Cannabis and Cannabinoids (PDQ®): Complementary and alternative medicine - Health Professional Information [NCI] - Human / Clinical Studies
When Cannabis is ingested by mouth, there is a low (6%–20%) and variable oral bioavailability.[1,2] Peak plasma concentrations of delta-9-tetrahydrocannabinol (THC) occur after 1 to 6 hours and remain elevated with a terminal half-life of 20 to 30 hours. Taken by mouth, delta-9-THC is initially metabolized in the liver to 11-OH-THC, a potent psychoactive metabolite. When inhaled, cannabinoids are rapidly absorbed into the bloodstream with a peak concentration in 2 to 10 minutes, declining rapidly for a period of 30 minutes and with less generation of the psychoactive 11-OH metabolite.
The initial approach to the patient is to evaluate the following parameters:
Detection of a monoclonal (or myeloma) protein (M protein) in the serum or urine.
Detection of more than 10% of plasma cells on a bone marrow examination.
Detection of lytic bone lesions or generalized osteoporosis in skeletal x-rays.
Presence of soft tissue plasmacytomas.
Serum albumin and beta-2-microglobulin levels.
Detection of free kappa and lambda serum immunoglobulin light...
Cannabinoids are known to interact with the hepatic cytochrome P450 enzyme system.[3,4] In one study, 24 cancer patients were treated with intravenous irinotecan (600 mg, n = 12) or docetaxel (180 mg, n = 12), followed 3 weeks later by the same drugs concomitant with medicinal Cannabis taken in the form of an herbal tea for 15 consecutive days, starting 12 days before the second treatment. The administration of Cannabis did not significantly influence exposure to and clearance of irinotecan or docetaxel, although the herbal tea route of administration may not reproduce the effects of inhalation or oral ingestion of fat-soluble cannabinoids.
A number of studies have yielded conflicting evidence regarding the risks of various cancers associated with Cannabis use.
A pooled analysis of three case-cohort studies of men in northwestern Africa (430 cases and 778 controls) showed a significantly increased risk of lung cancer among tobacco smokers who also inhaled Cannabis.
A large retrospective cohort study of 64,855 men aged 15 to 49 years from the United States found that Cannabis use was not associated with tobacco-related cancers and a number of other common malignancies. However, the study did find that, among nonsmokers of tobacco, ever having used Cannabis was associated with an increased risk of prostate cancer.
A population-based case-control study of 611 lung cancer patients revealed that chronic low Cannabis exposure was not associated with an increased risk of lung cancer or other upper aerodigestive tract cancers and found no positive associations with any cancer type (oral, pharyngeal, laryngeal, lung, or esophagus) when adjusting for several confounders, including cigarette smoking.
A systematic review assessing 19 studies that evaluated premalignant or malignant lung lesions in persons 18 years or older who inhaled marijuana concluded that observational studies failed to demonstrate statistically significant associations between marijuana inhalation and lung cancer after adjusting for tobacco use.
With a hypothesis that chronic marijuana use produces adverse effects on the human endocrine and reproductive systems, the association between marijuana use and incidence of testicular germ cell tumors (TGCTs) has been examined.[9,10,11] Three population-based case-control studies report an association between marijuana use and elevated risk of TGCTs, especially nonseminoma or mixed-histology tumors.[9,10,11] However, the sample sizes in these studies were inadequate to address marijuana dose by addressing associations with respect to recency, frequency, and duration of use. These early reports of marijuana use and TGCTs establish the need for larger, well-powered, prospective studies, especially studies evaluating the role of endocannabinoid signaling and cannabinoid receptors in TGCTs.