From: The relationship between cannabis and anorexia nervosa: a scoping review
Author/year | Study design | Participants | Methods, interventions, & observations | Outcomes of interest |
---|---|---|---|---|
Andries et al., 2014 (a) [27] | Crossover RCT (Parent Trial) | 24 women with AN | Participants were divided into 2 groups and given either 5 mg of dronabinol per day for 4 weeks or a placebo. After a 4-week break period, participants received the opposite intervention for 4 weeks. Measured weight weekly and Eating Disorder Inventory scores during the 1st and 4th week of each intervention period | Benefits: • Weight gain of 1.00 kg (95% CI: 0.40–1.62) during dronabinol vs. 0.34 kg (95% CI: 29.14-0.82) during placebo (p = 0.03 above placebo) Harms/Null Effects: • NS differences in eating disorder inventory scores |
Andries et al., 2014 (b) [28] | Report from Andries et al., 2014 (a) Parent Trial | 24 women with AN | Reported intensity and duration of PA measured through accelerometers worn by participants daily | Harms/Null Effects: • Increased moderate to hard PA intensity during dronabinol compared to placebo in inpatients (3,958.3 ± 789.2 accelerometer counts per minute vs. 3,732.6 ± 936.1 accelerometer counts per minute respectively, p = 0.04) • NS differences in PA intensity in outpatients • NS differences in PA duration in inpatients • Increased moderate to hard PA duration during dronabinol compared to placebo in outpatients (0.9 ± 0.6 h/day vs. 0.8 ± 0.6 h/day respectively, p = 0.02) |
Andries et al., 2015 [29] | Report from Andries et al., 2014 (a) Parent Trial | 24 women with AN | Reported bioactive IGF, IGF-1, IGFBP-2 and -3, leptin, and adiponectin measured through overnight fasted serum and cortisol measured through 24-h urine samples on the last day of each intervention period | Harms/Null Effects: • NS changes in bioactive IGF, IGF-1, or IGFBP -2/-3 • NS changes in leptin after controlling for age, weight, and cortisol • Decreased adiponectin (naturally transformed regression coefficient: -0.07, 95% CI: -0.11 to 0.04, p < 0.01) in a model including leptin during dronabinol • Decreased cortisol during dronabinol (naturally transformed regression coefficient: -0.19, 95% CI: -0.37 to 0.05, p = 0.04) |
Avraham et al., 2017 [30] | Non-randomized study | 10 females with AN | All participants received 1 mg THC for 1 week, then 2 mg THC for 3 weeks. Measured BMI, Eating Disorder Inventory, Eating Attitude Test, Beck Depression Inventory, Body Shape Questionnaire, and Spielberger State-Trait Anxiety Inventory at baseline and at the end of the intervention period | Benefits: • Decreased asceticism (10.00 ± 2.46 vs. 7.06 ± 1.61, p = 0.049) • Decreased depression (3.12 vs. 2.50, p < 0.049) • Increased body care (19.22 ± 1.87 vs. 20.22 ± 1.79, p = 0.02) Harms/Null Effects: • NS changes in BMI • NS changes in anxiety |
Graap et al., 2017 [31] | Case report | 1 male with AN | 7.5–15 mg dronabinol (increased dose weekly) during a 6-week period. Measured BMI weekly, steps through a pedometer daily, PA urge through a subjective 0–6 scale daily, Eating Disorder Examination questionnaire at baseline and at the end of the intervention, and leptin and cortisol through dexamethasone-suppression-tests at baseline and at week 5 of the intervention | Benefits: • Weight gain after dronabinol (BMI 19.5 kg/m2 pretreatment vs 21.0 kg/m2 posttreatment) • Decreased ED symptoms after dronabinol (sum score 5.2 pretreatment vs. 2.0 posttreatment) • Decreased PA levels after dronabinol (32,510 steps per day pretreatment vs. 17,493 steps per day posttreatment) • Decreased PA urge after dronabinol (average urge to move rating of 5 pretreatment vs. 3.5 posttreatment) Harms/Null Effects: • No changes in leptin • Dcreased cortisol levels during dronabinol (1.7 mg/dL pretreatment vs. < 1.0 mg/dL posttreatment) |
Hjorthøj et al., 2019 [35] | Retrospective cohort study | *Number of participants with AN could not be determined | Investigated polygenic risk scores for AN and CUD from participants followed from birth (between years 1981–2001) until 2017 | Harms: • Highest polygenic risk scores for AN were associated with CUD (Hazard Ratio = 1.41, 95% CI 1.27–1.56) |
Ihm et al., 2023 [36] | Retrospective cohort study | 16,992 individuals with AN, 55,525 HC *Gender/sex could not be determined | Investigated polygenic risk scores for AN and CUD from participants recruited between 2006–2010 | Null effects: • NS interconnections between the polygenic risk scores for AN and polygenic risk scores for CUD |
Brewerton et al., 2016 [37] | Case report | 1 Woman with BPAN | Patient presented to a treatment center with AN relapse symptoms. A urinary drug test, physical exam, mental status exam, and laboratory analysis was taken upon admission | Harms: • Patient reported using cannabis daily for at least 1 year and chronically for at least 7 years • Patient reported vomiting, which was originally mistaken as a relapse • Patient reported relief in vomiting symptoms after hot showers, which lead to the diagnosis of CHS |
Karayilan et al., 2013 [38] | Case report | 1 Woman with BPAN | Patient presented to a treatment center with weight loss, restrictive eating, and nervosity. Physical examination and review of life and medical history were taken upon admission | Harms: • Patient reported using cannabis daily for about 3 years • Decrease in BMI over the course of 3 years of daily cannabis use (22.08 kg/m2 at the start of cannabis use vs 15.6 kg/m2 after 3 years) • Patient reported engagement in postprandial compensatory behaviors after using cannabis |