Beach_Leech's short term memory loss

[chrish]

Marijuana has many dangers; through both immediate effects and damage to health over time.

Marijuana hinders the user's short-term memory (memory for recent events), and he or she may have trouble handling complex tasks. With the use of more potent varieties of marijuana, even simple tasks can be difficult.

Because of the drug's effects on perceptions and reaction time, users could be involved in auto crashes. Drug users also may become involved in risky sexual behavior. There is a strong link between drug use and unsafe sex and the spread of HIV, the virus that causes AIDS.

Under the influence of marijuana, students may find it hard to study and learn. Young athletes could find their performance is off; timing, movements, and coordination are all affected by THC.

Marijuana affects many skills required for safe driving: alertness, the ability to concentrate, coordination, and reaction time. These effects can last up to 24 hours after smoking marijuana. Marijuana use can make it difficult to judge distances and react to signals and sounds on the road.

There is data showing that marijuana can play a role in crashes. When users combine marijuana with alcohol, as they often do, the hazards of driving can be more severe than with either drug alone.

A study of patients in a shock-trauma unit who had been in traffic accidents revealed that 15 percent of those who had been driving a car or motorcycle had been smoking marijuana, and another 17 percent had both THC and alcohol in their blood.

In one study conducted in Memphis, TN, researchers found that, of 150 reckless drivers who were tested for drugs at the arrest scene, 33 percent tested positive for marijuana, and 12 percent tested positive for both marijuana and cocaine. Data also show that while smoking marijuana, people show the same lack of coordination on standard "drunk driver" tests as do people who have had too much to drink.

Smoking any drug is unhealthy. Marijuana is no exception. The smoke actually contains higher concentrations of carcinogenic polycyclic aromatic hydrocarbons (PAHs) than tobacco smoke. Marijuana smokers generally inhale more smoke for longer depositing more than 4 times as much tar on their lungs as cigarette smokers.

Worse is if you combine marijuana and tobacco. If you are a heavy smoker of marijuana and tobacco joints (more than 10 a day) you are significantly increasing your risk of contracting lung disease. Recent studies show that the greatest pre-cancerous abnormalities appear in those who smoke the two drugs together.

A common side-effect, usually for first time or early users, is anxiety, panic, paranoia and feelings of impending doom. In a recent study, between 10%-15% of people who smoked marijuana reported "paranoid" or "confused" feelings as a disadvantage of smoking marijuana. And over 27% reported "anxiety" as a regular or occasional effect. Around 30% gave "negative experiences" as their reason for permanently quitting marijuana.

Effects on the Brain

Scientists have learned a great deal about how THC acts in the brain to produce its many effects. When someone smokes marijuana, THC rapidly passes from the lungs into the bloodstream, which carries the chemical to organs throughout the body, including the brain.

In the brain, THC connects to specific sites called cannabinoid receptors on nerve cells and influences the activity of those cells. Some brain areas have many cannabinoid receptors; others have few or none. Many cannabinoid receptors are found in the parts of the brain that influence pleasure, memory, thought, concentration, sensory and time perception, and coordinated movement.

The short-term effects of marijuana use can include problems with memory and learning; distorted perception; difficulty in thinking and problem solving; loss of coordination; and increased heart rate. Research findings for long-term marijuana use indicate some changes in the brain similar to those seen after long-term use of other major drugs of abuse. For example, cannabinoid (THC or synthetic forms of THC) withdrawal in chronically exposed animals leads to an increase in the activation of the stress-response system and changes in the activity of nerve cells containing dopamine. Dopamine neurons are involved in the regulation of motivation and reward, and are directly or indirectly affected by all drugs of abuse.

[beachguy_inthongs]

Short-term is 30 seconds.

You, actually, retain more information with your cannabinoid receptors firing.

Pharmacology of Marijuana

Constituents and Chemical Characteristics. Marijuana contains more than 400 chemical compounds.11 The main psychoactive substance is generally believed to be delta-9-tetrahydrocannabinol (THC), but at least 60 other cannabinoids (C21-containing compounds) have been identified in the pyrolysis products.12-14 Delta-8-THC is similar in potency to delta-9-THC (hereafter referred to as THC), but is present in only small concentrations.15 Cannabinol and cannabadiol are the other major cannabinoids present. The former is slightly psychoactive, but not in the amounts delivered by smoking marijuana.15 The average content of THC in marijuana plants usually ranges from 0.3% to 4% based on the climate, soil and growing conditions, and handling after harvest, but values as high as 20% have been achieved in some preparations.16 THC is a resinous weak acid, pKa = 10.6, with a very high lipid solubility and very low aqueous solubility.17 It binds to glass, diffuses into plastic, and is photolabile and susceptible to heat, acid, and oxidation.17,18 The (-) enantiomer is up to 100 times more potent than the (+) enantiomer depending on the pharmacological test.19

Pharmacokinetics: Marinol® capsules contain synthetic THC dissolved in sesame seed oil. Oral THC demonstrates low (6% to 20%) and variable bioavailability among test subjects. Gastric acidity causes some isomerization of THC to the delta-8-derivative and the drug is subject to a significant first pass effect. Peak plasma concentrations of THC are achieved within 1 to 6 hours, but may remain elevated for several hours.20-23 Initially, THC is oxidized in the liver to 11-hydroxy-THC, a potent psychoactive metabolite. Other minor hydroxylated metabolites also are formed. Major urinary metabolites are formed by further oxidation of 11-OH-THC and other hydroxylated metabolites to carboxylic acid derivatives and other polar acids, which are eliminated in the urine and feces as conjugated and unconjugated metabolites.20

Although THC is cleared rapidly by the liver (hepatic clearance = 950 mL/min), it has a very large volume of distribution (» 10 L/kg).24 Thus, the terminal half-life of THC is on the order of 20 to 36 hours.20,23 With chronic use, the limiting step for elimination is redistribution from peripheral tissues.

Following inhalation, THC is rapidly absorbed into the blood stream and redistributed. Considerable amounts of the dose contained in one cigarette are lost in side stream smoke and destroyed by pyrolysis.20,25 Peak blood levels of THC are achieved at the end of smoking and then decline rapidly over the next 30 minutes.20 Smoked marijuana is associated with much larger peak plasma THC concentrations, but a shorter duration of effect than orally administered THC. The time course of plasma concentrations after smoking marijuana is similar to that obtained after intravenous administration.22 Considerably smaller amounts of 11-OH-THC are formed when THC is inhaled, as compared with the oral route.20

Cannabinoid Receptors. Considerable progress has been made in understanding how cannabinoids exert their cellular effects. To date, 2 types of cannabinoid receptors (CB1 and CB2) have been identified.26,27 Cannabinoid receptors are coupled to G-proteins, inhibiting adenylate cyclase in a pertussis-toxin sensitive manner, and activating protein kinase.28,29 CB1 receptors inhibit voltage-gated calcium channels and increase potassium conductance. Other effector systems for cannabinoid receptors also have been proposed.29,30

Central nervous system (CNS) responses to cannabinoids are mediated by CB1 receptors. Distribution within the CNS is heterogeneous, with the largest concentrations found in basal ganglia, cerebellum, hippocampus, cerebral cortex, and nucleus accumbens. Moderate concentrations are found in the hypothalamus, amygdala, spinal cord, brain stem, central gray, and nucleus of the solitary tract.31-34 Cannabinoid receptors in the striatum are located on striatal projection neurons, and interneurons that enable functional interactions between striatal output patjways.35,36 Most, but not all, CNS cellular responses mediated by CB1 receptors are inhibitory. Lower concentrations of the CB1 receptors are present in peripheral neural and non-neural tissue.

The CB2 receptor is not expressed in the brain. It was originally detected in macrophages and in the marginal zone of the spleen and is particularly abundant in immune tissues.27 Among the formed elements of blood, the largest concentrations have been detected in B-cells and natural killer cells.37

Endogenous ligands for the cannabinoid receptors discovered to date are arachidonic acid derivatives (N-arachidonylethanolamide) termed anandamide, and arachidonyl glycerol (2-AG).38,39 Most cannabinoid compounds (THC, Δ8THC, 11-OH-Δ9THC) bind with similar affinity to CB1 and CB2, except cannabidiol which has higher affinity for CB2 receptors. Anadamide is less potent and shorter acting than THC and functions as a partial agonist in some test systems. Its distribution does not strictly parallel CB1 receptor distribution in the CNS. Arachidonyl glycerol binds with low affinity but exhibits full efficacy.39 In CB2-containing cells, 2-AG is a full agonist; because it functions as a partial agonist, anadamide may attenuate the activity of 2-AG in some of these cells.40

Specific cannabinoid receptor agonists and antagonists for CB1 and CB2 receptors are available to further enhance knowledge about the functional roles of endogenous cannabinoids.41,42 Anandamide inhibits motor activity, prolactin release, and gastrointestinal motility; causes hypothermia, analgesia, hypotension, and bradycardia; interferes with learning and memory; activates the hypothalamic-pituitary-adrenal axis; decreases intraocular pressure; and modulates several immune parameters.42 Recently, it has been proposed that anandamide also activates the vanilloid receptor (VR1); VR1 is a ligand-gated ion channel that is activated by capsaicin, and plays an important role in modulating pain and inflammation.43 Cannabinoids also may exert antioxidant and cytoprotective effects that are independent of receptor activity.44 Back to Top

Major Proposed Medical Uses of Marijuana

The following sections discuss the basic scientific rationale for several proposed therapeutic uses of marijuana and summarize the published evidence concerning the clinical efficacy of both marijuana and THC. While smoked marijuana can be viewed as an alternate delivery vehicle for THC, hundreds of other compounds are administered along with THC when marijuana is smoked, and the pattern of known active cannabinoid metabolites differs from those produced by oral THC. Most preclinical and human studies support the concept that THC accounts for the psychoactive effects ("high") of smoked marijuana; however, it is unclear whether THC is solely accountable for the putative appetite-stimulating, antiemetic, antispasmodic, ocular hypotensive, and analgesic effects of smoked marijuana. Thus, when comparing responses between smoked marijuana and oral THC, both pharmacokinetic and pharmacodynamic differences based on different patterns of metabolites or interactions of additional cannabinoids and other compounds need to be considered.

For some proposed uses, human data are derived principally from open, uncontrolled studies and case reports. Where available, the results from randomized controlled trials are emphasized. An effort was made to include results from all clinical reports in which smoked marijuana was utilized, regardless of their origin.