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Official websites use. Share sensitive information only on official, secure websites. Cannabis sativa L. However, concern over the dangers of abuse led to the banning of the medicinal use of marijuana in most countries in the s. Only recently, marijuana and individual natural and synthetic cannabinoid receptor agonists and antagonists, as well as chemically related compounds, whose mechanism of action is still obscure, have come back to being considered of therapeutic value. However, their use is highly restricted. Despite the mild addiction to cannabis and the possible enhancement of addiction to other substances of abuse, when combined with cannabis, the therapeutic value of cannabinoids is too high to be put aside. Keywords: cannabinoids , therapeutics , medicinal , addiction. Las preparaciones de Cannabis sativa L. Numerous alkaloids were isolated in pure form or partially characterized. Morphine, cocaine, strychnine, and many others were purified and used in medicine. However, most of the terpenoids - a major class of secondary plant metabolites, to which the plant cannabinoids also belong - were not isolated until the end of the century or even much later, and in many cases their purity was doubtful. In , Schlesinger was apparently the first investigator to obtain an active extract from the leaves and flowers of hemp. The chemical research on the plant cannabinoids and their derivatives over nearly two centuries is described in ref 5. It took decades until cannabinoids came to be considered again as compounds of therapeutic value, and even now their uses are highly restricted. Here we present an overview of the addictive and side effects of cannabinoids vs their therapeutic potential. Marijuana may produce mild dependence in humans. Cannabinoids act on brain reward processes and reward-related behaviors by a mechanism similar to that found with other addictive drugs. In animal models they enhance electrical brain-stimulation reward in the core meso-accumbens reward circuitry of the brain and neural firing of a core dopamine DA component and thus elevate DA circuit. In the reward-relevant meso-accumbens DA circuit. In some animal models they produce conditioned place preference CPP and self-administration. The abuse of other substances is influenced by the cannabinoids. The cannabinoid system is involved in alcohol-consumption behavior. Cannabinoid CB1 receptor agonists have been found to specifically stimulate alcohol intake and its motivational properties in rats. Cocaine is another substance of abuse in whose acquisition and consolidation cannabinoids may be involved. High prevalence of alcohol dependence and cannabis dependence can be found in patients with cocaine dependences. 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. Most of them are noted as a result of early-onset cannabis use during adolescence. Furthermore, cannabis users did not differ from controls in terms of overall patterns of brain activity in the regions involved in these cognitive functions. The syndrome was first described in the s among patients with a history of longtime cannabis use. For example, cannabis can cause acute pancreatitis, although the exact mechanism remains unknown. Cannabis has been known for centuries to increase appetite and food consumption. Rimonabant administration caused suppression of the intake of a chocolate-flavored beverage over a day treatment period, without any apparent development of tolerance. Rimonabant leads to significant weight loss in obese human subjects. Treatment with rimonabant was also associated with beneficial effects on different metabolic parameters and cardiovascular risk factors linked with overweight. Many of the metabolic effects, including adiponectin increase, occur beyond weight loss, suggesting a direct peripheral effect of rimonabant. Surprisingly, the US Food and Drug Administration has declined to approve rimonabant, primarily due to its slight potential to enhance anxiety and suicidal thoughts. The atmosphere of consternation of possible legal action due to side effects may have led to this decision. The other side of the same coin is anorexia. While in obese populations weight loss is the main goal, in other populations, such as patients with cancer or AIDS, it is an immense problem. Dronabinol synthetic THC, known as Marinol and approved for the treatment of nausea and vomiting in cancer and AIDS patients is associated with consistent improvement in appetite. In clinical trials, weight was stable in dronabinol patients, while placebo recipients lost weight. However, while these antagonists are not effective in delayed vomiting, THC is known to reduce this side effect of chemotherapy. Cannabis has been used for millennia as a pain-relieving substance. Evidence suggests that cannabinoids may prove useful in pain modulation by inhibiting neuronal transmission in pain pathways. Considering the pronounced antinociceptive effects produced by cannabinoids, they were proposed to be a promising therapeutic approach for the clinical management of trigeminal neuralgia. These results do not support an overall benefit of THC in pain and quality of life in patients with refractory neuropathic pain. Other studies show much better results of pain relief. When THC was given to a patient with familial Mediterranean fever, with chronic relapsing pain and gastrointestinal inflammation, a highly significant reduction in pain was noted. Nabilone is a synthetic cannabinoid approved for treatment of severe nausea and vomiting associated with cancer chemotherapy. A significant decrease in disabling spasticity-related pain of patients with chronic upper motor neuron syndrome UMNS was found with nabilone. Cannabimimetic effects with ajulemic acid in rodents have also been recorded. It is efficacious and well tolerated in the treatment of symptoms of multiple sclerosis, notably spasticity and neuropathic pain. Inflammation, autoimmune response, demyelination, and axonal damage are thought to participate in the pathogenesis of MS. Increasing evidence supports the idea of a beneficial effect of cannabinoid compounds for the treatment of this disease. In clinical trials, it has been shown that cannabis derivatives are active on the pain related to MS, 84 , 85 , 95 , 97 , 98 However, this is not the only positive effect of cannabinoids in this disease. Reduction in the inflammatory response in the brain and spinal cord was also noted in animals treated with dexanabinol HU a nonpsychoactive synthetic cannabinoid. These observations may explain the efficacy of cannabinoid agonists in improving motor symptoms spasticity, tremor, ataxia typical of MS in both humans and animal models. Marijuana was suggested as treatment of muscle spasticity as early as the s. Responses varied, but benefit was seen in patients with tonic spasms. Improved motor coordination was seen when patients with MS, seriously disabled with tremor and ataxia, were given oral THC. MS is not the only disease state where the neuroprotective potential of cannabinoids can be seen. In animal experiments, 2 weeks after the application of 6-hydroxydopamine, a significant depletion of dopamine contents and a reduction in tyrosine hydroxylase activity in the lesioned striatum were noted, and were accompanied by a reduction in tyrosine hydroxylase-messenger ribonucleic acid mRNA levels in the substantia nigra. Daily administration of THC over 2 weeks produced a significant irreversible waning in the magnitude of these changes, which may be relevant in the treatment of Parkinson's disease see below The cannabinoids have a neuroprotective activity not only in vitro but also in vivo: HU, a potent synthetic analog of THC, increases survival of mouse cerebellar granule cells exposed to 6-hydroxydopamine. Rimonabant exerted neuroprotection independently of its cannabinoid receptor-blocking effect. A trend toward faster and better neurologic outcome was also observed. Atherosclerosis is a chronic inflammatory disease, and is the primary cause of heart disease and stroke in Western countries. Oral treatment with a low dose of THC inhibits atherosclerosis progression in an apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells. Thus, THC may be a valuable target for treating atherosclerosis. Its concentrations are significantly increased in three different inflammatory and neuropathic conditions. The enhanced levels may possibly be related to a protective local anti-inflammatory and analgesic action. In experiments with obese vs lean rats, rimonabant was found to be a potent inhibitor of sensory hypersensitivity associated with CFA-induced arthritis in obese rats, in which the inflammatory reaction is more severe than in lean rats. It may thus have therapeutic potential in obesity-associated inflammatory diseases. Parkinson's disease PD is a chronic, progressive neurodegenerative disorder. The main pathological feature of PD is the degeneration of dopamine DA -containing neurons of the substantia nigra, which leads to severe DAergic denervation of the striatum. 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. Natalya M. As a library, NLM provides access to scientific literature. Dialogues Clin Neurosci. Show available content in en es fr. Find articles by Natalya M Kogan. Find articles by Raphael Mechoulam. Issue date Dec. Similar articles. Add to Collections. 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Official websites use. Share sensitive information only on official, secure websites. Advocates for the legalization of medical and retail marijuana are quick to point out all the possible benefits that a community might see from such a venture. The more potent a drug is, the stronger the possibility of addiction and the more likely the person will continue to purchase and use the product. The active component in marijuana that people find so desirable was not really known until the s when a research team in Israel found that after injecting THC into aggressive rhesus monkeys, they became calm and sedate. It was not until the s that this same team discovered why we have these receptors in our brain. The primary problem with the current available cannabis in dispensaries in Colorado is that the THC content is not like it used to be. For example the Girl Scout Cookie strain has only 0. The flower or leaves that are generally smoked or vaped are only one formulation. There is absolutely no research that indicates this level of THC is beneficial for any medical condition. The purpose of these products is to produce a high, and the increased potency makes them potentially more dangerous and more likely to result in addiction. Because there was initially no regulation on the edibles they have been made to look very similar to regular products that people consume such as chocolates, gummy bears, PopTarts etc. Keep away from Children. According to the Monitoring the Future Study, marijuana is by far the number one drug abused by eighth and twelfth graders. However, there are significant consequences of long-term or heavy marijuana use beginning in adolescence. Adolescence is a time of significant brain development. Normally during this period there is a significant increase in dopaminergic and glutamatergic stimulatory neurotransmitters and a decrease in serotonergic and GABAergic suppressive neurotransmitters located in the pre-frontal motor cortex — the last part of the brain to fully develop. This equates to a great deal of learning, exploring and doing during this period, similar to stepping on the gas pedal and problems with impulse control and judgement, similar to problems stepping on the brake. The marijuana of old used to be classified as a hallucinogen and was thought to not cause addiction because there was no identified withdrawal syndrome. This has changed and with the increased potency of THC there is a definite recognized withdrawal syndrome which includes increased anger, irritability, depression, restlessness, headache, loss of appetite, insomnia and severe cravings for marijuana. All drugs of abuse cause a release of dopamine from the nucleus acumbens that signifies salience and starts the process of long term potentiation which reinforces the learning. At the same time, the hippocampus which is vitally important for new memory and learning is negatively impacted by the chronic use of any addictive substance. These substances decrease neurogenesis in the hippocampus and actually cause shrinkage of the hippocampus and impair the ability to learn new things. This is true for alcohol, cocaine, methamphetamine, heroin, nicotine, and THC. When the use of addictive drugs is stopped and the animals are allowed to be in a recovery environment where they are free to exercise voluntary exercise being one thing that improves neurogenesis they can again learn new things. A study of 40 male and 34 female long-term 15 years cannabis users versus 37 non-users, healthy controls divided the marijuana users into three groups; those that smoked predominantly THC in the previous three months, those who smoked a combination of THC and CBD in the previous three months and former uses with a sustained abstinence of 29 months. In the former users the hippocampal integrity was comparable to controls. The only problem with this study is they did not test for functional deficits to see if function improved along with hippocampal volume. There are other important neurotransmitters that are very active during adolescence and include acetylcholine receptors ACH and endocannabinergic receptors CB1. ACH helps us focus and concentrate and ACH innervation of the pre-frontal motor cortex reaches mature levels during adolescence. They are called nicotinic simply because nicotine binds to these receptors — not because we are supposed to use tobacco products. These receptors are involved in promoting or preventing neuronal cell death depending on the stage of brain development. Putting an exogenous form of nicotine in the developing brain, as in consuming tobacco, can dysregulate these fine tuning mechanisms during adolescence. CB1 receptors regulate the balance between excitatory and inhibitory neuronal activity utilizing our own natural anandamides. Exposure to cannabis during adolescence disrupts glutamate which plays an important role in synaptic pruning in the pre-frontal motor cortex; disrupting normal brain development. A study in New Zealand with a year follow-up showed an average loss of 8 IQ points with early persistent teen use of marijuana. A study out of Yale University tracked 1, students who achieved similar SAT scores and were enrolled in college. Those who drank alcohol without using marijuana had an average GPA of 3. Marijuana use is also correlated with creating or worsening many mental health problems including anxiety, depression, psychosis, and suicidal ideation. A prospective study in Australia followed 1, girls for seven years starting before they expressed symptoms of mental illness or substance abuse. A study of adults with depression assessed symptoms, functioning and marijuana use at baseline, and three- and six-month intervals. Numerous studies have demonstrated that using cannabis prior to the age of 15—18 significantly increases the risk of developing psychotic symptoms. A landmark study out of the UK analyzed adults, ages 18—65, with their first psychotic episode versus matched healthy controls. A growing number of states have identified PTSD as an approved condition for medical marijuana. However, this is not based on any research. There is no evidence that marijuana successfully treats PTSD and there is evidence that it can make it worse. All these compounds do is provide temporary relief by numbing the individual and disconnecting them from the traumatic emotion. It does not resolve the trauma, and they have to continue to use multiple times a day in order to continue with the benefit. This can lead to increased addiction potential and withdrawal symptoms, cognitive impairment, a-motivational syndrome, and the potential for psychosis or worsening psychosis from the PTSD. Those who were using marijuana but stopped using it in treatment had the lowest level of PTSD symptoms four months after treatment, and those who started smoking marijuana had the highest levels of violent behavior and PTSD symptoms four months after treatment. Another conundrum that impacts treatment for PTSD is the possibility that cannabis users have an increased susceptibility to memory distortions even when abstinent and drug free which can compromise reality monitoring. Riba et al. The study involved a memory paradigm including a study phase and a testing phase with the participant in an MRI scanner. They were given lists of four words to memorize and then shown a different list and they had to report if the words were on the previous list. Marijuana users were significantly more likely to have false recognition of the words and were less likely to reject that they had a false memory compared with the non-users. Multiple studies have documented a relationship between cannabis use and suicidality. A large, longitudinal study in Australia and New Zealand of over adolescents and maximum frequency of marijuana use found almost a seven fold increase in suicide attempts in daily marijuana users compared with non-users. According to the Colorado Department of Public Health and Environment, marijuana is by far the most frequently encountered drug on toxicology screens of suicides among adolescents ages 10 — 19 and has been increasing over the last eight years. Misguided marijuana advocates have recently been suggesting that marijuana is a solution for the opioid epidemic. A study of 5, adolescents in the UK with three or more measures of cannabis use from age 13—18 found a dose-response relationship between cannabis use trajectories in adolescence and nicotine dependence, harmful alcohol consumption, and other illicit drug use by age There is evidence that prenatal exposure of cannabis can alter opioid gene function in humans. Fetal brains obtained from aborted fetuses from women who were using marijuana during their pregnancy were compared to those from women not using marijuana during pregnancy. These findings are comparable to findings with animals. One study of prenatal cannabis exposure in rats found that the THC exposed rats exhibited shorter latency to first active lever press for heroin and had higher heroin-seeking during mild stress and drug extinction than animals not exposed to THC. Another interesting study that supports the idea that cannabis use and opioid use are linked was in a randomized, double-blind, placebo controlled trial of naltrexone in non-treatment seeking cannabis smokers. If states continue to commercialize marijuana as has been done in Colorado we are destined to see many more people requiring treatment for addiction, depression, anxiety, suicidal ideation, and psychosis. We need to continually educate every one of the risks and increase prevention efforts to prevent children and adolescents from initiating marijuana use. This should include a strong ban on any advertising that appears to be directed toward youth — for all drugs including marijuana, tobacco, and alcohol. States will need to commit to increased funding for and availability of treatment options. The strongest recommendation would be to initiate regulations to limit the concentration of THC. She is the medical director for a inpatient dual diagnosis treatment program in Pueblo, Colorado. As a library, NLM provides access to scientific literature. Mo Med. Find articles by Elizabeth Stuyt. Copyright by the Missouri State Medical Association. Contact: libbystuyt msn. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel.

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