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The CBG pain research that’s too compelling to ignore—and too early to promise.
The Broken Leg Study
In 2023, researchers at Penn State College of Medicine broke the legs of laboratory mice.
Specifically, they fractured their tibias—the shin bone.
Then they gave some mice ibuprofen. Others got CBG, a non-psychoactive cannabinoid from cannabis. And they waited to see what would happen.
The pain relief results?
CBG matched ibuprofen perfectly. Both groups showed the same reduction in pain sensitivity—to pressure, to cold, to heat. Equal analgesic effect.
But then something unexpected happened.
When the researchers examined the healed bones weeks later, they found a stark difference:
The ibuprofen group’s bones healed slower and weaker.
The CBG group’s bones healed faster and stronger—with higher bone density, better mineralization, and greater mechanical strength.
CBG didn’t just match ibuprofen for pain relief.
It beat it.
Here’s the problem:
Those were mice, not humans.
And every single impressive study on CBG for pain—and there are several now—has been conducted in rodents. Not a single human clinical trial exists yet for CBG and pain.
So we’re left with a question: Is CBG actually better than ibuprofen for pain and healing? Or are we getting excited about mouse data that won’t translate?
This article will show you:
- What the animal research actually found (it’s remarkable)
- Why the mechanisms make biological sense
- The honest limitations we can’t ignore
- What real CBG users are reporting
- Whether you should consider being an early adopter
Let’s start with that broken leg study, because it’s the foundation of everything else.
Pain Relief Without the Trade-Off
Study Details:
Published in the Journal of Bone and Mineral Research in 2023—a high-impact, peer-reviewed journal—this controlled experiment came from Penn State College of Medicine.
Mice with fractured tibias were divided into groups: some received CBG, some received NSAID pain medication (similar to ibuprofen), and some received no treatment as controls.
The researchers then measured two things: pain levels during healing, and the quality of the healed bone afterward.
Pain Relief Results – CBG Matched NSAIDs:
The researchers measured pain sensitivity using three different tests:
Mechanical sensitivity: How much pressure could the mice tolerate on their broken leg?
Cold sensitivity: How did they react to cold stimulation?
Heat sensitivity: How quickly did they pull away from heat?
Normally, a fractured bone makes you hypersensitive to all three. The area becomes painful to touch, painful in cold weather, painful with any temperature change.
CBG normalized all three pain responses—just as effectively as NSAIDs.
The mice treated with CBG showed pain sensitivity levels comparable to mice with no injury at all.
Same as the ibuprofen-like NSAID group.
In pain relief terms: tie game.
Healing Results – CBG Won Decisively:
But when the researchers examined the healed bones using micro-CT scans and mechanical testing, they found dramatic differences.
CBG-treated mice had:
- Higher bone mineral density (stronger, denser bone)
- Faster callus mineralization (the “new bone” that forms over a fracture hardened quicker)
- Increased recruitment of periosteal progenitor cells (the stem-like cells that build new bone)
- Greater mechanical strength in the healed bone (could withstand more force before breaking again)
- Better overall structural integrity
NSAID-treated mice had:
- Slower healing
- Lower bone density
- Impaired bone formation
- Weaker final structure
Think about that for a second.
Both groups got equal pain relief. But one group healed properly. The other group’s healing was compromised.
Why NSAIDs Impair Healing (And CBG Doesn’t):
NSAIDs work by blocking inflammation—specifically by inhibiting COX enzymes that produce inflammatory prostaglandins.
The problem?
You need some inflammation to heal.
The inflammatory phase of bone healing recruits immune cells and growth factors that trigger tissue repair. Block it completely, and you slow down the whole process.
NSAIDs are so effective at blocking inflammation that they actually impair fracture healing, delay surgical recovery, and can interfere with tissue repair throughout the body.
Orthopedic surgeons know this. They often tell patients to avoid NSAIDs during the first few weeks of bone healing—right when pain is worst.
CBG, on the other hand, modulates inflammation differently.
Instead of completely blocking the inflammatory cascade, CBG appears to dampen excessive inflammation while allowing the necessary inflammatory signals for healing to proceed.
It takes the edge off pain without derailing the repair process.
And somehow—through mechanisms the researchers are still investigating—it actually accelerates healing beyond normal rates.
The Clinical Implications (If This Translates to Humans):
Think about what this could mean:
Fracture patients could manage pain without compromising bone healing. No more choosing between pain relief and optimal recovery.
Post-surgical pain could be treated without slowing recovery. Patients could take something for pain without sabotaging the healing their surgery was meant to achieve.
Sports injuries—tendon strains, ligament damage, muscle tears—might heal faster while pain is controlled. Athletes could return to play sooner.
Chronic joint conditions might get both symptom relief and disease modification. Not just masking pain, but actually improving the underlying tissue health.
Currently, doctors face a dilemma: Give NSAIDs for pain, knowing they slow healing. Or withhold effective pain relief to optimize healing.
Patients suffer either way.
CBG might eliminate that trade-off.
The Massive Caveat:
This was in mice.
Mice with tiny fractured tibias, not humans with complex injuries.
The dose used was high—scaled to human weight, it would be hundreds of milligrams.
And bone healing in rodents doesn’t perfectly mirror bone healing in humans. We have different healing timelines, different bone structures, different metabolic responses.
Mouse bones heal in weeks. Human bones take months.
Will these results translate? We genuinely don’t know.
But the study was rigorous. Peer-reviewed. Published in a respected journal. And the findings were striking enough that pain researchers took notice.
Which brings us to the next question: Is the fracture study a fluke, or is there a pattern of CBG outperforming conventional pain treatments in preclinical research?
The Nerve Damage Evidence
The Broken Leg Study Wasn’t Alone:
While the fracture study grabbed headlines, quieter research was showing CBG might excel at a different type of pain—one that’s notoriously difficult to treat.
Neuropathic pain.
This is pain from nerve damage: sciatica, diabetic neuropathy, chemotherapy-induced nerve pain, post-shingles pain. The kind that standard painkillers often fail to touch.
The kind where patients cycle through gabapentin, Lyrica, antidepressants, and opioids—all with limited success and significant side effects.
Study #1: The Chemotherapy Pain Model (2022)
Researchers gave mice cisplatin—a chemotherapy drug known to cause severe peripheral neuropathy in cancer patients.
It’s a devastating side effect. Patients finish chemotherapy cancer-free, but they’re left with permanent nerve damage. Numbness. Tingling. Burning pain. Hypersensitivity.
The mice developed the hallmark signs: hypersensitivity to touch (light pressure became painful) and mechanical allodynia (things that shouldn’t hurt, did).
Then they gave them CBG.
Results:
- Significantly reduced mechanical hypersensitivity in both male and female mice
- Brought pain sensitivity closer to normal levels
- Effect was blocked when researchers used a CB2 receptor antagonist—proving CBG works through cannabinoid receptors
The mechanism: CBG activates CB2 receptors on immune cells, reducing inflammatory signaling that sensitizes nerves.
No CB1 activation means no “high”—just pain relief.
Study #2: The Comprehensive Pain Battery (2024)
A Brazilian research team took this further. They tested CBG in multiple pain models to see if the effect was specific to one type of pain or if CBG was a broader analgesic.
They tested:
Acute inflammatory pain (formalin test – injection that causes tissue inflammation)
Acute thermal pain (hot plate test – heat sensitivity)
Chronic neuropathic pain (spinal nerve ligation – permanent nerve injury model)
CBG showed analgesic effects in all three.
But the strongest effect was in chronic neuropathic pain.
Rats with nerve injury received CBG for 14 days. By the end:
- Thermal hyperalgesia (oversensitivity to heat) significantly reduced
- Mechanical allodynia significantly reduced
- No motor impairment or sedation—the rats weren’t just too drugged to feel pain, they were actually less sensitive to painful stimuli
- Molecular analysis showed reduced TNF-α (inflammatory marker) and downregulated Nav1.7 sodium channels (involved in pain signaling)
The researchers measured actual changes in the pain processing system, not just behavior.
Why This Matters More Than the Fracture Study:
Neuropathic pain affects an estimated 7-10% of the population.
That’s millions of people living with chronic nerve pain.
Current treatments are inadequate:
Gabapentin/Lyrica (pregabalin): Effective for some, but causes dizziness, cognitive fog, weight gain. Many patients can’t tolerate the side effects. Others build tolerance and lose effectiveness.
Antidepressants (off-label): SNRIs like duloxetine help some patients, but side effects (nausea, sexual dysfunction, withdrawal issues) limit long-term use.
Opioids: Don’t work well for nerve pain. High addiction risk. Doctors are (rightly) hesitant to prescribe them long-term.
Topical treatments: Lidocaine patches, capsaicin cream—limited penetration, only work for surface-level pain.
None of them are great.
Patients often suffer for years, cycling through medications, finding partial relief at best.
If CBG’s neuropathic pain results translate to humans, it could address a massive unmet medical need.
The Ibuprofen Connection:
Unlike the fracture study where CBG was directly compared to NSAIDs, these neuropathic pain studies didn’t include ibuprofen as a comparator.
Why?
Because NSAIDs barely work for neuropathic pain. They’re designed for inflammatory pain (arthritis, injuries, headaches), not nerve damage pain.
Ask someone with sciatica if ibuprofen helps. They’ll laugh.
So in this context, CBG isn’t just “as good as ibuprofen”—it might be targeting pain types where ibuprofen fails entirely.
The Limitation (Again):
Rats with induced nerve injuries aren’t humans with diabetic neuropathy.
The pain mechanisms might be similar. The CB2 receptor activation might work the same way.
But we don’t have human data yet.
Not a single clinical trial.
Targeting Pain at Its Source
The Colitis Study: When Inflammation IS the Pain
In 2013, Italian researchers published a landmark study on CBG and inflammatory bowel disease.
They induced severe colitis in mice using a chemical irritant that causes gut inflammation and ulceration—similar to what happens in Crohn’s disease or ulcerative colitis.
Then they treated some mice with CBG and measured what happened.
Results:
- Colon inflammation dramatically reduced
- Less tissue swelling (colon weight/length ratio normalized—a standard measure of inflammation)
- Lower myeloperoxidase activity (an enzyme marker of neutrophil inflammation)
- Pro-inflammatory cytokines (IL-1β, IFN-γ) dropped
- Anti-inflammatory cytokine (IL-10) increased
- Reduced oxidative stress (boosted antioxidant enzymes like superoxide dismutase)
- Less ulceration and intestinal damage visible under microscopy
The researchers didn’t just measure symptoms—they measured the actual molecular markers of inflammation and found CBG reduced them significantly.
Why This Matters for Pain:
Anyone with IBD knows: inflammation equals pain.
Severe abdominal cramping. Urgency. Constant discomfort. Sometimes debilitating.
The study didn’t specifically measure pain behaviors in mice (it’s harder to assess abdominal pain in rodents). But the inflammatory markers tell the story.
Less inflammation means less pain.
CBG reduced the underlying pathology driving the pain, not just masking symptoms.
The Broader Implication:
If CBG reduces gut inflammation this effectively through CB2 receptor activation, the same mechanism should work in other inflammatory conditions:
Arthritis: Joint inflammation is the primary driver of arthritis pain. If CBG dampens inflammatory cytokines in the gut, it should dampen them in joints too.
Tendinitis: Inflamed tendons cause pain and limit movement. Anti-inflammatory effects could address both.
Chronic inflammatory pain conditions: Any condition where inflammation drives pain could theoretically respond to CBG’s immune-modulating effects.
Autoimmune-related pain: Conditions where the immune system attacks the body’s own tissues might benefit from CBG’s ability to reduce pro-inflammatory signals.
Back to the Ibuprofen Comparison:
NSAIDs are powerful anti-inflammatory drugs. They work by blocking COX enzymes, which stops prostaglandin production.
Prostaglandins cause inflammation and pain, so blocking them equals pain relief.
CBG works differently—through the endocannabinoid system, modulating immune cell behavior rather than blocking a single enzyme.
Neither approach is inherently better. They’re just different mechanisms.
But here’s the advantage CBG showed in the fracture study: it reduced inflammation enough to relieve pain, without blocking the healing-promoting aspects of inflammation.
NSAIDs are a sledgehammer. Effective, but indiscriminate.
CBG might be a scalpel. More selective.
At least in mice.
The Pattern Emerging:
Across three different pain types—bone injury pain, neuropathic pain, inflammatory pain—CBG consistently shows analgesic effects in animal models.
Different mechanisms for different pain types:
- Fracture pain: Anti-inflammatory + healing promotion
- Neuropathic pain: CB2 receptor activation, reduced nerve sensitization
- Inflammatory pain: Immune modulation, reduced pro-inflammatory cytokines
But always, the same caveat.
Mice, not humans.
Pain’s Connection to Brain Inflammation
The Huntington’s Disease Study (2015):
CBG was tested in mouse models of Huntington’s disease—a devastating neurodegenerative condition that causes movement disorders, cognitive decline, and psychiatric symptoms.
It’s a brutal disease with no cure.
Researchers gave CBG to two different mouse models: one where HD was induced with a neurotoxin, and one with a genetic mutation that causes HD.
Results:
- Preserved neurons and motor function
- Reduced neuroinflammation—specifically, reduced activation of microglia (the brain’s immune cells)
- Lowered pro-inflammatory markers in the brain
- Boosted antioxidant defenses
- Improved movement scores on behavioral tests
- Small reduction in toxic protein aggregates
In the toxin model, the effect was dramatic. CBG-treated mice had significantly better motor function and less neuron death than untreated HD mice.
What Does Brain Research Have to Do With Pain?
More than you’d think.
Chronic pain isn’t just a peripheral problem—something happening at the injury site. It involves the central nervous system. Your brain. Your spinal cord.
Central sensitization is when chronic pain rewires your nervous system.
The pain signal gets amplified. Your pain threshold drops. Touch becomes painful. Temperature changes hurt. Your brain starts interpreting normal sensations as threats.
This process involves neuroinflammation—immune activation in the brain and spinal cord that makes pain processing go haywire.
Fibromyalgia. Complex regional pain syndrome. Chronic widespread pain. Many chronic pain conditions involve central sensitization.
If CBG reduces neuroinflammation in Huntington’s mice…
Could it reduce neuroinflammation in chronic pain conditions?
Could it address central sensitization?
Could it help reset a nervous system that’s been stuck in “pain mode” for years?
We don’t know.
But the neuroprotective findings add another layer to CBG’s potential pain-relieving mechanisms:
- Peripheral anti-inflammatory effects (at the injury site)
- CB2 receptor activation (immune modulation)
- Neuroprotective effects (protecting nerves from damage)
- Anti-neuroinflammatory effects (dampening central sensitization)
The Ibuprofen Comparison (Again):
Ibuprofen doesn’t do any of this.
It blocks COX enzymes. Reduces prostaglandins. That’s it.
It works at the injury site, but it doesn’t address central pain processing. It doesn’t protect nerves. It doesn’t modulate brain inflammation.
CBG’s multi-target approach might explain why it appears effective across such diverse pain types in animal research.
Or it might just be that mice aren’t humans and we’re reading too much into preclinical data.
Time will tell.
What Humans Are Reporting
The Survey Study (2022):
Researchers surveyed 127 people in the United States who were already using CBG-predominant cannabis products.
This wasn’t a clinical trial. It was a survey asking: Why are you using CBG? Is it working? Any side effects?
What they were using CBG for:
- Anxiety: 51%
- Chronic pain: 41% (second most common use)
- Depression: 33%
- Insomnia: 31%
How well did it work for pain?
The majority reported their pain was “much improved” or “very much improved.”
But here’s the striking finding:
74% said CBG worked better for their chronic pain than their conventional medications.
Better than prescription painkillers. Better than NSAIDs. Better than whatever else they’d tried.
Side effects:
- 44% reported NO adverse events at all
- When side effects occurred, they were mild: dry mouth (16%), sleepiness (15%), increased appetite (12%)
- 84% had no withdrawal symptoms when stopping CBG
Compare that to conventional pain medications:
Opioids: highly addictive, constipation, respiratory depression, tolerance, withdrawal.
Gabapentin/Lyrica: dizziness, cognitive fog, weight gain, difficult withdrawal.
Even NSAIDs: stomach ulcers, kidney damage, cardiovascular risks with long-term use.
Why This Matters:
This bridges the gap between “it works in mice” and “it might work in humans.”
Real people, using real CBG products, reporting real pain relief.
Better than their prescription meds, with minimal side effects, and no addiction or withdrawal issues.
It’s the kind of real-world data that should make researchers say “we need to study this properly.”
The Massive Limitations:
This was a survey, not a clinical trial.
Let’s be brutally honest about what’s wrong with this data:
No placebo control: We don’t know how much is placebo effect. Pain is highly subjective and responsive to expectation.
Self-reported data: People might overestimate benefits, especially if they’ve invested money and hope in CBG.
Selection bias: People who love CBG are more likely to complete a survey about CBG. People who tried it and it didn’t work probably didn’t bother responding.
No standardization: People were using different products, different doses, different formulations. Some were using CBG with small amounts of THC. We can’t draw specific conclusions.
No objective pain measurements: No validated pain scales, no functional assessments, no comparison to baseline.
This is Level C evidence—the weakest form.
In the hierarchy of medical evidence, surveys rank near the bottom. Below randomized trials, below observational studies, barely above anecdotes.
But it’s not nothing.
When 74% of chronic pain sufferers say CBG works better than their conventional medications, that’s a signal.
A signal that warrants investigation.
Not proof. But a reason to conduct actual clinical trials.
The Ibuprofen Connection:
Many of these survey respondents were likely comparing CBG to NSAIDs like ibuprofen.
And they preferred CBG.
Does that mean CBG is objectively better?
No—we need controlled trials with placebo comparisons.
But it means enough people are finding relief with CBG that the scientific community should take notice.
How CBG Actually Works for Pain
Why does CBG keep showing analgesic effects across such different pain types?
The answer lies in how it works at the molecular level.
Primary Mechanism: CB2 Receptor Activation
CBG binds to CB2 cannabinoid receptors—primarily located on immune cells throughout your body.
When activated, CB2 receptors:
- Reduce pro-inflammatory cytokine release (the chemical messengers that amplify pain signals)
- Dampen immune cell activation (less inflammation at the pain site)
- Modulate pain signaling pathways (reducing nerve sensitization)
Critically: CB2 activation doesn’t cause a “high.”
That’s CB1 receptors, mostly in the brain. CBG has minimal CB1 activity, which is why it’s non-intoxicating.
You get the anti-inflammatory and analgesic effects without psychoactive effects.
Secondary Mechanisms:
CBG also works through:
α2-adrenergic receptors: Pain modulation in the central nervous system. This is the same mechanism used by clonidine, a medication sometimes prescribed for neuropathic pain.
Antioxidant effects: Reduces oxidative stress that contributes to pain and tissue damage. In the colitis study, CBG boosted antioxidant enzymes.
Neuroprotective actions: Protects nerve cells from inflammatory damage. Relevant for preventing chronic pain from becoming worse over time.
Reduced glial activation: Dampens the brain and spinal cord immune response involved in chronic pain and central sensitization.
Why This Is Different From Ibuprofen:
Ibuprofen works by blocking COX enzymes, which stops prostaglandin production.
Prostaglandins cause inflammation and pain, so blocking them equals pain relief.
Simple. Effective.
But prostaglandins also:
- Trigger tissue repair
- Recruit stem cells for healing
- Coordinate the inflammatory phase of wound healing
- Protect the stomach lining
- Regulate blood flow to kidneys
Block them completely (like NSAIDs do), and you sabotage healing. You risk stomach ulcers. You potentially harm kidney function.
CBG’s approach is more nuanced:
Instead of blocking a single enzyme, it modulates the immune system’s behavior through cannabinoid receptors.
It reduces excessive inflammation (the kind causing pain) while allowing necessary inflammation (the kind promoting healing) to proceed.
It’s not an on/off switch.
It’s a volume dial.
At least, that’s the theory based on how it behaved in the fracture study.
Why Multiple Pain Types Respond:
Different pain requires different mechanisms:
Inflammatory pain (arthritis, injuries): CBG reduces inflammation at source via CB2 activation. Less inflammation equals less pain.
Neuropathic pain (nerve damage): CBG reduces nerve sensitization through CB2 and adrenergic pathways. Damaged nerves stop sending exaggerated pain signals.
Bone/tissue injury pain: CBG’s anti-inflammatory effects plus healing promotion. Pain relief that doesn’t compromise recovery.
Central pain (fibromyalgia, chronic widespread pain): Neuroprotective effects, reduced neuroinflammation. Addresses the brain and spinal cord amplification of pain signals.
One compound, multiple mechanisms, broad pain coverage.
At least in theory.
And in mice.
Why We Can’t Promise Anything Yet
Here’s what we need to acknowledge:
Every impressive CBG pain study—the fracture study, the neuropathic pain models, the colitis research, the neuroprotection findings—was conducted in rodents.
Not a single human clinical trial exists for CBG and pain.
Zero.
None.
Why This Matters:
Mouse studies fail to translate to humans all the time.
Constantly.
The pharmaceutical industry is littered with drugs that worked brilliantly in mice and did absolutely nothing in humans.
Examples:
Cancer treatments that shrank tumors in mice but failed Phase II or Phase III human trials. Billions of dollars invested. No benefit.
Alzheimer’s drugs that cleared amyloid plaques in mouse brains but didn’t slow cognitive decline in humans. Decades of research. Dead ends.
Pain medications that were effective in rat models but turned out to be useless—or actively harmful—in people.
We’ve been rightfully skeptical of companies making bold claims based solely on animal research.
It’s easy to cure cancer in mice. It’s hard to cure cancer in humans.
We can’t be hypocrites now just because the CBG data looks promising.
The Dosing Problem:
In the fracture study, mice received CBG doses scaled to their body weight—roughly 10-30 mg/kg.
For a 70 kg (154 pound) human, that would translate to 700-2,100 mg of CBG per dose.
The only human CBG trial that exists (the 2024 anxiety study) used 20 mg.
That’s a 35-100x difference.
Will the lower doses humans are likely to use show the same effects?
We don’t know.
Maybe humans are more sensitive to CBG and need less. Maybe we need higher doses. Maybe the optimal dose is somewhere in between.
Maybe dose-response curves are different across species.
We’re guessing.
The Healing Timeline Problem:
Mice bones heal in 3-4 weeks.
Human bones take 6-12 weeks minimum, sometimes longer.
Mouse metabolism is dramatically faster than human metabolism. Their hearts beat 600 times per minute compared to our 60-100. Everything happens faster.
Drug effects that last hours in mice might last days in humans—or might metabolize so quickly they don’t work at all.
The fracture study showed benefits over a few weeks of mouse healing. Will the same benefits appear over months of human healing?
Unknown.
The Pain Measurement Problem:
In mice, researchers measure pain by:
- Paw withdrawal latency (how quickly they pull away from painful stimuli)
- Grimace scales (analyzing facial expressions indicating pain)
- Activity levels (painful mice move less, groom less, explore less)
These are behavioral proxies for pain. Useful, but limited.
In humans, pain is:
- Subjective (“rate your pain 1-10”)
- Emotionally complex (pain catastrophizing, anxiety that amplifies perceived pain)
- Influenced by expectation (powerful placebo effects)
- Multidimensional (sensory component, emotional component, functional impact on daily life)
A mouse can’t tell you “it hurts less but the quality of pain changed” or “I can tolerate it better even though the intensity is the same.”
Will CBG’s effects in simplified mouse pain models translate to the complex, multifaceted experience of human chronic pain?
We genuinely don’t know.
What We DO Know (The Encouraging Parts):
Despite these limitations, some things work in our favor:
1. The mechanisms make biological sense
- CB2 receptors exist in humans
- They’re located on immune cells (same as in mice)
- The anti-inflammatory pathways are conserved across mammalian species
- The biological plausibility is strong
- We’re not talking about some mechanism that only exists in rodents
2. The one human trial showed safety
- 20 mg CBG in 34 healthy adults
- No intoxication, no impairment, no serious side effects
- Only mild issues: some dry mouth, slight sleepiness in a few people
- This establishes CBG is safe to give to humans (at that dose, at least)
- No red flags that would prevent pain trials from moving forward
3. The real-world survey data is promising
- 127 chronic pain sufferers reporting benefits
- 74% preferring CBG over conventional meds
- Minimal side effects
- While not rigorous, it’s a signal worth investigating
4. The animal data is consistent
- Multiple studies, multiple laboratories, multiple pain models
- Results consistently show analgesic effects
- Different researchers in different countries arriving at similar conclusions
- This reduces the chance it’s a fluke or an artifact of one lab’s methods
Where We Stand:
CBG for pain is exactly where CBD was 10-12 years ago:
- Compelling animal research showing promise
- Mechanisms that make theoretical sense
- Anecdotal human reports of benefits
- Safety profile seems favorable
- But no clinical proof
What Happens Next:
The scientific community is taking notice. The 2024 human anxiety trial was a first step—establishing that CBG can be safely given to humans and has measurable effects.
Likely next steps for pain research:
- Dose-finding studies in humans (what’s the lowest effective dose? What’s the ceiling?)
- Safety trials at higher doses (can humans tolerate 100mg? 200mg? 500mg?)
- Small pilot studies in specific pain conditions (maybe start with neuropathic pain since the animal data is strongest there)
- Eventually: randomized controlled trials comparing CBG to placebo
- Possibly: head-to-head trials comparing CBG to NSAIDs or gabapentin
But this takes years.
Clinical trials are expensive—millions of dollars for a proper Phase II trial.
Regulatory approval is slow—years from concept to completion.
Cannabis research faces additional hurdles—legal restrictions, banking issues, stigma affecting funding.
We’re probably 3-5 years away from definitive human data on CBG for pain.
Minimum.
Possibly longer.
So what do we do in the meantime?
Should You Try CBG for Pain?
The early adopter decision:
You’re faced with compelling animal research and zero human clinical trials.
Do you wait for the science to catch up? Or do you experiment now?
There’s no universally right answer. It depends on your situation, your pain, your risk tolerance, and your resources.
Here’s the honest framework for making that decision:
Consider CBG if:
1. NSAIDs work for you but you’re worried about long-term side effects
You’re taking ibuprofen daily for arthritis or chronic pain. It helps. But you’re concerned about:
- Gut issues (stomach ulcers, GI bleeding)
- Kidney concerns (NSAIDs can damage kidney function over time)
- Cardiovascular risks (some NSAIDs increase heart attack and stroke risk)
- Impaired healing (especially relevant if you’re recovering from injury or surgery)
You’d like an alternative that might be safer long-term.
2. You have neuropathic pain that hasn’t responded well to conventional treatments
- Gabapentin/Lyrica cause too much cognitive fog (you can’t think clearly, can’t work)
- Antidepressants (duloxetine) don’t work or cause intolerable side effects
- NSAIDs barely touch nerve pain anyway (they’re not designed for neuropathic pain)
- You’ve tried everything standard medicine offers and you’re still suffering
3. You’re dealing with inflammatory conditions
- Arthritis (joint inflammation driving pain)
- Tendinitis (tendon inflammation)
- IBD with pain component (abdominal cramping from gut inflammation)
- Any condition where reducing inflammation could meaningfully reduce pain
4. Healing is as important as pain relief
- Bone fractures (if the mouse study translates, this could be ideal)
- Post-surgical recovery (want pain management that doesn’t slow healing)
- Sports injuries—muscle, tendon, ligament damage (need to get back to activity ASAP)
- Anywhere you need tissue repair alongside pain management
5. You want to avoid or reduce opioid use
- No addiction potential with CBG
- No respiratory depression
- No tolerance buildup requiring ever-higher doses
- No risk of overdose
- If you’re trying to get off opioids or avoid starting them, CBG might be worth trying
6. Cognitive clarity matters to you
- The one human trial showed CBG didn’t impair cognition—it actually improved memory
- Unlike high-dose gabapentin or some pain meds that cause brain fog
- If you need to work, drive, think clearly while managing pain, this matters
Don’t consider CBG if:
1. You need FDA-approved, clinically proven treatments
Valid position. The evidence isn’t there yet.
If you’re someone who only uses treatments with robust clinical trial data, wait for those trials to happen.
Nothing wrong with this approach.
2. You’re on a tight budget
CBG products are expensive. Lab-tested, quality CBG oils typically cost €50-100+ per bottle.
No insurance coverage. All out-of-pocket.
If you can’t afford to experiment with unproven treatments, that’s completely reasonable.
Standard pain medications, for all their flaws, are at least covered by insurance or available as generics.
3. You have acute, severe pain requiring immediate, guaranteed relief
Don’t gamble on unproven treatments for acute emergencies.
Broken bone? Go to the hospital. Get proven pain management.
Post-surgical pain? Take what your surgeon prescribes—medications with known efficacy.
Severe pain crisis? Use established treatments.
CBG is for people with chronic pain exploring alternatives, not acute pain requiring immediate, reliable relief.
If you decide to try CBG:
What to look for:
- Lab-tested products with Certificates of Analysis (COAs) showing actual cannabinoid content
- Full spectrum formulations if possible (get the entourage effect—multiple cannabinoids and terpenes working together)
- Start with doses similar to the human anxiety study: 20-25 mg
- Give it time—effects might be subtle and cumulative, not immediate and dramatic
Track your results:
Be scientific about this. You’re essentially conducting an n=1 experiment on yourself.
- Rate pain levels (1-10 scale) before starting CBG and daily after
- Note functional improvements (What can you do now that you couldn’t before? Can you walk further? Sleep better? Work without distraction?)
- Track any side effects, even minor ones
- Compare to your previous pain management approach (Is this better, worse, or the same as what you were doing before?)
- Give it at least 2-4 weeks before drawing conclusions
Understand what you’re doing:
You’re an early adopter.
You’re betting that mouse studies translate to humans.
Sometimes they do. Sometimes they don’t.
The CBG you’re using hasn’t been proven to work in humans for pain. But it also hasn’t been proven NOT to work.
Manage expectations. Don’t expect miracles.
But stay open to the possibility it might help.
The “Better Than Ibuprofen” Reality Check:
The title of this article is “Better Than Ibuprofen (According to Mice With Broken Legs).”
The parenthetical is crucial.
We don’t know if CBG is better than ibuprofen in humans.
We know it matched or exceeded ibuprofen in several mouse pain models—fracture pain, inflammatory pain, even neuropathic pain where ibuprofen doesn’t work at all.
That’s exciting. It’s promising. It’s worth investigating.
But it’s not proof.
If you try CBG and it works better than ibuprofen for YOUR pain—great.
You’ve joined the 74% of survey respondents who reported similar results.
If you try it and it doesn’t work—that’s valid too.
Mouse results didn’t translate for you specifically. Or maybe you got a low-quality product. Or maybe the dose was wrong. Or maybe placebo effect wore off.
Either way, you’ve contributed to our collective understanding of whether these preclinical findings hold up in the real world.
The Promise, The Wait, and The Honest Position
Where we are:
CBG has shown remarkable pain-relieving effects in animal research.
In mice with broken legs, it matched NSAIDs for pain relief while accelerating bone healing—something NSAIDs actively impair.
In multiple neuropathic pain models, it reduced nerve hypersensitivity and pain behaviors.
In inflammatory bowel disease, it dampened gut inflammation and the molecular markers that drive inflammatory pain.
In neurodegenerative disease models, it showed neuroprotective effects that could theoretically address central sensitization in chronic pain.
The mechanisms make biological sense:
- CB2 receptor activation on immune cells
- Anti-inflammatory without blocking healing-promoting inflammation
- Multi-target approach covering different pain types
- Neuroprotective effects addressing both peripheral and central pain
The safety profile looks favorable:
- One human trial (anxiety) showed no serious side effects
- Survey data suggests minimal adverse events
- Non-addictive, non-intoxicating
- No reports of tolerance or withdrawal
But every pain study has been in rodents.
Not one human clinical trial for CBG and pain exists.
Where we’re going:
The scientific community is paying attention.
The fracture study made headlines. The neuropathic pain research is building. The survey data showed real-world interest.
Human trials are likely coming—but they take years and millions of dollars.
In the meantime, early adopters are experimenting. Some are reporting benefits similar to what the mouse studies predicted.
We’re in the “promising but unproven” phase.
Exactly where new treatments always start before they become standard medicine.
The honest position:
If someone asks me “Is CBG better than ibuprofen for pain?”, here’s my answer:
“In mice with broken legs—yes, definitively.
CBG matched ibuprofen for pain relief and beat it for bone healing. In neuropathic pain models, CBG worked where NSAIDs typically fail. In inflammatory bowel disease, CBG reduced the inflammation driving pain.
In humans—we don’t know yet. The research hasn’t been done.
But the animal data is compelling enough that if I had chronic pain not responding well to conventional treatments, I’d consider trying CBG while we wait for the clinical trials to give us definitive answers.
Just with eyes wide open about what we know and what we don’t.”
The bottom line:
The mouse studies are too impressive to ignore.
The human proof is too absent to promise anything.
CBG for pain sits in that uncomfortable middle ground—exciting potential, uncertain reality.
Some people will wait for clinical validation. That’s scientifically sound.
Some people will try it now as early adopters. That’s understandable given the limitations of current pain management.
Both positions are reasonable.
What’s not reasonable is overpromising based on animal data, or dismissing compelling preclinical research entirely.
The truth is in the nuance:
Better than ibuprofen?
According to mice with broken legs, neuropathic pain models, and inflammatory disease models—yes.
According to humans with chronic pain conditions?
Ask me again in 5 years when we have actual clinical trial data.
Until then, cautious optimism and radical honesty about what we know—and what we don’t—is the only intellectually honest position.
The mice tell us CBG might be remarkable for pain.
Now we wait to see if humans agree.
