A new study covering 100 million people links strokes with cocaine, methamphetamine, and cannabis use.

For people under 55, stroke risk nearly triples with amphetamine/methamphetamine, with cocaine not far behind.

Drug abuse is the most common predisposing condition for stroke in people under age 35.

Almost nobody gets a stroke if they’re 20, right? Stroke has been viewed for years as a disease of aging, hypertension, diabetes, hyperlipidemia, and atrial fibrillation. But when a much younger person uses illegal drugs, they may experience a stroke out of the blue.

Megan Ritson, Ph.D., and University of Cambridge colleagues just published a major study showing that illicit drugs, particularly amphetamines and cocaine, triple stroke risk in people under age 55. Cannabis has historically been considered relatively benign, but emerging evidence also suggests an important association with stroke risk. The meta-analysis found that cannabis use brought a 37 percent increase in stroke risk.

Ritson said, “This is the most comprehensive analysis ever conducted on recreational drug use and stroke risk and provides compelling evidence that drugs like cocaine, amphetamines, and cannabis are causal risk factors for stroke. These findings give us stronger evidence to guide future research and public health strategies.”

Stimulants like cocaine and methamphetamine have long been associated with acute cardiovascular complications, and now their role in cerebrovascular injury is clearly recognized. Cocaine increases stroke risks by 96 percent and amphetamines by 122 percent. Especially worrisome, stimulants can destabilize cerebral circulation in minutes. This means drug use among younger adults sometimes leads to preventable strokes. Consequently, when otherwise healthy younger patients experience ischemic or hemorrhagic stroke, substance use may be the cause.

Researchers suggest reasons why drug abuse is linked to increased stroke risks include sudden spikes in blood pressure, blood vessel spasm and constriction, heart rhythm problems, and inflammation or vasculitis. These are well-established pathways causing ischemic strokes from blood clots and hemorrhagic strokes

Methamphetamine and Amphetamine-Associated Stroke

Methamphetamine and related stimulant abuse strongly correlate with increased stroke risks. Previously reported large systematic reviews and meta-analyses show amphetamine exposure more than doubles stroke risk. In contrast to traditional vascular risk factors developing over decades, stimulant-related cerebrovascular injury may occur abruptly following drug exposure or drug-induced acute vascular stress. Patients frequently present with sudden neurologic deficits but little or no history of hypertension, diabetes, or other stroke risk factors.

Methamphetamine dramatically increases the release of dopamine and norepinephrine, resulting in tachycardia, systemic vasoconstriction, and profound blood pressure elevations. Acute hypertensive crises may rupture small intracerebral vessels or preexisting aneurysms, leading to intracerebral or subarachnoid hemorrhage. Sometimes stimulant exposure leads to reversible cerebral vasoconstriction syndrome, a condition of transient narrowing of cerebral arteries and recurrent severe headaches.

Chronic methamphetamine exposure is associated with endothelial injury and inflammatory vascular damage. Repeated stimulant use may produce chronic hypertension, progressive vascular injury, and remodeling. Cardiac complications represent an additional pathway linking methamphetamine to stroke.

Numerous studies demonstrated increased risks of ischemic and hemorrhagic stroke among cocaine users. Meta-analyses show cocaine exposure doubles stroke risks. Cerebrovascular events may occur within hours of cocaine use, underscoring its rapid acute physiologic effects. Like methamphetamine, cocaine produces potent sympathetic stimulation, resulting in marked elevations in heart rate and blood pressure. These acute hypertensive surges increase the risk of intracerebral hemorrhage and subarachnoid hemorrhage.

Cocaine is a powerful vasoconstrictor, leading to pronounced cardiac and cerebral vasospasm. Cocaine increases platelet activation and aggregation while promoting a prothrombotic state. These effects may facilitate arterial thrombosis and contribute to ischemic stroke. Cocaine exposure also has been associated with structural injury to the arterial wall, leading to thromboembolism and cerebral infarction.

Chronic cocaine use may accelerate atherosclerosis. Although many cocaine-associated strokes occur in individuals without established vascular disease, repeated exposure may contribute to premature atherosclerotic changes.

Cocaine-associated stroke may present in large vessel occlusion, intracerebral hemorrhage, and subarachnoid hemorrhage. Because these events frequently occur in young people without conventional vascular risk factors, clinicians should consider cocaine exposure when evaluating unexplained stroke in this population.

Stimulants produce intense sympathetic stimulation, elevating heart rate, blood pressure, and myocardial oxygen demand. At the same time, cocaine and methamphetamine can induce coronary vasospasm, decreasing blood flow to the myocardium. Use and vigorous physical exercise may be especially problematic. Platelet activation and thrombosis further increase the risk of coronary occlusion.

Cannabis (“weed”) has historically been regarded as less harmful than stimulants, but growing evidence suggests it, too, may contribute to cerebrovascular risk. Although the strength of association between cannabis and stroke is weaker than that of cocaine or methamphetamine, numerous observational studies have identified a relationship between cannabis exposure and subsequent cerebrovascular events.

Several epidemiologic analyses reported increased stroke risk among younger cannabis users, particularly with frequent or recent use. In large population-based datasets, young adults reporting recent cannabis use had higher odds of stroke compared with nonusers, and risks apparently increased with more frequent use.

Cannabis exposure has also been associated with reversible cerebral vasoconstriction syndrome, suggesting that transient arterial narrowing may affect ischemic events. Cannabis also affects autonomic balance, increasing sympathetic activity while reducing parasympathetic tone. These autonomic changes may influence vascular tone and cerebral blood flow regulation.

Fluctuations in blood pressure may likewise contribute. Cannabis can produce variable cardiovascular effects, including episodes of hypertension as well as postural hypotension. These fluctuations may impair cerebral autoregulation.

Some studies suggest cannabis may promote platelet activation and contribute to prothrombotic states. In addition, cannabis is associated with cardiac arrhythmias and cardiomyopathy, which could lead to cardioembolic stroke in susceptible individuals.

Cannabis is increasingly implicated in cardiovascular events. Emerging epidemiologic studies suggest cannabis use may be associated with increased risk of myocardial infarction, stroke, heart failure, and cardiovascular mortality in younger adults. Proposed mechanisms include tachycardia-induced increases in myocardial oxygen demand, coronary vasospasm, endothelial dysfunction, and prothrombotic effects.

Although the magnitude of stroke risk associated with cannabis remains smaller than that with stimulants, the rapidly increasing prevalence of regular cannabis use—notably among younger adults—makes this association significant.

Drug-Associated Heart Attack, Stroke, and Systemic Vascular Injury

The National Institutes of Health reports that drug use is a major driver of "unexplained" neurological emergencies, like seizures and strokes, estimating that users aged 15–44 are 6.5 times more likely to suffer a stroke than nonusers. Today, drug abuse is the most common predisposing condition for stroke in patients under age 35. In addition, many drug-associated heart attacks occur out of the blue, in people with little or no underlying coronary atherosclerosis. Angiographic studies have shown that a substantial proportion of cocaine-related myocardial infarctions occur in individuals with normal coronary arteries. In these cases, the infarction likely results from transient vasospasm, thrombosis, or severe oxygen supply–demand mismatch rather than plaque rupture. Stroke is a medical emergency in which blood flow to part of the brain is interrupted. Because brain tissue is extremely sensitive to oxygen deprivation, rapid recognition and treatment are critical. Even a delay of minutes can affect recovery. Warning signs are summarized in the BEFAST-Plus Table.

Stroke in younger adults is increasing. Although traditional vascular risk factors remain important contributors to cerebrovascular disease, drugs of abuse are newly recognized as significant preventable stroke causes.

Methamphetamine and cocaine use clearly increase strokes and stroke risks. Cannabis has a more modest effect, but evidence supporting the association with ischemic stroke among frequent users is mounting.

Substance use should be considered an important modifiable risk factor for stroke and myocardial infarction. Prevention and early intervention can prevent these complications caused by methamphetamine, cocaine, and cannabis.

Ritson M, Markus HS, Harshfield EL. Does illicit drug use increase stroke risk? A systematic review, meta-analyses, and Mendelian randomization analysis. Int J Stroke. 2026 Jan 21:17474930261418926. doi: 10.1177/17474930261418926. Epub ahead of print. PMID: 41566428.

Nehme A, Li L. The rising incidence of stroke in the young: Epidemiology, causes and global impact. Int J Stroke. 2026 Jan;21(1):14-23. doi: 10.1177/17474930251362583. Epub 2025 Jul 18. PMID: 40682212; PMCID: PMC12743130.

Cheng YC, Ryan KA, Qadwai SA, Shah J, Sparks MJ, Wozniak MA, Stern BJ, Phipps MS, Cronin CA, Magder LS, Cole JW, Kittner SJ. Cocaine Use and Risk of Ischemic Stroke in Young Adults. Stroke. 2016 Apr;47(4):918–922. doi: 10.1161/STROKEAHA.115.011417. Epub 2016 Mar 10. PMID: 26965853; PMCID: PMC6128285.

Ekker MS, Boot EM, Singhal AB, Tan KS, Debette S, Tuladhar AM, de Leeuw FE. Epidemiology, aetiology, and management of ischaemic stroke in young adults. Lancet Neurol. 2018 Sep;17(9):790–801. doi: 10.1016/S1474-4422(18)30233-3. PMID: 30129475.

Tsatsakis A, Docea AO, Calina D, Tsarouhas K, Zamfira LM, Mitrut R, Sharifi-Rad J, Kovatsi L, Siokas V, Dardiotis E, Drakoulis N, Lazopoulos G, Tsitsimpikou C, Mitsias P, Neagu M. A Mechanistic and Pathophysiological Approach for Stroke Associated with Drugs of Abuse. J Clin Med. 2019 Aug 23;8(9):1295. doi: 10.3390/jcm8091295. PMID: 31450861; PMCID: PMC6780697.

Rendon LF, Malta S, Leung J, Badenes R, Nozari A, Bilotta F. Cocaine and Ischemic or Hemorrhagic Stroke: A Systematic Review and Meta-Analysis of Clinical Evidence. J Clin Med. 2023 Aug 10;12(16):5207. doi: 10.3390/jcm12165207. PMID: 37629248; PMCID: PMC10455873.

Westover AN, McBride S, Haley RW. Stroke in young adults who abuse amphetamines or cocaine: a population-based study of hospitalized patients. Arch Gen Psychiatry. 2007 Apr;64(4):495–502. doi: 10.1001/archpsyc.64.4.495. PMID: 17404126.

Hemphill K, Tierney S, Tirschwell D, Davis AP. A review of methamphetamine use and stroke in the young. Front Neurol. 2024 Apr 24;15:1397677. doi: 10.3389/fneur.2024.1397677. PMID: 38721123; PMCID: PMC11076881.

Testai FD, Gorelick PB, Aparicio HJ, Filbey FM, Gonzalez R, Gottesman RF, Melis M, Piano MR, Rubino T, Song SY; American Heart Association Stroke Brain Health Science Subcommittee of the Stroke Council; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; Council on Lifestyle and Cardiometabolic Health; and Council on Peripheral Vascular Disease. Use of Marijuana: Effect on Brain Health: A Scientific Statement From the American Heart Association. Stroke. 2022 Apr;53(4):e176–e187. doi: 10.1161/STR.0000000000000396. Epub 2022 Feb 10. PMID: 35142225.

Parekh T, Pemmasani S, Desai R. Marijuana Use Among Young Adults (18-44 Years of Age) and Risk of Stroke: A Behavioral Risk Factor Surveillance System Survey Analysis. Stroke. 2020 Jan;51(1):308–310. doi: 10.1161/STROKEAHA.119.027828. Epub 2019 Nov 11. PMID: 31707926.

Rasing A, Hilkens NA, Leeuw FE. Young stroke: An update on epidemiology, emerging risk factors, and future research directions. Int J Stroke. 2026 Jan;21(1):6–13. doi: 10.1177/17474930251400524. Epub 2026 Jan 2. PMID: 41482721; PMCID: PMC12764685.

There was a problem adding your email address. Please try again.

By submitting your information you agree to the Psychology Today Terms & Conditions and Privacy Policy

© Psychology Today