BY BEN LYNCH, ND

Most pregnant women reach for Tylenol at some point, and for many, it feels like the only safe option for pain or fever relief.

Yet whether acetaminophen is truly “safe enough” during pregnancy depends less on the pill itself and more on how well a woman’s body can process it.

Tylenol is not inherently toxic; it becomes problematic when the body cannot move it through its normal detoxification pathways, and a reactive byproduct builds up.

At the center of this story is glutathione, often called the body’s “master antioxidant,” because it helps keep developing tissues—especially the brain—safe from damage. Glutathione neutralizes the most toxic acetaminophen metabolite and is critical for supporting healthy fetal brain development.^1,2,3,4,5

Women whose glutathione status is compromised—because of conditions such as polycystic ovary syndrome (PCOS),^17,37,40 blood sugar regulation issues, gallbladder dysfunction,^53,60 or in vitro fertilization (IVF)-related oxidative stress^18,19,41,46—may have less margin for error than they realize when it comes to repeated Tylenol use in pregnancy.

This matters because acetaminophen use in pregnancy is common, and pregnancy itself changes the way the body handles the drug. Studies suggest that over 60% of pregnant women take Tylenol at least once, with most using standard doses of 500–650 mg every 4–6 hours,^15,16,20 and the main metabolic pathway for clearing it can drop by nearly half or more in mid-to-late pregnancy.^60,102,104

Research points to a dose-response pattern: longer or heavier use tracks with higher odds of attention/focus disorders and neurodevelopmental risks in children, particularly when the most toxic metabolites show up at higher levels in cord blood.^11,14,77,79

The concern does not end at birth. The same vulnerable antioxidant systems that protect the fetal brain also matter for newborns, and many infants receive Tylenol (acetaminophen) after routine vaccinations.^47,48 The goal here is not to scare women away from every dose of Tylenol, but to invite a deeper conversation: your individual metabolic health, antioxidant status, and pregnancy context all influence what “safe use” looks like for you and your baby.

The Critical Question Is: What happens when women who already have low glutathione status take Tylenol during the critical window of fetal brain development?

Why Glutathione Matters for Brain Development

Glutathione acts as the body’s master antioxidant and the primary mechanism for supporting the healthy response of developing tissues to oxidative stress. During pregnancy, adequate glutathione levels are essential for proper brain development.^1,5

Glutathione’s Critical Roles^1,5

• Supports the developing brain’s healthy response to oxidative stress
• Supports healthy methylation (controls gene expression)
• Regulates homocysteine levels (elevated levels risk neural tube defects)
• Enables proper epigenetic programming
• Supports a healthy immune response within the brain and spinal cord and normal microglial activation

Children with neurodevelopmental disorders consistently show patterns of low glutathione, elevated homocysteine, impaired methylation capacity, increased oxidative stress markers, and mitochondrial dysfunction.^6,8 Low maternal glutathione during pregnancy has been linked with preeclampsia, HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets), intrauterine growth restriction, fetal brain inflammation, and a higher risk of attention/focus and neurodevelopmental disorders in offspring.^2,3,6,9,10

What the Research Shows: Several large human studies report associations between prenatal acetaminophen use and later neurodevelopmental outcomes. A 2021 meta-analysis of 73,881 mother-child pairs found that children exposed to acetaminophen use in utero were 19% more likely to have neurodevelopmental symptoms and 21% more likely to have attention/focus disorders.¹¹

A 2018 meta-analysis of 132,738 mother-child pairs found that these associations tended to strengthen with longer exposure duration,13 suggesting a possible dose-response pattern. More recent work measuring acetaminophen-related biomarkers in cord blood has linked higher exposure levels to higher odds of neurodevelopmental diagnoses,¹² and a 2024 review of 46 studies concluded that higher-quality studies were more likely to show positive associations.¹⁴

How Much Tylenol Do Pregnant Women Actually Take?

Current Tylenol usage patterns reveal widespread exposure:

• 62–65% of pregnant women use acetaminophen at least once^15,16

• 6% use it weekly or more often^15,16

• Typical adult dosing is 500–650 mg every 4–6 hours as needed^15,16,20

• 58% use it for fewer than 10 days; 9% use it for 45 or more days¹⁶

These “safe” therapeutic doses can significantly deplete glutathione in women who already have low levels.^21,23 Healthy individuals can generally tolerate up to 4 grams per day on occasion with only modest, reversible decreases in glutathione.

However, women with compromised glutathione—due to malnutrition, obesity, gestational blood sugar challenges, PCOS, liver disease, or genetic factors—may be at increased risk for significant glutathione depletion and acetaminophen toxicity.

The Math That Makes You Think

Currently, approximately 1 in 36 children are diagnosed with neurodevelopmental disorders. With 3.6 million births per year in the United States, that translates to roughly 100,000 children diagnosed annually.

Around 65% of pregnant women use acetaminophen—about 2.3 million women per year. A conservative estimate suggests that at least 10% of pregnant women have compromised glutathione status due to factors such as PCOS, IVF, poor diet, chemical exposure, obesity, liver disease, or genetic variants.

Even if only a fraction of these roughly 200,000 “glutathione-vulnerable” pregnancies each year experience additional glutathione depletion from acetaminophen, the potential impact on fetal brain resilience is significant enough to warrant serious attention.

How Your Body Processes Tylenol: Safe vs. Toxic Pathways

When you take acetaminophen, your liver processes it through three pathways:^{26,27,60,70,72}

1. Glucuronidation (Safe Pathway)

• Accounts for 50–60% of acetaminophen metabolism in healthy non-pregnant adults

• Attaches glucuronic acid to make the drug water-soluble for urinary excretion

• Increases during pregnancy (6% in first trimester, rising to 19% by third trimester)⁶⁰

• Severely underdeveloped in fetuses and newborns

2. Sulfation (Safe Pathway)

• Accounts for 30–35% of acetaminophen in healthy non-pregnant adults

• Attaches sulfate groups for safe elimination

• Decreases 33% during pregnancy (contrary to previous assumptions)⁶⁰

• Limited capacity—easily saturated with higher or repeated doses

• Predominant pathway in fetuses and children (60–70%), but quickly overwhelmed

3. Oxidation (Toxic Pathway)

• Accounts for only 5–10% of acetaminophen in healthy non-pregnant adults

• Increases by 80% during pregnancy⁶⁰

• Creates NAPQI (N-acetyl-p-benzoquinone imine)—the dangerous toxic metabolite

• NAPQI formation is 43% higher in the first trimester⁶⁰

• NAPQI must be immediately neutralized by glutathione; when glutathione is depleted, NAPQI causes cellular damage and crosses the placenta to damage the fetal brain

The Critical Problem: When the safe pathways are compromised, overwhelmed, or underdeveloped, more acetaminophen is forced through the toxic oxidation pathway. This generates more NAPQI when glutathione reserves are least able to handle it—creating a perfect storm for toxicity in vulnerable populations.

How Pregnancy Changes Acetaminophen Metabolism

During a normal, healthy pregnancy, natural metabolic shifts move acetaminophen metabolism away from safe routes toward increased NAPQI formation. This increases both maternal and fetal risk if glutathione reserves are compromised.

The Brookhuis et al. 2021 Study60 (published in Pharmaceutics) used physiologically-based pharmacokinetic modeling in pregnant women and documented critical shifts:

Oxidation to NAPQI Increases by 80%: Just before giving birth, the clearance level of acetaminophen via the toxic pathway was 1.8-fold higher than shortly after delivery—an 80% increase observed throughout the entire pregnancy.⁶⁰ This means 43% more of the toxic NAPQI metabolite is produced during pregnancy compared to non-pregnant women, with the highest NAPQI formation occurring in the first trimester (11% vs 7.7% in non-pregnant women)—precisely when the fetal brain is most vulnerable and undergoing critical early development.⁶⁰

Sulfation (Safe Pathway) Decreases 33%: The fraction of acetaminophen handled by sulfation drops from about 31% in non-pregnant women to around 20.7% by the third trimester.⁶⁰ This 33% decrease leaves the safe pathway more easily overwhelmed, especially with repeated doses.

Glucuronidation Increases but Is Insufficient: While glucuronidation does increase during pregnancy, this increase cannot compensate for the simultaneous 33% decrease in sulfation and 80% increase in oxidation to toxic NAPQI.

The Result: Significantly more acetaminophen is forced through the toxic CYP2E1 pathway, creating 43% more NAPQI—at precisely the time when glutathione reserves are most depleted.

Progressive Glutathione Depletion Across Trimesters: A 2024 study measuring glutathione across all three trimesters found significant decreases compared to non-pregnant women:¹⁰²

• 36% lower glutathione in the first trimester (48 vs 75 pg/mL)

• 55% lower in the second trimester (34 vs 75 pg/mL)

• 87% lower in the third trimester (9.76 vs 75 pg/mL)

The Study Concluded: “Pregnancy as a situation produces a huge amount of oxidants, so it reduces the capability of the body to overcome its effect, leading to oxidative stress.”¹⁰²

NAPQI Crosses the Placenta and Damages the Fetus

The Mian et al. 2020 study confirmed that NAPQI crosses the placenta and that the fetal liver has severely limited detoxification capacity, demonstrating direct fetal exposure to this toxic metabolite.^24,25,100

What NAPQI Does^73,75

• Directly binds to and damages cellular proteins

• Depletes glutathione rapidly

• Generates oxidative stress, which damages lipids, proteins, and DNA

• Triggers cell death (apoptosis)

• Damages mitochondria, disrupting energy production

Essential Point: NAPQI depletes fetal brain glutathione and induces oxidative stress and cell death in neural tissue at doses below those causing maternal liver toxicity.⁷⁵ The developing brain has limited antioxidant defenses and high metabolic demands, making it especially susceptible. This is why a pregnant woman can feel fine while her fetus is experiencing glutathione depletion and oxidative brain damage.

Why Low Glutathione Is Devastating for the Developing Brain

When NAPQI binds to glutathione, it reduces the capacity to detoxify other harmful chemicals in the developing brain:

Hydrogen Peroxide: Glutathione normally converts hydrogen peroxide into water. In the developing brain, hydrogen peroxide kills immature neurons at concentrations less toxic to mature neurons, disrupts the blood-brain barrier, and impairs visual system development and brain connectivity.

Formaldehyde: Naturally produced in the body but increased by environmental exposure (new clothes, carpets, foam mattresses, construction materials). In the developing brain, it disrupts learning and memory, causes oxidative stress and DNA damage, promotes inflammation and cell death, and disrupts neurotransmitter systems critical for learning.

Toxic Metals: Mercury (especially methylmercury from fish) crosses the placenta and accumulates in the fetal brain, causing dose-dependent deficits in IQ, memory, attention, language, and visual-spatial skills. Arsenic exposure (from rice, drinking water) is linked to cognitive deficits, lower IQ, impaired memory, language problems, and increased behavioral issues. The first trimester is a particularly vulnerable window.

Homocysteine: Maternal homocysteine can increase due to insufficient folate and vitamin B12. High homocysteine during pregnancy is associated with neural tube defects, delayed brain maturation, and cognitive deficits.

Why the Developing Brain Is More Vulnerable: The developing brain is much more susceptible to low glutathione than an adult brain. Rapid growth generates more reactive oxygen species, yet protective enzymes are less active, and the blood-brain barrier is more permeable to chemicals and toxins. Myelin (the fatty coating protecting neurons) is still immature for at least the first three years of life, and fetal and newborn liver capacity for detoxification is severely limited.

The Link to Neuro-developmental Disorders

Across multiple cohorts, the most consistent signal links prenatal acetaminophen exposure with later attention and hyperactivity disorders.^77,79 Higher reported use and higher cordblood levels of acetaminophen-related metabolites have been associated with roughly two-to three-fold higher odds of attention, hyperactivity, or broader neurodevelopmental concerns in some studies.

Other observational work has reported links with sleep and behavioral problems in exposed toddlers and modest increases in intellectual disability risk, though these findings are less consistent.^77,79,81,82

The Dose-Response Pattern: Short-term use (less than one week) tends to show minimal to modest risk increases. In contrast, longer duration, more frequent use, and higher metabolite levels are more commonly associated with increased odds of neurodevelopmental symptoms. This pattern is consistent with the hypothesis that a toxic metabolite, such as NAPQI, interacting with low glutathione, is part of the mechanism.^77,79

This Is Exactly What You’d Expect If NAPQI Is the Driver: More acetaminophen—more NAPQI—more glutathione depletion—more oxidative damage—higher neurodevelopmental risk.

What Slows and Speeds Up Your Detox Enzymes

Even without apparent genetic variations, everyday choices in diet, lifestyle, medications, and exposures can alter how efficiently the body processes acetaminophen.

When key detox enzymes run slowly or are overwhelmed, more of the drug is pushed toward the toxic NAPQI pathway.

Glucuronidation (UGT1A6 Enzyme) Safe Pathway

Glucuronidation is one of the main “safe exit routes” for acetaminophen, helping your body attach a glucuronic acid molecule so it can be excreted in urine. When UGT1A6 runs well, less acetaminophen is left over to form NAPQI.

What Slows UGT1A6

Environmental Chemicals: Persistent organochlorine pollutants (PCBs, DDT, BPA, dioxins); certain pesticides and herbicides; fabric and hair dyes; and polyaromatic hydrocarbons from grilling, charring, barbecuing, and deep-frying.

Lifestyle Factors: Advancing age, chronic inflammation and infections (including gut-derived LPS), and chronic stress.

Foods: Synthetic food dyes; frequent high-temperature cooking (burnt toast, charred meats, deep-fried foods); and regular intake of cured or smoked meats.

Medications: NSAIDs (ibuprofen, naproxen), aspirin, acetaminophen itself with repeated use, some diabetes medications (for example, glimepiride), certain sleep and pain medications, antifungals (such as ketoconazole, itraconazole), calcium-channel blockers (verapamil), and some antiretroviral drugs.¹⁰⁹

Herbs (especially when combined with medications): Milk thistle, astragalus, St. John’s wort, saw palmetto, cranberry, and high-coumarin herbs like wormwood, mullein, sweet clover, dong quai, peppermint, and spearmint.

What Speeds Up UGT1A6

Foods: Cruciferous vegetables (broccoli, kale, cauliflower, Brussels sprouts), onions and garlic, quality organic coffee, and polyphenol-rich teas like green, rooibos, honeybush, and dandelion.

Cooking Methods: Braising, stewing, and slow-cooking instead of high-heat charring; marinating meats several hours before grilling to reduce PAH formation.

Supplements (with practitioner guidance): Calcium-D-glucarate, quercetin, curcumin, vitamins C and E, and glutathione or N-acetylcysteine (NAC). These support a healthier response to oxidative stress and help keep glucuronidation pathways available.

Sulfation (SULT Enzymes) Safe Pathway

Sulfation is another major path for clearing acetaminophen; it depends heavily on sulfur-containing amino acids and adequate mineral and vitamin status.

In fetuses and young children, sulfation does more of the work than glucuronidation, but it is easily saturated.

What Slows Sulfation

Dietary Deficiencies: Low sulfur amino acid intake (common with vegetarian/vegan diets that lack adequate protein), overall low protein, and low intake of eggs, poultry, fish, and cruciferous vegetables.

Nutrient Depletions: Low molybdenum, vitamin B6, and magnesium, all of which are needed for efficient sulfur metabolism.

Environmental Exposures: Frequent intake of sulfite-preserved foods (wines, dried fruits, many processed foods) and a high toxic metal burden, which drains sulfur reserves.

Medications: Certain pain relievers, multiple NSAIDs (nimesulide, meclofenamate, piroxicam, aspirin, ibuprofen), fertility and gynecologic drugs (such as clomiphene and danazol), cardiovascular medications (spironolactone), vertigo/anti-nausea drugs, and some antihistamines.¹⁰⁸

Herbs and Concentrated Botanicals: Quercetin and resveratrol (in high supplemental doses), green tea extracts, grape seed, St. John’s wort, milk thistle, ginkgo, gymnema, banaba, turmeric, citrus juices, and strong tea infusions, especially when layered on top of medications using the same pathways.¹¹⁰

Genetic Factors: Variants in SUOX (sulfite oxidase) and CBS can slow sulfur handling and make sulfation more fragile.

What Speeds Up Sulfation

Foods: High-sulfur foods (eggs, garlic, onions, leeks, shallots, cruciferous vegetables) and quality animal protein (grass-fed beef, pasture-raised poultry, wild-caught fish).

Supplements (with practitioner guidance): MSM, taurine, alpha-lipoic acid, molybdenum, vitamin B6, magnesium, and NAC, which help replenish sulfur pools and support glutathione production.

CYP2E1 Enzyme (The Toxic Pathway)

CYP2E1 is the enzyme that converts acetaminophen into NAPQI, the toxic metabolite at the center of this discussion. During pregnancy, CYP2E1 activity increases by about 80%, which means anything that further induces this enzyme can add to fetal and maternal risk. Thus, ideally, you want to slow down this enzyme during pregnancy.

What Speeds Up CYP2E1 (Increases NAPQI)

Lifestyle: Chronic alcohol use, fasting or aggressive calorie restriction, high-fat ketogenic diets, obesity, and insulin resistance or diabetes.

Medications: Certain tuberculosis drugs (like isoniazid) and some anticonvulsants.

Environmental Exposures: Solvents such as acetone (nail polish remover, some industrial products) and benzene (industrial fumes, gasoline).

What Slows CYP2E1 (Reduces NAPQI Formation)

Foods and Compounds: Watercress, garlic (diallyl sulfide), green tea (EGCG), turmeric (curcumin), quercetin-rich foods (onions, apples), ellagic acid–rich foods (pomegranate, berries), and omega-3–rich fish oils.

Lifestyle: Avoiding alcohol completely in pregnancy, maintaining stable blood sugar, ensuring adequate protein (not fasting through meals), and avoiding ketogenic diets during pregnancy.

A Strategic Approach for Pregnant Women

Putting this together, a practical strategy to lower acetaminophen risk during pregnancy includes:

1. Supporting Glucuronidation: Emphasize cruciferous vegetables, onions, garlic, and gentle cooking methods; consider coffee and polyphenol-rich teas if tolerated.

2. Supporting Sulfation: Ensure adequate protein and sulfur-rich foods (eggs, garlic, onions, brassicas) and correct key deficiencies (B6, magnesium, molybdenum) under guidance.

3. Slowing CYP2E1: Avoid alcohol and extreme diets, keep blood sugar stable, and include foods that naturally temper CYP2E1 activity.

4. Maximizing Glutathione: Prioritize protein, vitamins C and E, B vitamins, and, when appropriate, targeted support such as NAC or glutathione with a knowledgeable clinician.

Risk Factors for Tylenol Use During Pregnancy

Dietary Factors: Low intake of sulfur-rich protein (vegetarian or vegan diets without adequate protein, or diets low in eggs, poultry, fish, and cruciferous vegetables), protein-energy malnutrition, and deficiencies in vitamins C, E, selenium, and B vitamins all reduce the body’s ability to maintain and recycle glutathione.

Polycystic Ovary Syndrome (PCOS) (5–10% of women): Women with PCOS have 50% lower glutathione levels, significantly increased oxidative stress, and 3–4x higher risk of preeclampsia and 3x higher risk of gestational diabetes—both of which further deplete glutathione. With a 50% lower baseline glutathione level, the “safe” acetaminophen dose is effectively cut in half.^17,37,40

Other Metabolic Conditions: Blood sugar dysregulation, chronic infections, pre-existing liver conditions, obesity, and metabolic syndrome all impair glutathione synthesis and status.

Environmental Exposures: Regular exposure to chlorinated water, volatile organic compounds from new furnishings and building materials, pesticides, heavy metals, urban air pollution, and harsh cleaning products all increase oxidative load.

Lifestyle Factors: High-intensity exercise without adequate recovery, chronic stress, and insufficient sleep increase oxidative stress and deplete glutathione.

Genetic Factors: Variants in CBS, CYP2E1, MTHFR, GSTM1/GSTT1, and UGT enzymes affect detoxification capacity.

Pregnancy-Specific Risk Factors

Gallbladder Dysfunction (10% of pregnant women): Up to 10% develop gallstones or biliary sludge. Intrahepatic cholestasis of pregnancy (ICP) occurs in 0.4–10% of pregnancies (up to 5.6% in Latina women). Sluggish gallbladder function impairs liver clearance; case reports document severe liver injury and even fatal outcomes after therapeutic acetaminophen doses in pregnant women with cholestasis.^{53,58,60,106,107}

Choline Deficiency (89% of pregnant women): Only 11% of pregnant women meet the recommended choline intake. Choline is essential for liver function, methylation, and phospholipid synthesis; deficiency increases susceptibility to liver injury and reduces resilience to acetaminophen.^61,63

IVF-Related Oxidative Stress (2–5% of births): Women who conceive via IVF experience dramatic antioxidant depletion: 70% reduction in plasma antioxidant capacity (3.4-fold lower than natural conception), 83% reduction in follicular fluid antioxidant capacity (six-fold lower), 10–30% decrease in total antioxidant activity after ovarian stimulation, and 15–25% decrease in vitamins E, C, and carotenoids during the IVF cycle. With 70–83% reduced antioxidant capacity, even a single 500mg dose of acetaminophen represents a much greater burden.^18,19,41,46

The Postnatal Risk: Tylenol After Vaccination

If prenatal acetaminophen creates vulnerability during fetal brain development, post-vaccination acetaminophen in infancy may add an additional oxidative-stress burden to a system that is already working hard to adapt.

How Common Is Post-Vaccination Tylenol Use?

• 64% of infants receive acetaminophen within 48 hours after vaccination⁴⁷

• 11% receive it prophylactically (before vaccination⁴⁷

• Acetaminophen is used 2.6x more frequently than ibuprofen⁴⁷

• Oral analgesics are used in 81% of practices during injection, 89% post-injection⁴⁸

Why Newborns Are Uniquely Vulnerable: At birth, the newborn loses maternal metabolic protection and must handle acetaminophen using its own immature enzyme systems.^24,25,49,50 Glucuronidation is severely underdeveloped (the primary adult pathway barely functions), sulfation predominates but is easily saturated, glutathione reserves are limited (especially in preterm or sick infants), and NAPQI detoxification is impaired. When sulfation is saturated, more acetaminophen is forced through the oxidative pathway to NAPQI—precisely when glutathione reserves are least able to handle it.^49,52

The Compounding Effect

Before birth: Mother has compromised glutathione—takes acetaminophen—developing fetal brain exposed to NAPQI—fetus cannot effectively detoxify—impaired neurodevelopment and neuronal damage

After birth: Baby loses maternal protection—immature detoxification systems—receives acetaminophen at 2, 4, 6, and 12 months with vaccinations—each dose further depletes limited glutathione—cumulative burden may exceed healthy neurodevelopmental threshold—neuronal damage and regression from previously achieved milestones may occur

The Math That Connects Prenatal and Postnatal Exposure: More than 200,000 pregnancies per year involve acetaminophen use in women with compromised glutathione. Of those pregnancies, approximately 128,000 infants will receive acetaminophen within 48 hours of their first vaccination. Many receive it repeatedly—after vaccinations at 2, 4, 6, and 12–15 months. Each dose represents another hit on an already compromised system.

This is not about vaccines causing neurodevelopmental disorders; it is about a common medication practice that may represent one exposure too many for infants already vulnerable from prenatal exposures and maternal metabolic dysfunction.

The Bottom Line: Is Tylenol Safe for Use During Pregnancy?

The dramatic rise in neurodevelopmental disorder rates points to environmental factors playing a significant role. Acetaminophen use during pregnancy—and after birth in infancy—appears to be one environmental factor among many that can interact with underlying vulnerabilities.

Acetaminophen itself is not toxic. It becomes toxic when your body cannot properly process it through safe detoxification pathways and instead converts it into the toxic metabolite NAPQI.

The evidence suggests that acetaminophen does not cause neurodevelopmental disorders in women with robust detoxification systems. However, in individuals with compromised glutathione status, impaired detoxification pathways, poor methylation, genetic variants, or multiple environmental stressors, the body generates more NAPQI—the toxic metabolite that crosses the placenta, depletes fetal brain glutathione, and damages developing neurons.

For some women, occasional acetaminophen use in pregnancy may still be a reasonable choice; for others with lower glutathione reserves, the same dose may carry more risk than is widely appreciated.

A thoughtful conversation with your obstetric provider about your individual risk factors—PCOS, IVF, liver function, nutrient status, and environmental exposures—can help you weigh alternatives for pain and fever control. Likewise, asking your pediatrician about non-acetaminophen strategies for post-vaccine comfort, or about dosing and timing if acetaminophen is used, allows you to support your child’s developing brain while still following recommended care.

The message is not “never use Tylenol,” but “use it with a clear understanding of your own detoxification capacity and your baby’s unique vulnerability.”

_________________________________________

Through his educational platform at drbenlynch.com and his StrateGene system, he helps individuals understand and address key genetic vulnerabilities and continues to teach globally on nutrigenomics, methylation, and glutathione. He received his doctorate in naturopathic medicine from Bastyr University and lives in Seattle, Washington, with his wife and three sons. Visit https://www.seekinghealth.com/ to learn more.

REFERENCES

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