Kratom affects several major organ systems, with the most well-documented impacts on the brain, liver, heart, and digestive tract. It also influences the endocrine (hormonal) system, kidneys, and lungs, though the severity varies widely depending on dose, frequency of use, and whether other substances are involved.
Brain and Nervous System
The brain is kratom’s primary target. Kratom’s main active compound, mitragynine, binds to the same receptors that opioid painkillers activate, producing pain relief, euphoria, and reduced anxiety at moderate doses. It also interacts with other receptor types in the brain and spinal cord, and it blocks certain calcium channels on nerve cells, which further dampens pain signaling. At lower doses, kratom acts more like a stimulant, increasing alertness and energy. At higher doses, it shifts toward sedation and pain relief.
The neurological side effects reflect this broad activity. Reported effects include agitation, drowsiness, tremor, loss of coordination, headache, slurred speech, and fainting. Seizures are among the more serious concerns. In poison control data, seizures appeared in roughly 6% to 17.5% of reported kratom cases, depending on the dataset. However, a 2025 systematic review noted there is no confirmed mechanism explaining how mitragynine would directly trigger seizures, and some researchers suspect the stimulant-like properties of kratom may play a role. The FDA has listed seizures among the serious risks associated with kratom products.
Liver
The liver is one of the organs most clearly affected by kratom. Liver injury from kratom typically follows a cholestatic or mixed pattern, meaning bile flow is disrupted rather than liver cells being directly destroyed (though both can happen). Lab work in affected patients shows elevated levels of enzymes that indicate liver stress, along with high bilirubin, the pigment that causes jaundice.
Early warning signs of kratom-related liver injury include fatigue, nausea, itching, and dark urine, followed by yellowing of the skin and eyes. In severe cases, bilirubin levels can climb to more than ten times the normal upper limit. These cases are serious enough to require hospitalization, though most patients recover after stopping kratom use.
Heart and Cardiovascular System
Kratom’s effects on the heart are a growing concern. The two most common cardiovascular side effects are a rapid heart rate (reported in about 30% of adverse event cases) and high blood pressure (about 12%). Cardiac palpitations and elevated blood pressure are frequently noted in clinical reports of kratom users seeking emergency care.
Lab studies using human heart cells have shown that mitragynine can prolong the electrical cycle of the heartbeat, a change known as QT prolongation that raises the risk of dangerous irregular rhythms. However, a clinical study of people who regularly consumed kratom did not find this same risk in living subjects, suggesting the real-world danger may be lower than what lab models predict. A handful of case reports have linked kratom to cardiac arrest and serious arrhythmias, but in most of those cases, the person was also using another substance, making it difficult to pin the blame on kratom alone.
Digestive System
Like traditional opioids, kratom slows the movement of food through the gut. Constipation is one of the most consistently reported side effects among regular users. Nausea, vomiting, dry mouth, and loss of appetite are also common, and the FDA lists gastrointestinal distress as a known adverse effect of kratom-related products. Weight loss is frequently reported with ongoing use, likely a combination of reduced appetite and disrupted digestion.
Hormonal System
Chronic kratom use can disrupt hormone levels in ways that mirror what traditional opioids do. In one well-documented case, a 42-year-old man developed low energy and reduced sex drive while using kratom regularly. Testing revealed his testosterone had dropped below the normal range while his prolactin (a hormone normally kept low in men) was nearly double the upper limit. His thyroid function remained normal. Within two months of stopping kratom, both his testosterone and prolactin returned to healthy levels.
This pattern, where the brain’s signaling hormones remain in the normal range but testosterone drops, points to a specific type of hormonal disruption driven by elevated prolactin. Opioid-like compounds are known to raise prolactin, which in turn suppresses the hormonal signals that drive testosterone production. Hypothyroidism has also been reported in the medical literature as a consequence of kratom use, though the evidence is more limited.
Kidneys
Kidney injury from kratom is less commonly reported than liver damage, but it does appear in the medical literature. In one case, a 21-year-old woman who had been self-treating headaches with kratom purchased online arrived at an emergency department with nausea, vomiting, and flank pain. Her creatinine level, a key marker of kidney function, was more than three times the normal upper limit. Her kidney function gradually improved with supportive care and fully normalized one month after she stopped using kratom. Notably, testing of her kratom supply revealed it had been adulterated with hydrocodone and morphine, raising the question of whether the kidney damage was caused by mitragynine itself or the contaminants.
This case highlights a broader issue with kratom products: because they are unregulated, adulteration with other drugs is a real possibility, and some organ damage attributed to kratom may partly stem from unknown additives.
Lungs and Breathing
Respiratory depression, where breathing slows dangerously, is the leading cause of death from opioid overdoses. Kratom’s main compound does slow breathing, but the effect appears to have a built-in safety ceiling that traditional opioids lack. In animal studies, mitragynine caused less respiratory depression than codeine, and increasing the dose beyond a certain point did not make the breathing suppression any worse. Researchers believe this ceiling exists because the body can only convert mitragynine into its more potent form (7-hydroxymitragynine) at a limited rate, so flooding the system with more of the raw compound doesn’t proportionally increase the danger.
That said, 7-hydroxymitragynine itself does not share this safety margin. It depresses breathing in a dose-dependent way similar to morphine. Products specifically marketed as containing concentrated 7-OH have prompted separate FDA warnings due to their potential for serious harm, including addiction and withdrawal symptoms.
Why Fatality Data Is Hard to Interpret
Establishing a clear lethal dose for kratom has proven difficult. A study of kratom-associated deaths in Northern Nevada found mitragynine blood levels ranging from about 9 to 1,800 ng/mL in cases where drug toxicity was the official cause of death. In only one of those cases was mitragynine the sole intoxicant, at a blood concentration of 950 ng/mL. Crucially, there was no statistically significant difference in blood concentrations between people who died from mitragynine toxicity and those who died from other causes but happened to have mitragynine in their system. This overlap makes it very difficult to define a threshold concentration that reliably predicts fatal outcomes, and it underscores that most kratom-associated deaths involve other substances.