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Similarly, the majority of dronabinol-treated patients (64%) reported increased appetite, whereas the majority of patients receiving placebo reported either decreased appetite (50%) or no change (20%). Total caloric intake per kilogram body weight did not differ significantly between treatment groups but did increase in both groups compared to baseline. Furthermore, compared to placebo, dronabinol-treated patients reported an increase in their protein intake as a proportion of total energy. According to the study authors, negative psychoactive effects were minimized by starting patients at a low dose (2.5 mg Δ9-THC once a day, for three days) followed by gradual dose escalation (up to a maximum of 7.5 mg dronabinol per day).
Significantly higher scores were also reported by occasional users on measures of “difficulty concentrating” and “altered sense of time” . The authors found that cannabis smoking significantly impaired psychomotor function up to 3.5 h after smoking a 6.8% THC cigarette. Cannabis smoking appeared to impair psychomotor function to a greater degree in occasional smokers compared to frequent smokers, raising the possibility of tolerance to some of the impairing effects of cannabis in frequent smokers.
This section covers human pharmacokinetics of smoked and vapourized cannabis, oral preparations including prescription cannabinoid medicines such as dronabinol (Marinol®) and nabiximols (Sativex®), and other routes of administration (e.g. rectal, topical). See Figure 2 for a graphical representation of the pharmacokinetics of THC. The endocannabinoid system is an ancient, evolutionarily conserved, and ubiquitous lipid signaling system found in all vertebrates, and which appears to have important regulatory functions throughout the human bodyReference 1.
Extreme anxiety was also observed at the 20 mg dose in a number of patients. Frequent adverse effects, likely caused by cannabis, included drowsiness, fatigue, dizziness, dry mouth, nausea and cognitive effects that were generally mild to moderate in severity and generally well tolerated. Serious adverse effects included urinary tract infection, head injury, and interstitial lung disease , delirium , and suicidal ideation and disorientation . Limitations of the findings relate mainly to the short duration and small sample sizes of the included trials and the modest effect sizes. RCTs of longer duration and with a larger sample size are needed to confirm efficacy signals reported by the smaller “proof of concept” studies, and for longer term monitoring of patients to assess long-term safety.
In addition, and as seen with tobacco smoke, cannabis smoke has the potential to induce CYP1A2 thereby increasing the metabolism of xenobiotics biotransformed by this isozyme such as theophyllineReference 473 or the anti-psychotic medications clozapine or olanzapineReference 474. Further detailed information on drug-drug interactions can be found in Section 6.2. Xenobiotics are not only metabolized by CYPs but they also modulate the expression level and activity of these enzymes; CYPs are therefore a focal point in drug-drug interactions and adverse drug reactionsReference 466.
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No significant adverse effects were noted in those using cannabis, with the exception of a reported reduction in memory in about 20% to 40% of the study sample. The reported decrease in memory among a proportion of the study sample could be a function of cannabis use along with the use of other medications such as opioids, anti-depressants, or even vary with age. Limitations of the study included its observational nature, the lack of an appropriate control group, and the reliance on self-report. An uncontrolled, open-label extension study of an initial five-week randomized trial of nabiximols in patients with MS and central neuropathic pain reported the absence of pharmacological tolerance to cannabinoid-induced analgesia, even after an almost two-year treatment period in a group of select patientsReference 327. Another long-term, open-label extension study of nabiximols in patients with spasticity caused by MS echoed these findings, also reporting the absence of pharmacological tolerance to the anti-spastic effects after almost one year of treatmentReference 325. A multi-centre, prospective, cohort, long-term safety study of patients using cannabis as part of their pain management regimen for chronic non-cancer pain reported small and non-significant increases in daily dose over a one-year study periodReference 216.
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Although in vitro studies show that THCV binds with relatively high affinity at CB1 receptorsReference 112Reference 748, THCV does not appear to be a potent CB1 receptor agonistReference 112Reference 263Reference 748. Instead, experimental studies suggest THCV acts more like a CB1 receptor antagonist and a potent CB2 receptor partial agonistReference 18Reference 112Reference 263Reference CBD-Öl-Tinktur FAQs 748Reference 749. At higher doses however, THCV appears to have some agonist activity at the CB1 receptorReference 18. Furthermore, in vitro studies suggest THCV has some anti-epileptiform effects at micromolar concentrationsReference 112 and in vivo studies suggest THCV (0.25 mg/kg) has some limited anti-convulsant effects in one mouse model of epilepsyReference 112Reference 266.
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In general, the findings from studies examining the effects of cannabis exposure on brain structure and function are mixed, mainly owing to the cross-sectional nature of the studies, the lack of consistent and extensive control for confounding variables and small sample sizesReference 1558. The long-term effects of cannabis exposure on cognition continue to be the subject of some debate. Some studies report a positive association between long-term cannabis consumption and cognitive deficitsReference 150Reference 151Reference 1549-Reference 1551, or suggest that some cognitive deficits persist after prolonged abstinence Reference 150Reference 235Reference 552-Reference 554Reference 1547Reference 1552. However, other studies did not find an association between cannabis use and certain long-term cognitive declineReference 554Reference 1552Reference 1553. One epidemiological study in relatively young clients of a health maintenance organization found an increased incidence of prostate cancer in those men who smoked cannabis and other non-tobacco materialsReference 358.
To further complicate the matter, THC interacts with numerous receptors in the body which are not considered part of the classical definition of the ECS. Research on D-10 THC is almost non-existent, with only very few studies investigating its nature, none of which involves humans. D-10 also can’t really be found in the cannabis plant in any interesting quantities, but can be produced in a lab synthetically, again using CBD and chemically converting it. The main reason for the sudden hype around D-8 is to do with supply and demand.
Another vapourization study also with the Volcano®, using the same cued-puff procedure, used 400 mg of dried cannabis of three variable strengths (1%, 4% and 7% THC or 4, 16 and 28 mg THC per dosing session)Reference 599. In another study, patients followed a similar “cued-puff” procedure and inhaled 4 puffs, followed by an additional round of between 4 and 8 puffs 2 h later for a total of between 8 and 12 puffs over a 2 h periodReference 598. Pharmacokinetic tolerance has also been documented to occur with repeated cannabinoid administration, but apparently occurs to a lesser degree than pharmacodynamic toleranceReference 507. Peak plasma values of the psycho-inactive metabolite, 11-nor-9-carboxy THC, occur 1.5 to 2.5 h after smoking, and are about one third the concentration of parent THCReference 475.
Because marijuana is still illegal at the federal level, doctors give recommendations or orders but are not legally permitted to give prescriptions. You can find state-by-state information regarding what conditions qualify for medical marijuana. Cannabinoid receptors are located throughout your body and help determine how cannabinoids affect you. So, you should pick of these male enhancement pills to bring the thrill back to your sex life by uplifting your sexual stamina. Above all, a supplement means nothing without proper lifestyle choices, and these need to be taken seriously.
This retrograde signaling mechanism permits the regulation of neurotransmission in a precise spatio-temporal mannerReference 3. In immune cells, activation of CB2 receptors inhibits cytokine/chemokine release and neutrophil and macrophage migration, giving rise to complex modulatory effects on immune system functionReference 19. Preliminary evidence from surveys suggests an association between use of ultra-high-potency cannabis concentrate products (e.g. butane hash oil, BHO) and higher rates of self-reported anxiety and depression and other illicit drug use as well as higher levels of physical dependence than with high-potency herbal cannabis. Epidemiological studies suggest an association between (THC-predominant) cannabis use, especially chronic, heavy use and the onset of anxiety, depressive and bipolar disorders, and the persistence of symptoms related to PTSD, panic disorder, depressive disorder, and bipolar disorder. Evidence from clinical studies suggests a dose-dependent, bi-phasic effect of THC on anxiety and mood, where low doses of THC appear to have an anti-anxiety and mood-elevating effect whereas high doses of THC can produce anxiety and lower mood.
If you want the very best of both worlds, there are many educational gaming activities for kids. Reference 1368Marconi A, Di Forti M, Lewis CM, Murray RM, Vassos E. Meta-analysis of the association between the level of cannabis use and risk of psychosis. Evidence from epidemiological studies also suggests a dose-dependent effect between cannabis use and suicidality, especially in men. Are Vegan CBD Gummy Bears suitable for children? COMT regulates the breakdown of catecholamines, including neurotransmitters such as dopamine, epinephrine, and norepinephrineReference 1120. A missense mutation at codon 158 in the COMT gene, causing a substitution to the methionine at the positional valine , results in an enzyme with decreased activity and correspondingly slower dopamine catabolismReference 1636Reference 1637.
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Nevertheless, animal models of OA are useful in understanding the potential therapeutic effects of cannabis and cannabinoids. A randomized, placebo-controlled, double-blind, crossover study of 12 healthy cannabis-naïve volunteers administered CBD Sprays a single oral dose of 20 mg Δ9-THC reported a lack of a significant analgesic effect following exposure to a multi-model pain test battery Reference 272. In addition, significant hyperalgesia was observed in the heat pain test.
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Increasing evidence suggests an important role for the ECS in the regulation of stress, mood, and psychiatric disordersReference 167Reference 1010Reference 1011. A preliminary clinical study assessing the effectiveness of nabiximols (Sativex®) for pain caused by RA reported a modest but statistically significant analgesic effect on movement and at rest, as well as improvement in quality of sleepReference 383. Administration of nabiximols was well tolerated and no significant toxicity was observed. The mean daily dose in the final treatment week was 5.4 pump actuations (equivalent to 14.6 mg THC and 13.5 mg CBD/day, treatment duration was three weeks). The differences observed were small and variable across the participants.
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In recent years, CBD started gaining popularity, eventually leading to the creation of an entire industry, with countless CBD infused products available, from oils, to bath bombs, dog treats and even infused fabrics. You can smoke, vape, apply topicals to your skin, or consume edibles. The way you take marijuana is about personal choice and the type of pain you are experiencing.
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Human spermatozoa have been shown to express functional CB1 and CB2 receptorsReference 1471. CB1 and CB2 receptors have been identified on the plasma membrane of human spermatozoa and the CB1 receptor has been further shown to be localized to the plasma membrane of the acrosomal region, although also to the midpiece, and the sperm tailReference 1471Reference 1472. The CB2 receptor on the other hand has been shown to be localized in the post-acrosomal region, midpiece and sperm tailReference 1471Reference 1473Reference 1474.
THCA at doses of 0.5 and 0.05 mg/kg (i.p.) reduced behaviours modelling acute nausea and vomiting, and at a dose of 0.05 mg/kg (i.p.) reduced behaviours modelling anticipatory nausea in animal models of acute and anticipatory nausea, and vomitingReference 623. Among the goals of palliative care described by the WHO are relief from pain and other distressing symptoms, and the enhancement of quality of life Reference 604. While integration of cannabis into mainstream medical use can be characterized as extremely cautious, its use appears to be gaining some ground in palliative care settings where the focus is on individual choice, patient autonomy, empowerment, comfort and especially QoLReference 605. Nevertheless, establishing the effectiveness of cannabis as a viable treatment option in a palliative care context requires a careful assessment of its effects in a wide range of conditions; such evidence is not yet abundant and further research is neededReference 606. Certain patient populations (e.g. the elderly or those suffering from pre-existing psychiatric disease) may also be more sensitive or susceptible to experiencing adverse psychotropic, cognitive, psychiatric or other effectsReference 607Reference 608. The observed regional variations in cellular adaptations to THC in the brain may also generalize to other tissues or organs, explaining why tolerance develops to some of the effects of cannabis and cannabinoids but not to other effects.
“The toxicity of D-9 THC is very low compared to other recreational and pharmaceutical drugs…It has been calculated that a lethal dose in a 70 kg human would be approximately 4 grams, and that such a dose could not be realistically achieved in a human following oral consumption, smoking or vaporizing the substance”. Many states that disagreed with the federal approach to cannabis started their own medical marijuana programs, and made it accessible for patients. This eventually led to the full legalization of cannabis in some states.
However, these CB1 receptor-mediated responses may be surmountable by the effects of local growth-promoting effectors at the growth cone and the balance between the effects of endocannabinoids and growth factors would determine the overall outcome of neuronal development. The CB1 receptor appears also to act as a negative regulator of synaptogenesis and in doing so can also affect the fate of neuronal communicationReference 60. For example, a study conducted in pregnant mice using a low dose of THC has been shown to alter the expression level of 35 proteins in the fetal cerebrumReference 62. Furthermore this study concretely identified a specific molecular target for THC in the developing CNS whose modifications can directly and permanently CBD + THC Gummies impair the wiring of neuronal networks during corticogenesis by enabling formation of ectopic neuronal filopodia and altering axonal morphologyReference 62. Another in vitro study with retinal ganglion cell explants showed that CBD decreased neuronal growth cone size and filopodia number as well as total projection length and induced growth cone collapse and neurite retraction (i.e. chemo-repulsion) through the GPR55 receptorReference 63. However, when using a continuous responder rate analysis as a secondary endpoint (i.e. comparing the proportion of active drug vs. placebo responders across the full spectrum of response from 0 to 100%), the study was able to report a statistically significant treatment effect in favour of nabiximols.
Sixty-percent of parents reported weaning their child from another anti-epileptic medication after starting CBD-enriched cannabis treatment. Parent-reported beneficial effects included better mood (79%), increased alertness (74%), better sleep (68%), and decreased self-stimulation (32%), while adverse effects included drowsiness (37%), and fatigue (16%). Limitations of such a survey include the self-selection bias, lack of a control group, the inability to independently verify any of the parents’ claims including information about dosing, as well as the small sample size and the under-representation of epilepsy types other than Dravet syndrome. A two-centre, phase II, randomized, double-blind, placebo-controlled, 22-day pilot study carried out in adult patients suffering from advanced cancer reported improved and enhanced chemosensory perception among patients treated with dronabinol (2.5 mg Δ9-THC b.i.d.) compared to those receiving placeboReference 611. The majority (73%) of dronabinol-treated patients self-reported an increased overall appreciation of food compared to those receiving placebo (30%).
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Other synthetic routes include acyl-chain removal from NAPE by α/β-hydrolase 4 to yield glycerophospho-N-arachidonoylethanolamine followed by phosphodiester bond hydrolysis of glycerophospho-N-arachidonoylethanolamine by phosphodiesterase 1 to yield anandamideReference 16. In contrast, 2-AG is principally synthesized through phospholipase C-β-mediated hydrolysis of phosphatidylinositol-4,5-bisphosphate, with arachidonic acid on the sn-2 position, to yield diacylglycerol . While anandamide and 2-AG are both derivatives of arachidonic acid, they are synthesized by pathways distinct from those used to synthesize eicosanoidsReference 17. Nevertheless, it appears that there may be a certain amount of cross talk between the eicosanoid and endocannabinoid pathwaysReference 17.
Symptom patterns can be divided into diarrhea predominant (IBS-D), constipation predominant (IBS-C), and an alternating pattern (alternating constipation/diarrhea) (IBS-A)Reference 1189Reference 1190. There is also some emerging evidence that suggests an association between genetic alterations in genes coding for certain ECS proteins (e.g. FAAH and CNR1) and the pathophysiology of IBSReference 1191-Reference 1193. Importantly, therefore, alternate methods of Δ9-THC delivery by aerosol or oral administration have been studied.
THC was relatively less potent than the other synthetic cannabinoid agonists (CP 55,940, Win 55,212-2, and anandamide); the other cannabinoid agonists only required 0.7 to 14 nM to inhibit embryonic development. The developmental arrest primarily occurred between the four-cell and eight-cell stagesReference 1379. Because of the long half-life of elimination of cannabinoids and their metabolites, drug tests screening for cannabinoids can be positive for weeks after last cannabis/cannabinoid useReference 1398Reference 1399 depending on among other things, the sensitivities of the tests used, frequency of cannabis use and timing of testing.
The study concluded that during a one-year treatment period, patients using cannabis exhibited less treatment compliance and higher levels of overall illness severity, mania, and psychosis compared to non-users. Patients using cannabis also reported experiencing less satisfaction with life. Studies investigating the effects of cannabis consumption on testosterone levels in men have yielded conflicting resultsReference 397.
Evidence from clinical and epidemiological studies suggests a dose-response effect, with increasing doses of THC increasing the risk of motor vehicle crashes that can lead to injuries and death. Limited evidence from human clinical imaging studies suggests THC and CBD may exert opposing effects on neuropsychological/neurophysiological functioning. Pre-clinical studies suggest that ultra-low doses of THC may be cardioprotective on experimentally-induced myocardial infarction. However, limited and conflicting evidence from epidemiological studies has thus far been unable to find a robust and consistent association between cannabis use and various types of cancer, with the possible exception of a link between cannabis use and testicular cancer (i.e. testicular germ cell tumours).
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Smoking cannabis may also increase the risk of developing respiratory infections in chronic usersReference 1413 through exposure to infectious organisms such as fungi and molds which can be found in the plant materialReference 1414, or alternatively by decreasing natural host defensesReference 1415. However, further epidemiological research is also required to establish a causal relationship between cannabis smoking and respiratory infections. However, limited and conflicting evidence from epidemiological studies has thus far been unable to find a robust and consistent association between cannabis use and various types of cancer, with the possible exception of a link between cannabis use and testicular cancer (i.e testicular germ cell tumours).
CBD administered immediately following the induction of ischemia, or at 90 min of reperfusion, still attenuated hepatic injury measured at 6 h of reperfusion, though to a lesser extent than when administered prior to the induction of the ischemia-reperfusion injury. The Canadian Guidelines for the Diagnosis and Management of Les bienfaits des oursons au CBD ? Fibromyalgia Syndrome recommend that with regards to possible treatments, a trial of a prescribed pharmacologic cannabinoid may be considered in a patient with fibromyalgia, particularly in the setting of important sleep disturbance Reference 838. D Determine substance abuse history; history of psychiatric or mood disorders.
Complementing these findings, an in vivo study showed that combined treatment with Δ9-THC (15 mg/kg/day) and temozolomide (5 mg/kg/day) reduced the growth of glioma tumour xenografts in mice in a synergistic mannerReference 1331. These Cecilia studies suggest that cannabinoids might sensitize certain tumours to the anti-neoplastic action of conventional chemotherapeutic drugs. There have been very few clinical studies of cannabis or cannabinoids for the treatment of AD.
Drug interactions involving cannabis and cannabinoids can be expected to vary considerably in their clinical significance given the wide variability in products, potencies, ratios of THC and CBD, doses, routes of administration, populations using cannabinoids and other factorsReference 468. However, some of the more clinically significant interactions may occur when cannabis is taken with other CNS depressant drugs such as sedative-hypnotics or alcoholReference 159Reference 219-Reference 221Reference 1373-Reference 1375Reference 1387Reference 1388. An overdose can occur if a patient is smoking/vapourizing cannabis and consuming orally administered cannabinoids, whether from prescription cannabinoid medications (e.g. dronabinol, nabilone), or from consumption of teas, baked goods or other productsReference 227Reference 431. Pre-clinical in vitro and in vivo studies investigating the effects of combining cannabinoids with frequently used chemotherapeutic agents have also been performed. One in vitro study showed that combining sub-maximal doses of Δ9-THC (0.75 μM) with cisplatin or doxorubicin reduced the viability of an astrocytoma cell line in a synergistic mannerReference 1330. Likewise, combining sub-maximal doses of Δ9-THC with temozolomide reduced the in vitro viability of several human glioma cell lines and primary cultures of glioma cells derived from human glioblastoma multiforme biopsiesReference 1331.
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Therefore, the upregulation of COX-2 expression in chronic pain states may promote the additional production of these pro-nociceptive metabolites both peripherally and centrally thus contributing to nociception and painReference 765. While prescription cannabinoids present clear advantages over placebo in the control of CINV, the evidence from randomized clinical trials shows cannabinoids to be clinically only slightly better than conventional dopamine D2-receptor antagonist anti-emeticsReference 210Reference 637. In some cases, patients appeared to prefer the cannabinoids to these conventional therapies despite the increased incidence of adverse effects such as drowsiness, dizziness, dysphoria, depression, hallucinations, paranoia, and arterial hypotension. This may be explained in part by the notion that for certain patients a degree of sedation and euphoria may be perceived as beneficial during chemotherapy. In humans, sex-dependent differences have been often observed in the biological and behavioural effects of substances of abuse, including cannabisReference 559. In male animals, higher densities of CB1 receptors have been observed in almost all cerebral regions analyzed whereas in females a more efficient coupling of the CB1 receptor to downstream G-protein signaling has been observedReference 560.
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Furthermore, the findings from this study further support the idea that the CB1 receptor plays an age-related differential role in bone turnover processes. It is important to note that the study had a number of considerable limitations and as such, the results should be interpreted with caution. Animal models of OA suffer from a number of limitations such as differences in anatomy, functionality, dimensions, cartilage repair processes, and thickness in comparison with human jointsReference 877. In addition, the lesions that develop in animal models of OA correspond to those found in humans only in a particular stage of the diseaseReference 877. Furthermore, no animal model of OA completely reproduces the whole variety of signs and symptoms of human OA. Taken together, these factors all pose a number of significant challenges in translating findings obtained in animal models of OA to OA patients.
Study limitations included study design, subject selection bias, the lack of a proper control group and placebo, small number of subjects, and the inability to establish a dose-response effect. Two randomized, double-blind, placebo-controlled clinical studies suggested oral Δ9-THC provided an analgesic benefit in patients suffering from moderate to severe continuous pain due to advanced cancer. The first study was a small dose-ranging study of 5, 10, 15, and 20 mg Δ9-THC, given in successive days, to 10 cancer patientsReference 840. Significant pain relief was found at the 15 and 20 mg dose levels, but at these higher doses patients were heavily sedated and mental clouding was common. A second, placebo-controlled study compared 10 and 20 mg oral Δ9-THC with 60 and 120 mg codeine in 36 patients with cancer painReference 285.
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Much of what is known about the beneficial properties of the non-psychotropic cannabinoids (e.g. CBD, THCV) is derived from in vitro and in vivo studies and few well-conducted, rigorous clinical studies of these substances exist. For more in-depth information on the pharmacology of cannabinoids, the reader is invited to consult the following resourcesReference 22Reference 46Reference 48Reference 101Reference 114. The evidence thus far from some observational studies and clinical studies suggests that cannabis and prescription cannabinoids (e.g. dronabinol, nabilone, or nabiximols) may be useful in alleviating a wide variety of single or co-occurring symptoms often encountered in the palliative care setting. A double-blind, counter-balanced, placebo-controlled driving simulator study reported that driving performance was more impaired in subjects who co-consumed alcohol and low or high doses of THC by smoking cannabis cigarettesReference 231.
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MS is an immune-mediated, demyelinating and neurodegenerative chronic disease of the CNS that affects between 2 and 3 million people worldwide and is characterized by periods of relapsing and remitting neurological attacks and accumulating disability over many yearsReference 667Reference 668. Demyelination and axonal and neuronal loss within different neural pathways of the CNS lead to a variety of different cognitive, sensory and motor problems (e.g. pain and spasticity) that accumulate as the disease progressesReference 667. ALS is a progressive neurodegenerative disease caused by the selective damage of motor neurons in the spinal cord, brainstem, and motor cortexReference 669. Although most cases are sporadic, familial cases can occur in an autosomal recessive or dominant or dominant X-linked inheritance patternReference 670.
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Indeed, it is important to highlight that two studies reported that individuals using cannabis for therapeutic purposes indicated they used approximately similar gram amounts of cannabis regardless of route of administrationReference 216Reference 580. Cannabis has many variables that do not fit well with the typical medical model for drug prescribingReference 405. Whereas the acute effects on the CNS and physiological effects occur within minutes by the smoking route or by vapourizationReference 149Reference 417, the acute effects proceed on a time scale of hours in the case of oral ingestionReference 417Reference 418. Acute oral administration results in a slower onset of action, lower peak blood levels of cannabinoids, and a longer duration of pharmacodynamic effects compared to smokingReference 78. The psychotropic effect or “high” occurs much more quickly by the smoking than by the oral route, which is the reason why smoking appears to be the preferred route of administration by many, especially among non-medical usersReference 419. Pre-clinical evidence suggests certain cannabinoids can have negative effects on a variety of measures of reproductive health.