How the American Kratom Association Misled Kansas to Pass the KCPA
When Kansas lawmakers were asked to pass the Kratom Consumer Protection Act (KCPA), they were told a reassuring story: that kratom is not an opioid, not addictive, and safe enough to regulate rather than restrict.
That story was built on selective citations, incomplete science, and critical omissions—many of them drawn from the very exhibits submitted as “evidence.”
Primary Exhibits (as submitted)
These PDFs are provided exactly as uploaded for independent review.
Exhibit A: “Kratom Science Update – Evidence-Based Facts” (Pinney Associates / AKA)
What Kansas was handed:
A glossy “science update” that looks like an objective report written by credentialed experts.
What it really is:
The authors admit in their own disclosure that this document was paid work and was drafted for the
American Kratom Association (AKA). That doesn’t automatically make every sentence false, but it matters
because Kansas lawmakers were asked to treat it like a neutral source.
What this document admits (and why Kansas should have been alarmed):
- Your body turns kratom into a stronger opioid-like chemical. The paper says the main kratom alkaloid (mitragynine) is metabolized into 7-hydroxymitragynine (7-OH) in humans.
- 7-OH is not mild. The paper says 7-OH has stronger opioid effects than mitragynine.
- The market has been “enhancing” products. The paper admits that some makers have boosted 7-OH to levels far higher than what exists in the plant.
- Dependence and withdrawal are real. Even this pro-KCPA document warns that frequent, chronic use can lead to dependence and withdrawal and tells consumers to monitor use to reduce that risk.
- Adulteration has included real opioids. The paper admits that some kratom products were found adulterated with substances like fentanyl, heroin, and morphine.
What Kansas lawmakers were not told plainly:
- If a product is routinely converted in the human body into a more potent opioid-like compound, you cannot keep selling it to the public as if it’s just “a plant” or “non-opioid.”
- This document describes the exact mechanisms that drive drug harm in the real world (stronger opioid-active compounds, product boosting, dependence, withdrawal, and contamination), then asks lawmakers to believe that labels and testing will solve it.
Why Exhibit A actually helps the case for stricter control (including scheduling arguments):
- Abuse potential: the paper admits a pathway to a more potent opioid-active compound (7-OH) and admits product boosting.
- No accepted medical use: people report benefits, but there is no FDA-approved use or standardized dosing.
- Safety problems: the paper admits dependence/withdrawal risk and a history of adulterated products in commerce.
Exhibit B: Systematic Review of Overdose Risk (Stanciu et al.)
What Kansas lawmakers were told:
Supporters emphasized that most kratom-related deaths involved other drugs, implying that kratom by itself is relatively low risk.
What the study actually found:
- Serious medical emergencies are repeatedly reported. Poison center data and medical case reports include seizures, slowed or stopped breathing, coma, cardiac arrest, and cases where patients had to be placed on breathing machines.
- Kratom can look like an opioid overdose. At least one documented case showed slowed breathing that improved after naloxone, the same medication used to reverse opioid overdoses.
- Modern U.S. kratom products are much riskier. The authors explain that today’s kratom extracts, concentrates, and pure alkaloid products greatly increase overdose risk compared to traditional leaf chewing or tea.
- Kratom interferes with common medications. Kratom compounds block important liver enzymes that process many prescription drugs. This makes drug–drug interactions more dangerous, especially with antidepressants, opioids, alcohol, and sedatives.
What lawmakers were not clearly told:
- Deaths involving multiple substances do not make kratom harmless. The paper explains that kratom often worsens the effects of other drugs, which is exactly how opioid-related deaths occur in the real world.
- The authors repeatedly warn that safety claims based on traditional use do not apply to the unregulated, high-potency products sold in the United States.
Why this matters for regulation:
- Safety has not been established. The authors state there are no human trials testing kratom’s toxicity, yet life-threatening outcomes are documented.
- Overdose patterns resemble opioid harm. Lung congestion, slowed breathing, naloxone response, and drug interactions mirror known opioid overdose mechanisms.
- Unregulated product potency is a core risk factor. The study shows that variability, concentration, and interactions—especially in U.S. products— are central to why severe outcomes occur.
Exhibit C: Abuse Liability Study of 7-Hydroxymitragynine (Hemby et al.)
What Kansas lawmakers were led to believe:
Animal studies show kratom has low addiction risk.
What this study actually found:
- One kratom chemical behaves like an addictive drug. In this study, animals repeatedly pressed a lever to give themselves 7-hydroxymitragynine (7-OH). That behavior is the standard scientific sign that a substance is reinforcing and addictive.
- Animals treated 7-OH like morphine. When researchers swapped out morphine for 7-OH, the animals kept using it. This means 7-OH acted like an opioid in the brain.
- Exposure made animals want more opioids later. After being exposed to 7-OH, animals went on to take significantly more morphine than before. That did not happen with mitragynine.
What lawmakers were not clearly told:
- This study does not identify a harmless compound. It singles out 7-OH as the most dangerous part of kratom.
- 7-OH is not theoretical. It exists naturally in kratom, is produced in the body, and has been found at elevated levels in commercial products.
Why this matters for policy decisions:
- High abuse potential: The study shows classic addiction behavior with 7-OH.
- Risk of escalation: Exposure increased later opioid use, a red flag for addiction policy.
- No approved medical use: There are no FDA-approved treatments using 7-OH, and no clinical trials establishing safe therapeutic use.
Exhibit D: “Kratom Tea as a Therapeutic Option” (Wilson et al.)
What Kansas lawmakers were told:
This study was cited to suggest that kratom can help people get off opioids and does not seriously affect breathing.
What the study actually shows:
- Kratom tea works through opioid receptors. The study shows that even a traditional tea preparation activates the same brain receptor (the mu-opioid receptor) targeted by drugs like morphine. When that receptor was removed in mice, kratom tea stopped working.
- Breathing was affected, even if briefly. The tea caused a short-term drop in breathing rate. It was less severe than morphine, but it was not zero risk.
- The body turns kratom into a stronger opioid compound. The authors explain that mitragynine is converted in the body into 7-hydroxymitragynine, a much more potent opioid-active chemical.
- This is not proven safe in people. The authors are clear that there are no completed human trials establishing safety or medical use. Studies in humans are still underway.
What lawmakers were not clearly told:
- This study used a carefully prepared tea with known ingredients. It does not reflect the high-potency extracts, concentrates, or enhanced products commonly sold in U.S. stores.
- Calling something “therapeutic” in a mouse study does not mean it is an approved or accepted medical treatment in humans.
Why this matters for regulation:
- Opioid pharmacology is confirmed. The study shows kratom tea acts through opioid receptors.
- Physiologic risk is documented. Even under controlled conditions, respiratory effects occurred.
- No accepted medical use has been established. There is no FDA-approved kratom product and no completed human safety trials.
Exhibit E: Mitragynine Self-Administration in Rats (Yue & Katz)
What Kansas lawmakers were told:
This study was used to claim that kratom’s main ingredient is not addictive
because animals did not repeatedly take it.
What the study actually found:
- Mitragynine acts on opioid receptors. The researchers showed that mitragynine binds to the same brain receptor targeted by drugs like morphine and heroin—the mu-opioid receptor.
- It changes opioid-seeking behavior. When rats were given mitragynine before a session, they took less heroin. That means mitragynine is active in the brain’s opioid reward system.
- The experiment tested mitragynine alone. The study did not examine what happens after the body processes kratom, and it did not include kratom’s stronger opioid byproducts.
Why this animal study does not translate to human safety
Rats do not process kratom the way people do. Humans convert mitragynine into 7-hydroxymitragynine (7-OH), a much stronger opioid-active compound. Rats do not make this conversion in the same way or to the same extent.
This is basic pharmacology. We would never judge the safety of codeine in an animal that cannot convert it into morphine. Yet that is exactly what happened here—without explaining it to lawmakers.
What lawmakers were not told:
- The authors themselves warn that failure to see self-administration in one animal model does not rule out addiction risk.
- Other studies show kratom compounds can produce reward-related effects, and this paper does not contradict that.
Why this matters for policy decisions:
- The animal model misses the human risk pathway. People are exposed to a more potent opioid metabolite that rats do not model.
- Claims of “low abuse potential” rest on incomplete science. The study was never designed to answer the question lawmakers were told it answered.
Exhibit F: The KCPA Advocacy Deck
What Kansas was told:
The KCPA solves the problem through regulation.
What the deck itself admits:
- Products must limit 7-OH.
- Synthetic alkaloids must be banned.
- Adulteration is a known problem.
- Youth access is a concern.
What this really means:
If a substance requires potency caps, metabolite limits, bans on chemical manipulation, and strict age controls, lawmakers are not treating it like a supplement. They are treating it like a drug.
Why this supports Schedule I logic:
- The market predictably drifts toward higher opioid potency.
- Consumer regulation cannot fix a pharmacologic problem.
Final Synthesis: Kansas Was Given the Case for Schedule I—Not the KCPA
From the materials submitted to Kansas:
- Kratom works the same way opioids do. It activates opioid receptors in the brain. That’s not opinion — that’s pharmacology.
- When a human takes kratom, the body turns it into 7-hydroxymitragynine — a much stronger opioid than the plant itself. The danger doesn’t show up later. The body makes it.
- That stronger opioid has clear addiction risk. Animals will work to get it. People keep escalating doses to chase it.
- The harms are already on the record: overdoses, slowed or stopped breathing, seizures, coma, and lethal drug interactions. This is not hypothetical.
- There is no FDA-approved medical use. No dosing standard. No physician oversight. No accepted treatment role. Calling it “therapeutic” doesn’t change that.
- The safety claims collapse because they rely on animal studies that don’t process kratom the way humans do. Rats don’t make the opioid humans are exposed to and lawmakers were never told that.
Kansas lawmakers were not given neutral science. They were given a curated narrative—one that collapses under its own citations.
The evidence used to justify the KCPA actually satisfies the core criteria for Schedule I placement.