Table. Somatic consequences of non-medicinal cannabis use.
Region and symptoms or consequences | Study type, evidence level, statistical risk (reference) |
---|---|
Mouth and throat | |
Gingival proliferation, inflammation of oral mucosa (stomatitis) or uvula (uvulitis) | Case reports (16), no statistical analysis |
Respiratory tract | |
Irritation of the respiratory system, damage to the bronchioles, and chronic bronchitis | Meta-analysis (17); (review [e24]; cohort study [e25]): association between cannabis consumption and cough (OR = 2.00; 95% CI: 1.32–3.01) (evidence level: 1b) |
Dyspnea, hoarseness, chronic-obstructive lung disease, or pharyngitis with combined consumption of cannabis and tobacco; the findings for tobacco and cannabis inhalation do not go in the same direction; several cohort studies with differing results | Systematic review (e24, e26) (evidence level: 2a); case report (e27) |
Life-threatening respiratory problems (experimentally unproved; in contrast, review points to a bronchodilatory effect) | Systematic reviews (e28, e29) (evidence level: 2a) |
Emphysema: effects of cannabis controversial | Systematic reviews (17, e29, e30) (evidence level: 2a) |
Gastrointestinal tract | |
Worsening of hepatic steatosis (particularly in hepatitis C) with potential steatogenic and fibrotic effects | Systematic review (18), cohort study (e31) (evidence level: 2b); in cannabis users (N = 270) daily cannabis consumption predicted more rapid progression of hepatic fibrosis (>0.15) (OR = 3.6; 95% CI: 1.5–7.5). |
Cannabis-hyperemesis syndrome: repeated episodes of nausea and vomiting | Case series (e32), review of these case reports (e33) (evidence level: 4) |
Cardiovascular system | |
Tachycardia, increased BP, arrhythmias up to and including atrial fibrillation | Reviews (19, 20), case reports, reviews of the cases (e.g., e34, e35; evidence level: 4) |
Deaths due to cerebral and cardiac ischemia | Case reports (e36, e37), case–control study: increased risk of MI up to 60 min after cannabis consumption (OR = 4.8; 95% CI: 2.4–9.5) (e38) (evidence level: 1b); part of prospective study (e39) (evidence level: 1b): in n = 1913 patients (follow-up time: 3.8 years) there was a dose-dependent relationship between cannabis consumption and mortality after MI: cannabis consumption (<1 x per week) was connected with an hr of 2.5 (95% ci: 0.9–7.3), and the hr for weekly consumption was 4.2 (95% ci: 1.2–14.3). the age- and sex-adjusted hr for persons who had ever used cannabis was 1.9 (95% ci: 0.6–6.3) for cardiovascular and 4.9 (95% ci: 1.6–14.7) for other causes of death |
Effects on skin and mucosae | |
Conjunctivitis, inflammation of posterior palate | Individual cases, review (18) (evidence level: 4) |
Isolated cases: urticaria, pruritus, excoriative prurigo, type-1 allergies (asthmatic and anaphylactic reactions) | Case reports (23), review (18) (evidence level: 4) |
Consequences for hormone metabolism | |
Elevated visceral fat deposition and insulin resistance | Case–control cohort study (e40): cannabis users had a higher proportion of abdominal fat, while other parameters (glucose, insulin, cholesterol, LDL, triglycerides) showed no difference. Adipocyte resistance to insulin and oral glucose tolerance results were lower (p<0.05) (evidence level: 2b) |
Comatose states | |
Individual cases of comatose states in children who had ingested cannabis | Case reports (e41) (evidence level: 4) |
Overall mortality | |
Some unfavorable effects of cannabis use (e.g., increased risk of road traffic accidents and tumors) can influence overall mortality | Systematic review of studies (12, 21, 22), some of them with low case numbers; no epidemiological findings (evidence level: 3a) |
Consequences for the reproduction system | |
In women: adverse effects on frequency of menstrual cycle, oogenesis ("maturation of oocytes"), implantation of embryo, development of brain in embryo, increased risk of birth complications, decreased birth weight of child | Systematic reviews (24, 25), cohort studies (e42, e43) (evidence level: 2a): low birth weight (OR = 1.7; 95% CI: 1.3–2.2), preterm births (OR = 1.5; 95% CI: 1.1–1.9), reduced gestation (OR = 2,2; 95% CI: 1.8–2.7), admission to neonatal intensive care unit (OR = 2.0; 95% CI: 1.7–2.4) |
In children of women exposed to cannabis during pregnancy: increased impulsiveness, impairment of learning, memory, and executive functions, particularly following exposure in the third trimester | Systematic review without statistical analysis, cohort study (e44) (evidence level: 3a) |
In men: ejaculation problems, decreased sperm count, libido loss or impotence | Systematic review (25) (evidence level: 3a) |
Tumor diseases | |
Nasopharyngeal tumors (independent of tobacco consumption) | Case–control cohort study (e45) (evidence level: 2b): for intensive cannabis consumption (>2000 x in total) the OR was 2.62 (95% CI: 1.00–6.86) after statistical control for tobacco consumption |
Increased risk of lung tumors, although simultaneous tobacco consumption is a potential confounding factor | Cohort study (e46) (evidence level: 2b): in cannabis users the OR for lung tumors was 2.4 after statistical ‧adjustment for various factors, e.g., tobacco consumption (95% CI: 1.6–3.8). If the amount of tobacco consumed is taken into account (cigarettes/d), the risk (compared with non-users of cannabis) rises to 10,9 (95% CI: 6.0–19.7). Case–control study (e47) (evidence level: 2b): the risk of a lung tumor rose by 8% with every year of cannabis use (95% CI: 2.00–15.00), after controlling for tobacco consumption. The risk of a lung tumor rose by 7% with every year of tobacco consumption (95% CI: 5–9) after controlling for cannabis use. |
Tumors of head and neck | Systematic reviews (18), cohort study (e48) (evidence level: 2b): cannabis smoke is carcinogenic and cannabis use can cause tumors of the upper respiratory tract, the GIT, the lungs, and the bladder; cohort case–control study (e48): n = 75 patients and n = 319 controls; cannabis consumption (even at a high level) was not associated with an increased risk of head and neck tumors (after adjusting for potential confounding variables) (evidence level: 2b). |
Effects on the immune system | |
Immunosuppressive effect in a number of autoimmune diseases or inflammatory processes (e.g., multiple sclerosis, atherosclerosis, asthma, rheumatic, gastrointestinal, and liver diseases) | Basic science–oriented review without statistical analysis (26) (evidence level: 4) |
Evidence level according to Oxford CEBM classification; CI: confidence interval of OR; OR: odds ratio; LDL: low-density lipoprotein; HR: hazard ratio; MI: myocardial infarction; GIT: gastrointestinal tract; BP: blood pressure; d: day