Cannabidiol (CBD) is widely available and marketed as having therapeutic properties. Over-the-counter CBD is unregulated, many of the therapeutic claims lack scientific support, and controversy exists as to the safety of CBD-liver interaction. The study aims were to compare the pharmacokinetics of commercial CBD and CBD metabolites following the ingestion of five different CBD formulations, determine the influence of CBD on food induced thermogenesis, determine the influence of food on CBD pharmacokinetics, and determine the influence of CBD on markers of liver function. Fourteen males (body mass index ³ 25 kg/m2) were studied in a placebo-controlled, randomized, crossover design. On five occasions, different CBD formulations were ingested (one per visit). On two additional occasions, CBD or placebo was ingested following a meal. CBD servings were standardized to 30 mg. Considerable pharmacokinetic variability existed between formulations; this pharmacokinetic variability transferred to several of the metabolites. CBD did not influence food induced thermogenesis but did favorably modify early insulin and triglyceride responses. Food appreciably altered the pharmacokinetics of CBD. Finally, CBD did not evoke physiologically relevant changes in markers of liver function. Collectively, these data suggest that consumers should be aware of the appreciable pharmacokinetic differences between commercial CBD formulations, CBD is unlikely to influence the caloric cost of eating but may prove to be of some benefit to initial metabolic responses, consuming CBD with food alters the dynamics of CBD metabolism and increases systemic availability, and low-dose CBD probably does not represent a risk to normal liver function.

The purpose of the study was to describe and compare the pharmacokinetics of five commercial edible marijuana products, determine the influence of body composition on pharmacokinetics, and, in light of epidemiology suggesting marijuana may offer diabetes protection, explore the influence of edible marijuana on glucose tolerance. Seven regular users of marijuana self-administered five edible products in a randomized crossover design; each product contained 10 mg of delta-9-tetrahydrocannabinol (THC). Thirty minutes following marijuana ingestion, participants imbibed a 75 g glucose beverage. Time-to-peak plasma THC concentration ranged between 35 and 90 min; maximal plasma THC concentration (Cmax) ranged between 3.2 and 5.5 ng/mL. Differences between products in plasma THC concentration during the first 20–30 min were detected (p = 0.019). Relations were identified between body composition and pharmacokinetic parameters for some products; however, none of these body composition characteristics were consistently related to pharmacokinetics across all five of the products. Edible marijuana had no effect on oral glucose tolerance compared with a marijuana-free control (Matsuda Index; p > 0.395). Commercially available edible marijuana products evoke different plasma THC concentrations shortly after ingestion, but do not appear to influence acute glucose regulation. These data may allow recreational marijuana users to make informed decisions pertaining to rates of edible marijuana ingestion and avoid overdose.

Introduction:The release of interleukin (IL)-6 from contracting skeletal muscle is thought to contribute to some of the health benefits bestowed by exercise. This IL-6 response seems proportional to exercise volume and to lactate production. Unfortunately, high volumes of exercise are not feasible for all people. Caffeine augments the magnitude of increase in circulating IL-6 in response to high-intensity and long-duration exercise. Caffeine also increases circulating concentrations of lactate during exercise. We hypothesized that caffeine, ingested before short-duration, moderate-intensity exercise, would lead to greater circulating concentrations of lactate and IL-6 in a study population comprising both male and female individuals. Methods: Twenty healthy adults (10 men and 10 women age 25 ± 7 yr (mean ± SD)) completed 30 min of moderate-intensity cycle ergometer exercise, at an intensity corresponding to 60% peak oxygen uptake, after ingesting either caffeine (6 mg•kg −1 ) or placebo. Arterialized-venous blood was collected throughout each of the exercise sessions. Results: Compared with placebo, caffeine increased circulating concentrations of lactate at the end of exercise (5.12 ± 3.67 vs 6.45 ± 4.40 mmol•L −1 , P < 0.001) and after 30 min of inactive recovery (1.83 ± 1.59 vs 2.32 ± 2.09 mmol•L −1 , P = 0.006). Circulating IL-6 concentrations were greatest after 30 min of inactive recovery (P < 0.001) and higher with caffeine (2.88 ± 2.05 vs 4.18 ± 2.97, pg•mL −1 , P < 0.001). Secondary analysis indicated sex differences; caffeine increased the IL-6 response to exercise in men (P = 0.035) but not in women (P = 0.358). Conclusions: In response to moderate-intensity exercise, caffeine evoked greater circulating lactate concentrations in men and women but only increased the IL-6 response to exercise in men. These novel findings suggest that for men unwilling or unable to perform high-intensity and/or long-duration exercise, caffeine may augment the health benefits of relatively short, moderate-intensity exercise.

The release of interleukin 6 (IL‐6) from contracting skeletal muscle is thought to contribute to some of the health benefits bestowed by exercise. This IL‐6 response appears proportional to exercise volume. Unfortunately, high volumes of exercise are not feasible for all people. Caffeine augments the magnitude of increase in circulating concentration of IL‐6 in response to high‐intensity and long‐duration exercise, in men. Caffeine is also known to increase circulating concentrations of lactate during exercise. One of the mechanisms thought to contribute to IL‐6 release from exercising skeletal muscle is lactate production. We hypothesized that caffeine, ingested prior to moderate‐intensity exercise, would lead to greater circulating concentrations of lactate and IL‐6 in a study population comprising both men and women. 15 healthy adults (9 males and 6 females, aged 26±7 years, (mean ± SD)) completed 30‐minutes of moderate‐intensity cycle ergometer exercise, equivalent to the ventilatory threshold, after ingesting either caffeine (6 mg/kg) or placebo. Arterialized‐venous blood was collected throughout each of the exercise sessions. Compared with placebo, caffeine increased end‐exercise circulating concentrations of lactate (5.72±3.95 vs. 7.14±4.66 mmol/L, P<0.001) but not end‐exercise IL‐6 (1.84±0.97 vs. 2.37±1.04 pg/mL, P=0.139). However, when women were excluded from the analysis, caffeine augmented (P=0.04) the magnitude of increase of end‐exercise IL‐6 concentration (1.80±0.86 vs. 2.57±1.21 pg/mL); this effect was further exaggerated after 30‐minutes of inactive recovery (3.81±2.32 vs. 5.06±3.22 pg/mL). Noteworthy, caffeine evoked greater end‐exercise lactate concentrations in data sets containing only men (P=0.02) and only women (P=0.002) but did not influence the IL‐6 response in women (P=0.94). Our preliminary data imply that in men unable/unwilling to perform high‐intensity and/or long duration exercise, caffeine may potentially enhance the IL‐6 mediated health benefits of relatively short, moderate intensity exercise.