Cannabinoids that have developed and taken from hemp plants are Common Types of Cannabinoids Found In Cannabis Like any other drug taken for a prolonged time, Cannabinoids can impact your body in a negative. It takes a little longer to feel the effects if you eat or drink marijuana. . Using marijuana while pregnant can also affect the brain of your unborn. Cannabinoids likely have a role in the brain's control of movement and memory, as well as natural pain modulation. It is clear that cannabinoids can affect pain.
the Body? What on Types Effects Can of Have Cannabinoids
The irreversible loss of the DA-mediated control of striatal function leads to the typical motor symptoms observed in PD, ie, bradykinesia, tremor, and rigidity. It has been proposed that cannabinoids may have some beneficial effects in the treatment of PD.
The majority of PD patients undergoing levodopa therapy develop disabling motor complications dyskinesias within 10 years of treatment. Recent studies in animal models and in the clinic suggest that CB1 receptor antagonists could prove useful in the treatment of both parkinsonian symptoms and levodopa-induced dyskinesia, whereas CB1 receptor agonists could have value in reducing levodopa-induced dyskinesia.
This effect was significantly reduced by coinjection with the cannabinoid receptor agonist WIN 55, The simultaneous administration of the CB1 antagonist rimonabant with quinpirole and WIN 55, blocked the effect of WIN 55, on quinpirole-induced alleviation of akinesia.
This effect was also reversed by rimonabant. The injection of 0. In clinical trials, the cannabinoid receptor agonist nabilone significantly reduced levodopainduced dyskinesia in PD. Advanced grades of HD showed an almost total loss of CB1 receptors and a further depletion of Dl receptors in the caudate nucleus, putamen, and globus pallidus internus, and an increase in GABA A receptor binding in the globus pallidus internus.
Indeed, arvanil, a hybrid endocannabinoid and vanilloid compound, behaves as an antihyperkinetic agent in a rat model of HD generated by bilateral intrastriatal application of 3-nitropropionic acid 3-NP.
However, both capsaicin VR1 agonist and CP55, an CB1 agonist had antihyperkinetic activity Quinolinic acid QA is an excitotoxin which, when injected into the rat striatum, reproduces many features of HD by stimulating glutamate outflow. Perfusion with WIN 55, significantly and dose-dependently prevented the increase in extracellular glutamate induced by QA.
Thus, the stimulation of CB1 receptors might lead to neuroprotective effects against excitotoxic striatal toxicity. Tourette syndrome TS is a complex inherited disorder of unknown etiology, characterized by multiple motor and vocal tics. Anecdotal reports have suggested that the use of cannabis might improve tics and behavioral problems in patients with TS.
There was a significant improvement of motor tics, vocal tics and obsessive-compulsive behavior after treatment with THC. Amyotrophic lateral sclerosis ALS is a fatal neurodegenerative disorder characterized by a selective loss of motor neurons in the spinal cord, brain stem, and motor cortex. Many effects of marijuana may be applicable to the management of ALS. These include analgesia, muscle relaxation, bronchodilation, saliva reduction, appetite stimulation, and sleep induction.
In addition, its strong antioxidative and neuroprotective effects may prolong neuronal cell survival. Furthermore, genetic ablation of the FAAH enzyme, which results in raised levels of the endocannabinoid anandamide, prevented the appearance of disease signs in these mice. Ablation of the CB1 receptor, in contrast, had no effect on disease onset in these mice, but significantly extended life span.
Together these results show that cannabinoids have significant neuroprotective effects in this model of ALS, and suggest that these beneficial effects may be mediated by nonCB1 receptor mechanisms. Administration at the onset of tremors delayed motor impairment in treated mice when compared with vehicle controls ; moreover, AM prolonged survival in these mice.
Studies on cannabinoid anticonvulsant activity began in , when CBD, and four CBD derivatives, CBD-aldehyde-diacetate, 6-oxo-CBD-diacetate, 6-hydroxy-CBD-tri-acetate and 9-hydroxy-CBD-triacetate were shown to protect against maximal electroshock convulsions in mice, to potentiate pentobarbital sleeping-time and to reduce spontaneous motor activity. Furthermore, it appears that CBD enhances the anticonvulsant effects of drugs in major seizures and reduces their effects in minor seizures.
The induction of status epilepticus-like activity by CB1 receptor antagonists was reversible and could be overcome by maximal concentrations of CB1 agonists. Cannabis use is common in patients with bipolar disorder, and anecdotal reports suggest that some patients use marijuana to alleviate symptoms of both mania and depression. The effect of cannabinoids on schizophrenia is controversial.
Neuropsychological results in THC-intoxicated normal volunteers exhibit strong similarities with data acquired from patients suffering from productive schizophrenic psychoses, as regards disturbances in internal regulation of perceptual processes.
Data from experimental-psychological tests show that personality changes generated by schizophrenia progression are comparable to psychopathological phenomenon due to cannabis intoxication. This argues against a distinct schizophrenia-like psychosis caused by cannabis. The group receiving the CB1 antagonist did not differ from the group receiving placebo on any outcome measure.
CBD causes antipsychotic effects. Posttraumatic stress disorder PTSD is a term for severe psychological consequences of exposure to, or confrontation with, stressful, highly traumatic events. Cannabinoids are believed to help in such cases. AMtreated animals showed decreased shock-induced reinstatement of fear. SRI blocked the effects of OL, suggesting that endogenous anandamide plays a facilitator role in extinction through a CB1 receptor mechanism of action.
However, upon repeated stress or acute severe stress, CB1 receptor deficiency causes persistent behavioral inhibition. Repeated bell stress seemed to cause a cumulative fear in CB1 receptor knockout mice. CB1 receptor gene polymorphism is known to modify transcription of the gene. In patients with Parkinson's disease, the presence of two long alleles, with more than 16 repeated AAT trinucleotides in the CNR1 gene, was associated with a reduced prevalence of depression.
CBD, and some derivatives, were found to cause a selective anxiolytic effect in the elevated plus-maze, within a limited range of doses. The effects of marijuana on human sleep patterns were noticed long ago. Asthma is a chronic disease of the respiratory system in which the airway occasionally constricts, becomes inflamed, and is lined with excessive amounts of mucus.
In animal experiments, after methacholine-induced or exercise-induced bronchospasm, marijuana caused a prompt improvement of the bronchospasm and associated hyperinflation. The daily use of THC was not associated with clinical tolerance. Maximal bronchodilatation was achieved more rapidly with salbutamol, but at 1 hour both drugs were equally effective. No cardiovascular or mood disturbance was detected, and plasma total cannabinoids at 15 minutes were not detected by radioimmunoassay.
The mode of action of THC differed from that of sympathomimetic drugs. In another study, THC induced sympathetic stimulation and parasympathetic inhibition of cardiovascular control pathways. The peak heart rate rise after THC was attenuated by atropine and by propranolol, and nearly abolished by atropine-propranolol pretreatment. With repetitive dosing supine bradycardia and decreased blood pressure with tolerance to orthostatic hypotension were observed. A number of studies suggest that there is a correlative, but not necessarily causal, relationship between glaucoma and systemic hypertension.
Ocular hypertension OHT refers to any situation in which intraocular pressure is higher than normal, and is the most important risk factor for glaucoma. In contrast, noladin ether decreased IOP immediately after topical administration, and no initial IOP increase was observed.
CB2 mRNA was undetectable. Ocular toxicity was seen after THC treatment, consisting of conjunctival erythema and chemosis as well as corneal opacification. Although these changes also occurred with marijuana extract, their intensity was much reduced. In contrast, no ocular toxicity was apparent during administration of plant cannabinoids other than THC. The results indicate that THC may have value as a hypotonizing ocular drug.
The intensity and duration of the arterial and ocular pressure responses to THC were greater in hypertensives than in normotensive patients; the changes in ocular pressure paralleled the changes in blood pressure in glaucoma patients.
The antiproliferative action of cannabinoids on cancer cells was first noticed in the s. Since then cannabinoids were found to act on various cancer cell lines, through various mechanisms. Moreover, cannabinoid challenge decreased the efficiency of glioma stem-like cells to initiate glioma formation in vivo.
Activation of these receptors decreased growth, proliferation, angiogenesis, and metastasis, and increased apoptosis, of melanomas in mice. These effects were prevented by blockade of the CB2 cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo.
THC inhibited tumor-cell proliferation in vitro, decreased tumor-cell Ki67 immunostaining and prolonged the survival time of two of the patients. Many drugs used today can cause addiction and are misused and abused, for example opiates, cocaine, benzodiazepines, barbiturates, cholinergic agonists, ketamine, , dopaminergic agonists, amphetamines, and others. Nevertheless they are still an important part of our pharmacopeia.
Marijuana was used for centuries as a medicinal plant, but during the last century, because of its abuse and addictive potential it was taken out of clinical practice.
Now, we believe that its constituents and related compounds should be brought back to clinical use. The endocannabinoid system is a very complex one and regulates numerous processes, in parallel with other wellknown systems, such as the adrenergic, cholinergic, and dopaminergic systems.
National Center for Biotechnology Information , U. Journal List Dialogues Clin Neurosci v. Kogan , MSc Natalya M. Author information Copyright and License information Disclaimer. This is an open-access article distributed under the terms of the Creative Commons Attribution License http: This article has been cited by other articles in PMC. Abstract Cannabis sativa L. Abstract Las preparaciones de Cannabis sativa L. Addiction to canabis, and the influence of cannabis on addiction to other substances Marijuana may produce mild dependence in humans.
Negative effects of cannabis other than addiction There are some negative effects of cannabis use other than addiction, most of them related to alterations of attentional and cognitive functions or other neuropsychological and behavioral effects. Therapeutic uses of cannabinoids Obesity, anorexia, emesis Cannabis has been known for centuries to increase appetite and food consumption.
Pain Cannabis has been used for millennia as a pain-relieving substance. Multiple sclerosis, neuroprotection, inflammation Inflammation, autoimmune response, demyelination, and axonal damage are thought to participate in the pathogenesis of MS. Parkinson's disease, Huntington's disease, Tourette's syndrome, Alzheimer's disease, epilepsy Parkinson's disease PD is a chronic, progressive neurodegenerative disorder. Bipolar disorder, schizophrenia, post-traumatic stress disorder PTSD , depression, anxiety, insomnia Cannabis use is common in patients with bipolar disorder, and anecdotal reports suggest that some patients use marijuana to alleviate symptoms of both mania and depression.
Asthma, cardiovascular disorders, glaucoma Asthma is a chronic disease of the respiratory system in which the airway occasionally constricts, becomes inflamed, and is lined with excessive amounts of mucus. Cancer The antiproliferative action of cannabinoids on cancer cells was first noticed in the s. Conclusion Many drugs used today can cause addiction and are misused and abused, for example opiates, cocaine, benzodiazepines, barbiturates, cholinergic agonists, ketamine, , dopaminergic agonists, amphetamines, and others.
Early medical use of cannabis. Untersuchung der Cannabis sativa. Repertorium fur die Pharmacie. Note sur le haschisch. A historical overview of chemical research on cannabinoids. Isolation, structure and partial synthesis of the active constituent of hashish. J Am Chem Soc. Marihuana, an annotated bibliography. Withdrawal symptoms in cannabis indica addicts. The addictive potential of cannabis. Clinical studies of cannabis tolerance and dependence. Ann N Y Acad Sci.
Treatment of cannabis use disorders: Cannabis addiction and Telic Dominance Scale. Clinical trial of abstinencebased vouchers and cognitive-behavioral therapy for cannabis dependence. J Consult Clin Psychol. Addictive potential of cannabinoids: Failure of Delta 9 -tetrahydrocannabinol and CP 55, to maintain intravenous self-administration under a fixed-interval schedule in rhesus monkeys.
Endocannabinoid system and alcohol addiction: Endocannabinoid signaling via cannabinoid receptor 1 is involved in ethanol preference and its age-dependent decline in mice. SR, a central cannabinoid CB 1 receptor antagonist, blocks the motivational and dopaminereleasing effects of nicotine in rats. The diagnosis of alcohol and cannabis dependence addiction in cocaine dependence addiction. Behavioral effects of cocaine alone and in combination with ethanol or marijuana in humans.
Marihuana smoking increases plasma cocaine levels and subjective reports of euphoria in male volunteers. Involvement of cannabinoid CB1 receptors in drug addiction: Rimonabant, a CB1 antagonist, blocks nicotineconditioned place preferences.
Nicotine-associated cues maintain nicotine-seeking behavior in rats several weeks after nicotine withdrawal: The role of the cannabinoid system in nicotine addiction. Successful control of lipids, kilos and cigarettes]. Advances in pharmacotherapy for tobacco dependence.
Expert Opin Emerg Drugs. Expert Opin Investig Drugs. Adenosine A2a blockade prevents synergy between mu-opiate and cannabinoid CB1 receptors and eliminates heroin-seeking behavior in addicted rats. Unresponsiveness to cannabinoids and reduced addictive effects of opiates in CB1 receptor knockout mice. The roles of cannabinoid and dopamine receptor systems in neural emotional learning circuits: Cell Mol Life Sci. Cannabinoid CB1 receptor antagonists as promising new medications for drug dependence.
J Pharmacol Exp Ther. Cognitive functioning of longterm heavy cannabis users seeking treatment. Chronic cognitive impairment in users of 'ecstasy' and cannabis. Cannabis use, cognitive performance and mood in a sample of workers. Long-term effects of frequent cannabis use on working memory and attention: Maternal smoking, drinking or cannabis use during pregnancy and neurobehavioral and cognitive functioning in human offspring.
A literature review of the consequences of prenatal marihuana exposure. An emerging theme of a deficiency in aspects of executive function. Cannabis, the mind and society: Cannabis and cognitive dysfunction: The psychotomimetic effects of intravenous deItatetrahydrocannabinol in healthy individuals: Amotivational syndrome in organic solvent abusers. Characteristics of abnormal behavior induced by delta 9-tetrahydrocannabinol in rats.
Psychiatric aspects of cannabis use in adolescents and young adults. Related, induced and associated psychiatric disorders to cannabis. Operant acquisition of marihuana in man. Cannabis, motivation, and life satisfaction in an internet sample. Subst Abuse Treat Prev Policy. Endocannabinoids in the regulation of appetite and body weight. Endocannabinoids in appetite control and the treatment of obesity. Genetic variations at the endocannabinoid type 1 receptor gene CNR1 are associated with obesity phenotypes in men.
J Clin Endocrinol Metab. Lack of tolerance to the suppressing effect of rimonabant on chocolate intake in rats. Consuming a drink laced with marijuana, such as a tea, will lead to a similar absorption process as an edible.
Here, however, the drink will often dilute the THC, making it less potent. Much like other drugs absorbed in the stomach, such as alcohol, the effects of THC will be realized much more quickly on an empty stomach than on a full stomach. Consuming marijuana on an empty stomach can produce other unpleasant symptoms, including stomach pain and nausea. The primary differences between smoking a joint and eating an edible are in the magnitude of the effects, the time lapse before the effects are realized, and the longevity of the effects.
Edibles do not carry some of the negative and potentially dangerous consequences of smoking marijuana through a joint. Edibles do not create habitual smoking urges, do not lead to smoking-related health problems, and do not produce second-hand residue. Many medical marijuana consumers report that it is easier to identify an effective dosage through smoking than through eating an edible, which factors into their decision to use joints.
The most important factor to remember, however, is that THC remains the active ingredient in both methods of marijuana intake — carrying with it the same psychoactive qualities and potentially adverse consequences.
Call and speak with a marijuana rehab professional today. For those seeking addiction treatment for themselves or a loved one, the DrugAbuse. Our helpline is offered at no cost to you and with no obligation to enter into treatment. Drug Abuse , Understanding Addiction. Data accurate as of In the tonsils the CB2 receptors appear to be restricted to B-lymphocyte -enriched areas.
THC and its endogenous equivalent anandamide additionally interact with glycine receptors. Cannabinoids usually contain a 1,1'-di-methyl-pyran ring, a variedly derivatized aromatic ring and a variedly unsaturated cyclohexyl ring and their immediate chemical precursors, constituting a family of about 60 bi-cyclic and tri-cyclic compounds.
Like most other neurological processes, the effects of cannabis on the brain follow the standard protocol of signal transduction , the electrochemical system of sending signals through neurons for a biological response. It is now understood that cannabinoid receptors appear in similar forms in most vertebrates and invertebrates and have a long evolutionary history of million years.
There are at least two types of cannabinoid receptors CB1 and CB2. The CB2 receptor is most abundantly found on cells of the immune system.
Cannabinoids act as immunomodulators at CB2 receptors, meaning they increase some immune responses and decrease others. For example, nonpsychotropic cannabinoids can be used as a very effective anti-inflammatory.
It is clear that cannabinoids can affect pain transmission and, specifically, that cannabinoids interact with the brain's endogenous opioid system and may affect dopamine transmission. Most cannabinoids are lipophilic fat soluble compounds that are easily stored in fat, thus yielding a long elimination half-life relative to other recreational drugs.
The THC molecule, and related compounds, are usually detectable in drug tests from 3 days up to 10 days according to Redwood Laboratories; long-term users can produce positive tests for two to three months after ceasing cannabis use see drug test.
No fatal overdoses with cannabis use have been reported. THC , the principal psychoactive constituent of the cannabis plant, has an extremely low toxicity and the amount that can enter the body through the consumption of cannabis plants poses no threat of death. It is important though to note that cannabinoids and other molecules present in cannabis can alter the metabolism of other drugs, especially due to competition for clearing metabolic pathways such as cytochromes CYP ,  thus leading to drug toxicities by medications that the person consuming cannabis may be taking.
A study found that while tobacco and cannabis smoke are quite similar, cannabis smoke contained higher amounts of ammonia , hydrogen cyanide , and nitrogen oxides , but lower levels of carcinogenic polycyclic aromatic hydrocarbons PAHs.
Cannabis smoke contains thousands of organic and inorganic chemical compounds. This tar is chemically similar to that found in tobacco smoke or cigars. Other observations include possible increased risk from each cigarette; lack of research on the effect of cannabis smoke alone; low rate of addiction compared to tobacco; and episodic nature of cannabis use compared to steady frequent smoking of tobacco.
Further, he notes that other studies have failed to connect cannabis with lung cancer, and accuses the BLF of "scaremongering over cannabis". When smoked, the short-term effects of cannabis manifest within seconds and are fully apparent within a few minutes,  typically lasting for 1—3 hours, varying by the person and the strain of cannabis. The psychoactive effects of cannabis, known as a " high ", are subjective and vary among persons and the method of use.
When THC enters the blood stream and reaches the brain, it binds to cannabinoid receptors. The endogenous ligand of these receptors is anandamide , the effects of which THC emulates.
This agonism of the cannabinoid receptors results in changes in the levels of various neurotransmitters, especially dopamine and norepinephrine ; neurotransmitters which are closely associated with the acute effects of cannabis ingestion, such as euphoria and anxiety.
Abstract or philosophical thinking, disruption of linear memory and paranoia or anxiety are also typical. Anxiety is the most commonly reported side effect of smoking marijuana. Cannabidiol CBD , another cannabinoid found in cannabis in varying amounts, has been shown to ameliorate the adverse effects of THC, including anxiety, that some consumers experience. Cannabis produces many other subjective and highly tangible effects, such as increased enjoyment of food taste and aroma, and marked distortions in the perception of time and space where experiencing a "rush" of ideas from long-term memory can create the subjective impression of long elapsed time, while in reality only a short time has passed.
In some cases, cannabis can lead to dissociative states such as depersonalization   and derealization. Any episode of acute psychosis that accompanies cannabis use usually abates after 6 hours, but in rare instances, heavy users may find the symptoms continuing for many days. While psychoactive drugs are typically categorized as stimulant , depressant , or hallucinogen , cannabis exhibits a mix of all of them, perhaps leaning more towards hallucinogenic or psychedelic properties, though with other effects quite pronounced.
THC is considered the primary active component of the cannabis plant. Scientific studies have suggested that other cannabinoids like CBD may also play a significant role in its psychoactive effects.
Electroencephalography or EEG shows somewhat more persistent alpha waves of slightly lower frequency than usual. Peak levels of cannabis-associated intoxication occur approximately 30 minutes after smoking it and last for several hours.
The total short-term duration of cannabis use when smoked depends on the potency, method of smoking — e. Peak levels of intoxication typically last an average of three to four hours. When taken orally in the form of capsules, food or drink , the psychoactive effects take longer to manifest and generally last longer, typically lasting for an average of four to ten hours after consumption.
Also, oral ingestion use eliminates the need to inhale toxic combustion products created by smoking and therefore negates the risk of respiratory harm associated with cannabis smoking.
The areas of the brain where cannabinoid receptors are most prevalent are consistent with the behavioral effects produced by cannabinoids. Brain regions in which cannabinoid receptors are very abundant are the basal ganglia , associated with movement control; the cerebellum , associated with body movement coordination; the hippocampus , associated with learning , memory, and stress control; the cerebral cortex , associated with higher cognitive functions; and the nucleus accumbens , regarded as the reward center of the brain.
Other regions where cannabinoid receptors are moderately concentrated are the hypothalamus , which regulates homeostatic functions; the amygdala , associated with emotional responses and fears ; the spinal cord , associated with peripheral sensations like pain; the brain stem , associated with sleep , arousal , and motor control; and the nucleus of the solitary tract , associated with visceral sensations like nausea and vomiting.
Experiments on animal and human tissue have demonstrated a disruption of short-term memory formation,  which is consistent with the abundance of C receptors on the hippocampus, the region of the brain most closely associated with memory. Cannabinoids inhibit the release of several neurotransmitters in the hippocampus such as acetylcholine , norepinephrine , and glutamate , resulting in a decrease in neuronal activity in that area.
Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of A aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may impact the progression of this debilitating disease.
While several studies have shown increased risk associated with cannabis use by drivers, other studies have not found increased risk. In Cannabis and driving: Where they can compensate, they do A meta-analysis found that acute cannabis use increased the risk of an automobile crash. In the largest and most precisely controlled study of its kind carried out by the U.
Likewise better controlled studies have found lower or no elevated crash risk estimates". Short-term one to two hours effects on the cardiovascular system can include increased heart rate, dilation of blood vessels, and fluctuations in blood pressure.
Indeed, marijuana may be a much more common cause of myocardial infarction than is generally recognized. In day-to-day practice, a history of marijuana use is often not sought by many practitioners, and even when sought, the patient's response is not always truthful".
A analysis of 3, myocardial infarction survivors over an year period showed "no statistically significant association between marijuana use and mortality". A study by the National Institutes of Health Biomedical Research Centre in Baltimore found that heavy, chronic smoking of marijuana joints per week changed blood proteins associated with heart disease and stroke. A study by researchers at Boston's Beth Israel Deaconess Medical Center , Massachusetts General Hospital and Harvard School of Public Health found that a middle-age person's risk of heart attack rises nearly fivefold in the first hour after smoking marijuana, "roughly the same risk seen within an hour of sexual activity".
Cannabis arteritis is a very rare peripheral vascular disease similar to Buerger's disease. There were about 50 confirmed cases from to , all of which occurred in Europe.
A confounding factor in cannabis research is the prevalent usage of other recreational drugs, especially alcohol and nicotine. Some critics question whether agencies doing the research make an honest effort to present an accurate, unbiased summary of the evidence, or whether they "cherry-pick" their data to please funding sources which may include the tobacco industry or governments dependent on cigarette tax revenue; others caution that the raw data, and not the final conclusions, are what should be examined.
The Australian National Household Survey of  showed that cannabis in Australia is rarely used without other drugs. Evidence from a controlled experimental study undertaken by Lukas and Orozco  suggests that alcohol causes THC to be absorbed more rapidly into the blood plasma of the user.
Data from the Australian National Survey of Mental Health and Wellbeing  found that three-quarters of recent cannabis users reported using alcohol when cannabis was not available, this suggests that the two are substitutes.
Studies on cannabis and memory are hindered by small sample sizes, confounding drug use, and other factors. In a study looking at neuropsychological performance in long-term cannabis users, researchers found "some cognitive deficits appear detectable at least 7 days after heavy cannabis use but appear reversible and related to recent cannabis exposure rather than irreversible and related to cumulative lifetime use". From neuropsychological tests, Pope found that chronic cannabis users showed difficulties, with verbal memory in particular, for "at least a week or two" after they stopped smoking.
Within 28 days, memory problems vanished and the subjects "were no longer distinguishable from the comparison group". Their findings were published in the July issue of the Journal of the International Neuropsychological Society. Researchers looked at data from 15 previously published controlled studies involving long-term cannabis users and nonusers.
Cannabinoids in health and disease
More and more Americans are using marijuana for medical and recreational reasons. Whether you smoke it or eat it, learn how this drug can. I do recall the last time that I did, I thought I was a soldier in war. That's the kind of effect the strong BC weed has on me. Well, I smoked a little bit of “Jamaican”. Cannabis sativa, also known as hemp, is a species of the The effects experienced by the cannabis user are variable and will depend upon the dose While cannabis remains a Schedule 1 substance, research has resulted.