When Pain Relief Backfires: The Hidden Risks of Tylenol, NSAIDs, Steroids & Opioids
How Common Pain Medications Deplete Nutrients, Injure the Gut and Liver, Disrupt Hormones, and Undermine the Body’s Natural Healing Capacity
The Double-Edged Sword of Modern Pain Management
Pain and inflammation are not problems to eliminate—they are biological signals indicating that something in the body needs attention. Yet in modern medicine, treatment often focuses on quieting those signals quickly rather than understanding what is driving them.
Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, naproxen, and aspirin are commonly used as first-line pain relievers. As awareness grows around their potential risks—including gastrointestinal irritation, cardiovascular strain, and kidney stress—many people turn to what is often perceived as a “safer” alternative: acetaminophen (Tylenol).
Acetaminophen and corticosteroids are among the most widely used medications worldwide for pain, fever, and inflammation. While they can provide rapid symptom relief, their effects extend far beyond pain suppression.
Rather than supporting the body’s natural repair processes, these medications can strain detoxification pathways, suppress immune signaling, and deplete critical nutrients and antioxidants—including glutathione, selenium, zinc, magnesium, and vitamin C.
When these protective reserves decline, the body becomes less capable of neutralizing oxidative stress, repairing damaged tissues, regulating inflammation, and defending against toxins and infections. Over time, this can contribute to fatigue, persistent inflammation, delayed healing, and increased vulnerability to chronic illness.
→ Detoxification & Environmental Medicine
Conventional Pain Strategies: Why Relief Often Comes at a Cost
Conventional pain management is designed primarily to reduce symptoms quickly, not to identify or correct why pain is occurring. In acute or emergency situations, this approach can be appropriate and necessary. However, when used as a long-term strategy, it often fails to resolve underlying drivers of pain—and may introduce new problems over time.
Common Conventional Approaches
Over-the-counter medications: acetaminophen and NSAIDs to blunt pain and inflammation
Prescription medications: opioids, gabapentin, muscle relaxers, and corticosteroids
Injections: steroid injections and epidurals for localized pain relief
These tools work by suppressing pain signaling or inflammatory pathways, not by repairing damaged tissue, restoring biomechanics, or addressing metabolic, immune, or nervous system dysfunction.
Limitations of a Symptom-Suppression Model
While medications and injections may reduce pain temporarily, they often:
Do not correct structural imbalance or tissue degeneration
Fail to resolve inflammatory or immune-driven pain
Overlook metabolic contributors such as blood sugar instability or nutrient depletion
Ignore nervous system sensitization that perpetuates chronic pain
As a result, pain frequently returns—sometimes requiring higher doses, repeated injections, or additional medications to maintain relief.
The Chronic Pain Cycle
For many patients, this leads to a familiar pattern:
short-term relief → symptom return → escalating intervention → increasing side effects
Over time, this cycle can contribute to nutrient depletion, impaired detoxification, hormonal disruption, immune suppression, and delayed tissue repair, making pain harder—not easier—to resolve.
When Conventional Care Falls Short
If pain persists despite medications, injections, or physical therapy, it is often a sign that:
Inflammation is being driven by systemic factors
Tissue damage is not healing adequately
The nervous system remains stuck in a pain-sensitive state
Foundational supports like nutrition, sleep, and recovery are insufficient
At this point, continuing to suppress symptoms without addressing root causes can prolong suffering rather than resolve it.
A Root-Cause, Integrative Model of Pain Relief
Where conventional pain strategies focus on suppressing symptoms, a root-cause, integrative approach asks a different question: why is pain occurring in the first place?
Rather than overriding pain signals, this model works to identify and address the drivers beneath them—such as chronic inflammation, tissue injury, biomechanical imbalance, nutrient depletion, metabolic dysfunction, gut-immune disruption, or nervous system sensitization.
An integrative pain strategy typically layers multiple supportive inputs, including:
Therapies that restore nervous system regulation and reduce pain sensitivity
Approaches that support tissue repair, circulation, and cellular energy
Nutritional and metabolic support to lower inflammatory load
Movement and biomechanical correction to prevent reinjury
Lifestyle strategies that improve sleep, stress resilience, and recovery
Instead of cycling through medications and injections, this approach aims to repair what is broken, rebalance what is stressed, and restore the body’s capacity to heal—often leading to more durable pain relief and fewer downstream complications.
Why Common Pain Medications Can Undermine Long-Term Healing
Instead of cycling endlessly through medications and injections, a root-cause approach focuses on repairing what is damaged, rebalancing what is stressed, and restoring the body’s innate capacity to heal—often leading to more durable pain relief and fewer downstream complications.
Understanding this distinction helps explain why many commonly used pain medications—particularly corticosteroids—can provide short-term symptom relief while quietly worsening long-term metabolic, immune, and tissue health.
Corticosteroids (e.g., Prednisone, Dexamethasone, Hydrocortisone)
Corticosteroids are powerful anti-inflammatory medications that act by mimicking cortisol, the body’s primary stress hormone. While they can be lifesaving in acute or emergency settings, repeated or long-term use has profound metabolic, immunologic, and musculoskeletal consequences.'
Key Nutrients Depleted
Corticosteroids are associated with depletion of multiple nutrients essential for tissue repair, immune defense, and metabolic stability, including:
Calcium, vitamin D, magnesium, potassium, zinc, selenium, vitamin C, and protein (1)
Mechanisms of Depletion
Calcium & vitamin D: Reduced intestinal absorption and increased urinary loss → osteopenia and fracture risk
Zinc, selenium & vitamin C: Impaired immune function, delayed wound healing, increased infection risk
Protein: Accelerated protein breakdown → muscle wasting and connective tissue weakness
Magnesium & potassium: Electrolyte imbalance → fatigue, weakness, and cardiac rhythm disturbances
Why This Matters
By chronically elevating cortisol signaling, corticosteroids shift the body into a catabolic, stress-dominant state. Over time, this disrupts blood sugar regulation, suppresses immune surveillance, impairs collagen synthesis, and weakens bone, muscle, and connective tissue integrity.
Documented Health Impacts
Bone loss and fractures due to calcium and vitamin D depletion and impaired osteoblast activity (2)
Blood sugar dysregulation and steroid-induced diabetes through increased insulin resistance and gluconeogenesis (3)
Muscle wasting and impaired connective tissue repair from protein catabolism and suppressed synthesis (4)
Weakened immunity, delayed healing, and prolonged infections related to micronutrient depletion and immune suppression (5)
Weight gain, mood changes, and insomnia driven by hormonal and circadian disruption (6,7)
Abnormal blood lipids, hypertension, and increased cardiovascular risk, including heart attack, with long-term use (8)
Thinning skin and easy bruising from collagen breakdown and connective tissue loss (9)
Psychiatric effects, including anxiety, irritability, depression, and—in severe cases—steroid-induced psychosis, particularly at higher doses or with prolonged exposure (10)
⚠️ Even short-term corticosteroid use can cause side effects in susceptible individuals. Long-term or repeated use requires careful monitoring and a proactive strategy to mitigate downstream damage.
→ Metabolic Health & Weight Loss
Supportive Strategies During or After Steroid Use
Herbal & Nutritional Support
Milk thistle (Silybum marianum): Supports liver cell protection and regeneration during medication stress
N-acetylcysteine (NAC): Replenishes glutathione and reduces oxidative burden
Vitamin C & zinc: Essential for collagen synthesis, immune recovery, and wound healing
Vitamin D + K2: Support bone density, calcium balance, and immune regulation
Adaptogens (e.g., ashwagandha, rhodiola): Help buffer adrenal stress and support circadian rhythm balance
Nutritional & Lifestyle Foundations
Emphasize adequate protein intake (collagen, eggs, wild-caught fish) to counter muscle and connective tissue loss
Include antioxidant-rich foods such as citrus, berries, cruciferous vegetables, and green tea
Support vitamin D status through sunlight exposure and appropriate D3 + K2 supplementation
Incorporate weight-bearing exercise and supportive modalities (e.g., red-light therapy) to preserve bone and muscle
Functional Medicine Considerations
Assess and monitor: vitamin D, magnesium, zinc, selenium, fasting glucose, and bone density
Support detoxification: use strategies such as sulforaphane and NAC to assist liver and mitochondrial function
Taper thoughtfully: when appropriate, work with a qualified clinician to gradually reduce steroid use while restoring adrenal balance and nutrient status
While corticosteroids exert their effects by overriding the body’s stress and immune signaling, other commonly used pain relievers disrupt healing through different mechanisms. One of the most widely trusted alternatives—acetaminophen (Tylenol)—is often perceived as gentler, yet it places a distinct and significant burden on the liver’s detoxification and antioxidant systems.
2. Acetaminophen (Tylenol / Paracetamol)
Acetaminophen is widely used for pain and fever and is often perceived as a safer alternative to NSAIDs. However, its metabolism places a significant burden on the liver’s detoxification and antioxidant systems, particularly through depletion of glutathione.
Key Nutrient Depleted
Glutathione — the body’s primary antioxidant and detoxification molecule
Why This Matters
Acetaminophen is metabolized in the liver through pathways that consume glutathione, a compound essential for neutralizing oxidative stress, detoxifying hormones and chemicals, and protecting cells from damage.
When glutathione levels fall:
Liver cells become more vulnerable to injury
Oxidative stress increases
Detoxification of toxins and hormones becomes impaired
Importantly, the margin between a “therapeutic” dose and a toxic dose is narrow. In adults, taking approximately 4 grams in a 24-hour period—about six extra-strength 650 mg tablets—can damage the liver. Acetaminophen overdose accounts for nearly half of all acute liver failure cases in the United States, according to a 2023 analysis (11).
Documented Health Impacts
Liver toxicity and increased risk of liver disease, particularly when combined with alcohol use
Fatigue, brain fog, and chemical sensitivity related to impaired detox capacity
Increased oxidative stress contributing to systemic inflammation and tissue damage
Reduced ability to handle environmental toxins and heavy metals
Beyond the Liver: Systemic Risks Linked to Acetaminophen
Emerging research shows that acetaminophen’s effects extend beyond hepatic stress:
Kidney toxicity: A subset of overdoses results in acute kidney injury (12)
Gastrointestinal irritation: Despite being marketed as “stomach-friendly,” reviews report GI reactions comparable to—or worse than—NSAIDs in some cases (13)
Cardiovascular concerns: Associations with hypertension, cardiovascular events, and heart failure have been reported with frequent or long-term use (14)
Hematologic cancer associations: Observational studies link repeated use with increased risk of certain blood cancers (15)
Immune and respiratory effects: Higher rates of allergies and asthma, particularly in children, have been observed with ongoing use (16)
What Many People Don’t Realize About Tylenol
During acetaminophen metabolism, a highly reactive byproduct—NAPQI (N-acetyl-p-benzoquinone imine)—is produced. NAPQI damages liver cells by binding to proteins and disrupting cellular function.
Under normal conditions, NAPQI is rapidly neutralized by glutathione. When intake is frequent, doses accumulate, or detox capacity is impaired, glutathione becomes depleted—allowing NAPQI to build up and trigger liver cell injury and death (17).
In the U.S., this results in approximately (18):
~56,000 emergency room visits annually
~2,600 hospitalizations
~500 deaths from liver failure each year
Many people assume they are using acetaminophen safely without realizing how narrow the dosing window truly is.
Pregnancy & Childhood Outcomes: A Growing Warning Signal
Acetaminophen has long been recommended as the preferred pain reliever during pregnancy. However, accumulating evidence has prompted renewed scrutiny.
Systematic reviews and meta-analyses suggest that frequent or prolonged prenatal exposure may be associated with (19–25):
Higher rates of hyperactivity and attention-related disorders
Increased likelihood of ADHD medication use
Elevated risk of autism-related neurobehavioral patterns
Increased childhood asthma risk, particularly with late-pregnancy exposure
A large systematic review of 46 studies found that neurodevelopmental risks appeared dose-dependent and were more pronounced in higher-quality studies (26).
As a result, many researchers and clinicians now advocate for more cautious, limited use during pregnancy.
What This Means for You
Acetaminophen may be appropriate in specific, short-term situations—but it is not metabolically neutral. With frequent use, or in the context of alcohol intake, chronic illness, pregnancy, or nutrient depletion, its impact on liver health, oxidative stress, detoxification capacity, and immune development becomes far more significant.
When acetaminophen use is unavoidable, proactive support of glutathione and detox pathways is essential.
→ Detoxification & Environmental Medicine
Supportive Strategies During or After Acetaminophen Use
Herbal & Nutritional Support
N-acetylcysteine (NAC): Direct glutathione precursor; primary antidote for acetaminophen toxicity
Alpha-lipoic acid (ALA): Regenerates antioxidants and supports liver mitochondrial function
Milk thistle: Protects hepatocytes and supports liver detox enzymes
Sulforaphane: Activates Nrf2, increasing glutathione synthesis and detox capacity
Vitamin C + selenium: Replenish antioxidant reserves depleted by acetaminophen use
Nutritional & Lifestyle Foundations
Support liver function with bitter greens (dandelion, arugula), beets, and lemon water
Include sulfur-rich foods (garlic, onions, eggs) to support glutathione production
Maintain hydration and avoid alcohol, which compounds liver toxicity
Use supportive detox modalities such as infrared sauna when appropriate
Functional Medicine Considerations
Assess ALT, AST, GGT, glutathione status, and oxidative stress markers (e.g., 8-OHdG)
Evaluate detox capacity, including relevant genetic SNPs (GST, MTHFR, COMT)
Support phase I/II detox pathways with NAC, glycine, and cruciferous extracts
Explore drug-free pain and fever strategies such as acupuncture, red-light therapy, PEMF, peptide therapy, magnesium, and hydrogen-rich water
3. NSAIDs (Ibuprofen, Naproxen, Aspirin)
NSAIDs are among the most commonly used medications for pain and inflammation. They work by blocking cyclooxygenase (COX) enzymes, which reduces prostaglandin production and dampens pain signaling. While this can provide short-term relief, prostaglandins play essential roles far beyond pain (27).
Why NSAIDs Backfire Long Term
Prostaglandins are also responsible for:
Protecting the stomach and intestinal lining (27,31)
Supporting kidney blood flow and electrolyte balance (30)
Regulating vascular tone and cardiovascular function (30)
Facilitating tissue repair, particularly in tendons and ligaments (32)
When these pathways are chronically suppressed, pain relief may come at the cost of impaired healing and increased systemic inflammation.
Key Downstream Effects
Regular or long-term NSAID use has been associated with:
Damage to the gut lining, increasing intestinal permeability (“leaky gut”) and immune activation (27,29,31)
Reduced absorption of key nutrients, including iron, folate, and vitamin C (28,29)
Delayed tissue repair, especially in connective tissue where prostaglandins are required for healing (32)
Kidney stress and electrolyte imbalance, particularly with dehydration or endurance activity (30)
Increased cardiovascular risk, especially with higher doses or prolonged use (30)
These effects help explain why NSAIDs may temporarily reduce pain while contributing to persistent inflammation, fatigue, recurrent injuries, and poor recovery over time.
Why This Matters for Chronic Pain
When gut integrity is compromised and nutrient absorption declines, inflammation becomes harder to regulate. Pain may return more quickly, require higher doses, or shift locations—driving a cycle of escalating medication use without resolution (27,31).
For a deeper look at how NSAIDs and other medications disrupt digestion, nutrient status, and detox pathways::
→ Your Gut, Hormones & Medications: How Common Drugs Disrupt Digestion and Detox Pathways
While NSAIDs undermine healing by damaging the gut lining and impairing tissue repair, opioids affect pain through a completely different pathway—by suppressing pain perception within the central nervous system rather than addressing inflammation or injury.
4. Opioids (e.g., Hydrocodone, Oxycodone, Morphine)
Opioids reduce pain by binding to opioid receptors in the brain and spinal cord, dampening the transmission of pain signals. This can be appropriate for short-term severe pain or end-of-life care. However, opioids do not reduce inflammation, repair tissue, or restore function—and with ongoing use, they often worsen pain physiology (35).
Why Opioids Backfire Over Time
With repeated exposure, the nervous system adapts to opioids, leading to:
Tolerance, requiring higher doses for the same effect (33,35)
Dependence, with withdrawal symptoms when doses wear off (35)
Opioid-induced hyperalgesia, a paradoxical increase in pain sensitivity (33,36)
Rather than calming pain long term, opioids can sensitize the nervous system, making everyday stimuli feel more painful (33,36).
Key Downstream Effects
Chronic or recurrent opioid use has been associated with:
Central nervous system suppression, affecting alertness, coordination, and mood (35,36)
Disrupted gut motility and microbiome balance, contributing to constipation, dysbiosis, and inflammation (38)
Hormonal suppression, including reduced testosterone and altered HPA-axis signaling, which can worsen fatigue, depression, and pain perception (34)
Impaired immune function, increasing susceptibility to infection (37)
Reduced motivation and physical activity, slowing rehabilitation and tissue recovery (35)
Why This Matters for Chronic Pain
Because opioids silence pain signals without correcting underlying drivers, pain often returns when doses decrease—sometimes more intensely. Over time, this can create a cycle of escalating doses, worsening sensitivity, and declining function without meaningful healing (33,35,36).
When pain medications repeatedly fail—whether through immune suppression, detox depletion, gut injury, or nervous system sensitization—it becomes clear that lasting relief requires a fundamentally different strategy.
Why Pain Persists Despite Medication
When pain becomes chronic, the issue is rarely a lack of stronger medication. More often, it’s that the biological systems required for healing have been progressively undermined.
Across corticosteroids, acetaminophen, NSAIDs, and opioids, a consistent pattern emerges:
Inflammation is suppressed, but tissue repair is impaired
Pain signals are blocked, but nervous system sensitivity increases
Symptoms are quieted, but root causes remain unaddressed
Over time, this creates a widening gap between symptom relief and true recovery.
The Common Thread Behind Medication Failure
Although each drug class acts differently, many share downstream effects that perpetuate pain:
Nutrient depletion that weakens connective tissue, nerves, and immune resilience
Gut and liver dysfunction that increases systemic inflammation and toxin load
Hormonal disruption that impairs sleep, metabolism, and tissue repair
Nervous system sensitization, where the brain becomes more reactive to pain signals
When these systems are compromised, the body may temporarily feel better—but it becomes less capable of healing.
Why Escalation Rarely Solves the Problem
As healing capacity declines, pain often returns faster or spreads. This can lead to:
Higher doses or additional medications
Repeated injections without lasting benefit
Increased side effects with diminishing returns
At this point, pain is no longer just a symptom—it is a reflection of underlying system imbalance.
A Different Question Changes the Outcome
Instead of asking, “What will quiet this pain?” a more effective question is:
“What does this pain need in order to resolve?”
Answering that requires shifting focus toward:
Restoring metabolic and detox capacity
Rebuilding nutrient reserves
Repairing gut and connective tissue integrity
Regulating the nervous system
Supporting movement and circulation
This is where a root-cause, integrative approach becomes essential.
Understanding why medications fall short opens the door to strategies that support repair rather than suppress symptoms—approaches designed to calm inflammation, restore resilience, and help the body heal naturally.
The Nervous System’s Role in Chronic Pain
Chronic pain is not solely a tissue problem—it is also a nervous system problem. When pain persists, the brain and spinal cord can become sensitized, amplifying signals even after the original injury has healed.
This process, often referred to as central sensitization, occurs when the nervous system remains stuck in a heightened threat or stress response. Instead of accurately interpreting sensory input, the brain begins to overreact—turning normal movement, pressure, or inflammation into persistent pain.
How Medications Can Worsen Pain Sensitivity
Several commonly used pain medications influence nervous system signaling in ways that may unintentionally reinforce pain over time:
Opioids can increase pain sensitivity through opioid-induced hyperalgesia
Corticosteroids alter stress-hormone signaling and sleep architecture
NSAIDs may impair tissue repair, prolonging nociceptive input
Acetaminophen reduces antioxidant capacity needed for neuronal resilience
When combined with chronic stress, poor sleep, nutrient depletion, or unresolved inflammation, the nervous system may lose its ability to “turn pain off.”
When Pain Becomes a Learned Response
Over time, pain can become conditioned—linked not only to injury, but also to:
Movement patterns
Emotional stress
Previous flare experiences
Sleep disruption
At this stage, treating pain as a purely structural or inflammatory issue often fails. Even aggressive interventions may offer only temporary relief because the pain-processing circuits themselves remain dysregulated.
Why This Matters
If the nervous system is not addressed, pain may:
Spread beyond the original injury site
Return quickly after medications wear off
Worsen during stress or fatigue
Become resistant to escalating interventions
This helps explain why chronic pain frequently persists despite “normal” imaging, labs, or repeated treatments.
When pain-processing circuits remain dysregulated, restoring nervous system balance becomes a foundational step in breaking the chronic pain cycle.
→ Bioenergetic & Nervous System Therapies
Once pain becomes neurologically reinforced, healing depends on restoring the body’s biological capacity to recover—including nutrient availability, detoxification, sleep quality, and metabolic stability.
Nutrient Depletion and Impaired Tissue Repair
Healing from pain requires raw materials. Muscles, tendons, ligaments, nerves, and connective tissue all depend on adequate nutrients to repair microdamage, regulate inflammation, and maintain structural integrity.
When pain medications are used repeatedly, many of those foundational nutrients are quietly depleted—often without obvious early symptoms.
How Medications Undermine Repair Capacity
Across multiple drug classes, common patterns emerge:
Corticosteroids accelerate protein breakdown and deplete calcium, vitamin D, magnesium, zinc, and vitamin C—nutrients required for bone strength, collagen synthesis, and immune repair
Acetaminophen consumes glutathione, increasing oxidative stress and impairing cellular recovery
NSAIDs interfere with iron, folate, and vitamin C absorption while disrupting prostaglandin-driven tissue healing
Opioids suppress endocrine and immune signaling that supports regeneration
Individually, these effects may seem modest. Over time, however, they create a state in which the body is asked to heal without the necessary building blocks to do so.
Why Pain Lingers or Recurs
When nutrient reserves are low:
Collagen and connective tissue repair slows
Micro-injuries accumulate faster than they can be resolved
Inflammation becomes harder to regulate
Muscles fatigue more easily and recover more slowly
Nerve tissue becomes more vulnerable to irritation
This helps explain why some people experience:
Recurrent strains or tendon injuries
Persistent joint pain despite “normal” imaging
Slow recovery from physical therapy or exercise
Pain flares during stress, illness, or poor sleep
In these cases, pain is not simply a signal to suppress—it reflects insufficient repair capacity.
The Compounding Effect of Detox Burden
Nutrient depletion often coincides with increased detox demand. The liver and mitochondria require adequate antioxidants, minerals, and amino acids to neutralize oxidative byproducts from medications, inflammation, and environmental exposures.
When detox capacity is overwhelmed, oxidative stress rises—further impairing tissue repair and amplifying pain sensitivity.
When nutrient reserves are depleted and repair pathways are strained, factors like sleep quality, metabolic health, and stress physiology become even more influential in determining whether pain resolves—or becomes chronic.
→ Detoxification & Environmental Medicine
Sleep, Stress, and Metabolic Dysfunction in Chronic Pain
Pain does not exist independently of sleep, stress, or metabolism. These systems are tightly interconnected, and when they are disrupted, the body’s capacity to resolve pain is significantly reduced.
Sleep is a primary window for healing. During deep sleep, the body repairs tissue, regulates inflammation, recalibrates pain processing, and releases growth hormone. Chronic pain—and several pain medications—disrupt normal sleep architecture, limiting the body’s ability to recover. When sleep becomes shallow or fragmented, pain sensitivity increases and inflammation becomes harder to control.
→ Why Poor Sleep Is More Dangerous Than You Think — And How to Fix It
Chronic stress keeps the body in a prolonged threat response. Ongoing pain is interpreted as stress, dysregulating the hypothalamic–pituitary–adrenal (HPA) axis. Over time, this leads to altered cortisol signaling, increased muscle tension, impaired circulation, and reduced immune and repair capacity. In this state, resources are diverted away from healing and toward short-term survival.
Metabolic instability further amplifies pain. Blood sugar fluctuations and insulin resistance increase inflammatory signaling, oxidative stress, and mitochondrial strain—factors that worsen pain sensitivity and slow tissue repair. Even subtle metabolic dysfunction can make pain more persistent and resistant to treatment.
When sleep, stress physiology, and metabolism are misaligned, pain is less likely to resolve—regardless of the intervention used.
→ Metabolic Health & Weight Loss
Why Pain Relief Often Backfires — and What That Tells Us
Across medications, a consistent pattern emerges: pain is quieted, but the systems required for healing are progressively weakened.
Whether through immune suppression, detox depletion, gut injury, nervous system sensitization, or metabolic strain, symptom-focused pain relief often leaves the body less capable of resolving the underlying problem.
This is why pain so often returns—sometimes stronger, more widespread, or more resistant to treatment.
At that point, the question is no longer “What can suppress this pain?”
It becomes “What does my body need in order to heal?”
That shift is where durable recovery begins.
Next Steps
If pain or inflammation is being managed with medications that quietly strain the liver, immune system, and nutrient reserves, a root-cause approach can help identify what is driving the problem—and support restoration of the systems those medications deplete.
Rather than simply rotating medications or escalating doses, addressing inflammation, detox capacity, metabolic stress, and tissue repair often leads to more durable relief and better long-term outcomes.
→ Detoxification & Environmental Medicine
Request a free 15-min consultation with Dr. Martina Sturm at Denver Sports & Holistic Medicine to explore a personalized plan for restoring balance, resilience, and natural healing capacity from the inside out.
Frequently Asked Questions About Pain Relief
Are corticosteroids ever necessary?
Yes. In acute, severe situations—such as asthma flares, autoimmune crises, anaphylaxis, or other life-threatening inflammatory conditions—corticosteroids can be lifesaving. The concern is not appropriate short-term use, but chronic or repeated reliance without addressing root causes or monitoring nutrient depletion and downstream effects.
How quickly can steroids cause nutrient depletion?
Some effects, such as blood sugar elevation or reductions in vitamin C and zinc, can occur within days. Bone loss, adrenal suppression, connective tissue breakdown, and immune shifts typically develop with longer-term or repeated exposure.
Can Tylenol be used safely?
Occasional, low-dose use is generally well tolerated in individuals with good liver function and adequate antioxidant reserves. Risk increases significantly with frequent use, alcohol consumption, preexisting liver or gallbladder issues, nutrient deficiencies, or pregnancy.
Is ibuprofen safer than Tylenol?
Ibuprofen does not deplete glutathione the way acetaminophen does, but it carries its own risks, including gut lining damage, kidney stress, and cardiovascular strain. “Safer” depends on the individual, dose, duration, and overall health status. No pain medication is metabolically neutral.
Can antioxidant supplements help reverse damage from past steroid or Tylenol use?
In many cases, yes. Nutrients such as NAC, selenium, sulforaphane, vitamin C, vitamin D3 with K2, and zinc can help rebuild detox pathways, antioxidant capacity, and immune resilience. The most effective approach is personalized and guided by functional testing.
What are the best natural alternatives for pain relief?
Many patients experience meaningful relief from approaches that support healing rather than suppress symptoms, including acupuncture, red-light therapy, PEMF, targeted herbal formulas such as boswellia and curcumin, peptide therapy, magnesium, and omega-3 fatty acids.
How do I know if I’ve depleted glutathione or other key nutrients?
Possible signs include persistent fatigue or low stamina, poor stress tolerance, slow recovery after illness, brain fog, chemical sensitivity, recurring inflammation, or easy bruising and thinning skin. Functional testing can confirm deficiencies and guide targeted repair.
Why does pain sometimes get worse after stopping pain medications?
In some cases, pain may temporarily worsen when medications are reduced or stopped because the underlying systems they were suppressing—such as inflammation, nervous system sensitivity, or metabolic stress—have not yet been repaired. This does not mean the medication was healing the problem; it often reflects a period of adjustment while the body recalibrates and repair pathways are restored.
Can imaging or lab tests be normal even when pain is real?
Yes. Chronic pain often involves nervous system sensitization, metabolic strain, nutrient depletion, or low-grade inflammation that does not always appear on standard imaging or routine labs. Normal results do not invalidate pain—they simply indicate that the driver may be functional rather than structural.
When should someone consider a root-cause approach to pain?
A root-cause approach is especially appropriate when pain persists despite medications, injections, or physical therapy; when pain keeps returning after temporary relief; or when treatment side effects begin to outweigh benefits. These patterns suggest that healing systems—not pain suppression—need to be addressed.
Resources
Nutrients – Evidence of Drug–Nutrient Interactions with Chronic Use of Commonly Prescribed Medications: An Update
Osteoporosis International – Calcium and Vitamin D for Corticosteroid-Induced Osteoporosis
Endocrine Practice – Glucocorticoid-Induced Hyperglycemia: A Neglected Problem
PubMed – Glucocorticoids and Skeletal Muscle
Nutrients – Nutritional Risk of Vitamin D, Vitamin C, Zinc, and Selenium Deficiency on Risk and Clinical Outcomes of COVID-19: A Narrative Review
Cell Reports – Flattening of Circadian Glucocorticoid Oscillations Drives Acute Hyperinsulinemia and Adipocyte Hypertrophy
Endocrine Reviews – Functional and Clinical Significance of the 24-Hour Rhythm of Circulating Glucocorticoids
PubMed – Adverse Effects of Corticosteroids on the Cardiovascular System
Dermatology and Therapy – Glucocorticoid-Induced Skin Atrophy: The Old and the New
Mayo Clinic Proceedings – Psychiatric Adverse Effects of Corticosteroids
StatPearls – NCBI Bookshelf – Acetaminophen Toxicity
Toxins – Acetaminophen-Induced Nephrotoxicity: Pathophysiology, Clinical Manifestations, and Management
Arthritis Care & Research – Incidence of Side Effects Associated With Acetaminophen in People Aged 65 Years or More: A Prospective Cohort Study
Circulation – Regular Acetaminophen Use and Blood Pressure in People With Hypertension: The PATH-BP Trial
Cancer Epidemiology, Biomarkers & Prevention – Long-Term Use of Acetaminophen, Aspirin, and Other Nonsteroidal Anti-Inflammatory Drugs and Risk of Hematologic Malignancies: Results From the VITAL Study
Clinical & Experimental Allergy – Prenatal Exposure to Acetaminophen and Asthma in Children
Archives of Toxicology – Mechanisms of Acetaminophen-Induced Liver Injury and Its Implications for Therapeutic Interventions
PubMed – Acetaminophen and the U.S. Acute Liver Failure Study Group: Lowering the Risks of Hepatic Failure
Food and Drug Administration – FDA Responds to Evidence of Possible Association Between Autism and Acetaminophen Use During Pregnancy
PubMed – Acetaminophen in Pregnancy and Attention-Deficit and Hyperactivity Disorder and Autism Spectrum Disorder
Environmental Health Perspectives – Prenatal Acetaminophen Exposure and Its Associated Risk for Attention Deficit Hyperactivity Disorder
Nature Reviews Endocrinology – Paracetamol Use During Pregnancy — A Call for Precautionary Action
JAMA Pediatrics – Association of Cord Plasma Biomarkers of In Utero Acetaminophen Exposure With Risk of Attention-Deficit/Hyperactivity Disorder and Autism Spectrum Disorder in Childhood
Environmental Health Perspectives – Evaluation of the Evidence on Acetaminophen Use and Neurodevelopmental Disorders Using the Navigation Guide Methodology
New England Journal of Medicine – Nonsteroidal Anti-Inflammatory Drugs and the Gastrointestinal Tract
Gastroenterology – NSAID-Induced Damage to the Gastrointestinal Tract: Clinical Implications
Alimentary Pharmacology & Therapeutics – Small Intestinal Injury Caused by Non-Steroidal Anti-Inflammatory Drugs
American Journal of Medicine – Cardiovascular Risks of Nonsteroidal Anti-Inflammatory Drugs
Clinical Gastroenterology and Hepatology – NSAIDs and Increased Intestinal Permeability
Journal of Applied Physiology – Prostaglandins and the Regulation of Skeletal Muscle and Tendon Healing
Pain – Opioid-Induced Hyperalgesia: A Qualitative Systematic Review
The Journal of Clinical Endocrinology & Metabolism – Opioid-Induced Androgen Deficiency in Men
The Lancet – Long-Term Opioid Therapy for Chronic Non-Cancer Pain
Nature Reviews Neuroscience – Mechanisms of Central Sensitization in Chronic Pain
Journal of Neuroimmune Pharmacology – Opioids and Immune System Suppression
Gut – Opioid Effects on Gastrointestinal Motility and Microbiome Function