simply on organ removal, but on organ preservation, demonstrating that future cancer treatments can aim to save not just the patient's life, but also its quality.
3. Immunotherapy's Two-Front War: Attacking the Tumor and Its Bodyguards
Immunotherapy has revolutionized cancer treatment, but a major obstacle remains: the Tumor Microenvironment (TME). This complex ecosystem of non-cancerous cells, including immune cells like macrophages, can form a "protective shield for the tumor," making it difficult for therapies to penetrate and for the patient's own immune system to launch an effective attack. New therapies are now being designed to fight a two-front war, simultaneously targeting the tumor and the very cells that protect it.
A novel CAR-T cell therapy from Mayo Clinic, known as MC9999, is a prime example of this new strategy. Traditional CAR-T therapies engineer a patient's T-cells to attack a specific protein on the surface of cancer cells. The challenge is that the TME often suppresses these engineered cells before they can do their job. MC9999 gets around this by targeting PD-L1, a protein found on the surface of both the tumor cells and the immunosuppressive cells within the TME.
The strategy is explained by the researchers who developed it:
"PD-L1 is a very good target for us, because it allows us to simultaneously hit tumor cells and the immunosuppressed cells in the tumor microenvironment."
This approach is also being explored in glioblastoma, a deadly brain cancer. Researchers are mapping how immunosuppressive macrophages and glioblastoma cells co-evolve—with the macrophages changing the tumor cells and the tumor cells, in turn, changing the macrophages. This dynamic interaction creates a potent protective barrier, and by understanding it, scientists are identifying new targets on both cell types.
This represents a critical shift in immunotherapy strategy. Instead of just sending T-cells to storm the fortress (the tumor), these new therapies are designed to simultaneously dismantle the fortress walls and neutralize its guards, leaving the cancer exposed and vulnerable.
4. The "Undruggable" Is Finally Being Drugged
In oncology, some targets have been considered "undruggable" for decades. These are cancer-driving proteins whose structure and function make them incredibly difficult to block with conventional drugs. Among the most notorious of these are mutations in the RAS family of genes, which are found in a huge proportion of human cancers, including some of the deadliest. After years of effort, this frontier is finally beginning to yield.
The most prominent example of this progress is Daraxonrasib (RMC-6236), a first-of-its-kind pan-RAS inhibitor. Unlike earlier drugs that could only hit one specific type of RAS mutation, Daraxonrasib is designed to target the active form of all major RAS variants. This makes it a potential game-changer for cancers driven by this historically intractable target, particularly pancreatic ductal adenocarcinoma (PDAC), where progress has been notoriously slow.
The early results in this difficult-to-treat cancer are impressive. In patients with advanced PDAC who had already received other treatments, Daraxonrasib achieved an Objective Response Rate (ORR) of 29-35%, a median Progression-Free Survival (PFS) of approximately 8 months, and disease control rates over 90%. This translated to a median Overall Survival (OS) of 13-16 months—a level of durable benefit rarely seen in this setting. In previously untreated patients, the results were even more striking: when combined with chemotherapy, Daraxonrasib delivered an ORR of 55% and a disease control rate of approximately 90%.
The significance of these findings cannot be overstated. They demonstrate that a target long considered the "holy grail" of oncology is now vulnerable to innovative drug design. For patients with pancreatic cancer and other RAS-driven tumors, this breakthrough offers real, tangible hope where there was once very little.
5. Cancer's "Smart Bombs" Are Getting a Double-Tap Upgrade
Antibody-Drug Conjugates (ADCs) are one of the most sophisticated tools in modern oncology. They function like "smart bombs," combining a highly specific monoclonal antibody that seeks out a target on cancer cells with a potent cytotoxic payload that kills them. Now, the next generation of these smart bombs is being engineered with even greater complexity to overcome one of cancer's greatest strengths: its ability to adapt and resist treatment.
One new evolution, now in early-phase clinical trials, is the dual-payload ADC. These constructs are designed to "deliver two different cytotoxic agents simultaneously" from a single antibody. The strategic goal is to overcome drug resistance driven by tumor heterogeneity—the fact that a single tumor is often made up of different types of cells, some of which may be resistant to one type of chemotherapy but vulnerable to another.
Another powerful example of this increasing complexity is the development of bispecific ADCs, where the antibody itself is engineered to hit two targets at once. Iza-bren (izalontamab brengitecan) exemplifies this multi-pronged approach. It is a first-in-class bispecific ADC whose antibody targets two different proteins: EGFR and HER3. By co-targeting both and delivering a potent topoisomerase-I payload, Iza-bren is designed to attack the cancer’s signaling architecture and its DNA simultaneously. The power of this highly engineered weapon is clear from its practice-changing results in nasopharyngeal carcinoma, where it more than doubled the confirmed Objective Response Rate (54.6% vs 27.0%) compared to standard chemotherapy in heavily pretreated patients.
This trend shows that oncology is moving beyond single-target, single-payload drugs to create complex, multi-layered molecular weapons designed to preemptively counter cancer's most evasive tactics.
Conclusion: A Shift in Thinking
The breakthroughs of 2025 reveal a clear strategic evolution in the fight against cancer. We are moving beyond simply inhibiting the disease to a more sophisticated approach: destroying its core components, reprogramming its protective environment, preserving vital organs and functions, and deploying multi-pronged molecular weapons to overcome its defences.
These advances show that the future of oncology isn't just about better drugs, but about a fundamentally smarter, more holistic way of fighting the disease. As we continue to rewrite the biological rulebook, what long-held assumptions about cancer will be the next to fall?
