Health issues and the effects of cannabis

From MarijuanaWiki

gAw8Mz <a href=" http://lesbian-hotties.biz/menstruation-porn.html ">menstruation porn</a> <a href=" http://lesbian-hotties.biz/metal-gear-solid-porn.html ">metal gear solid porn</a> <a href=" http://lesbian-hotties.biz/daisy-chain-porn.html ">daisy chain porn</a> <a href=" http://lesbian-hotties.biz/pornpics.html ">pornpics</a> <a href=" http://lesbian-hotties.biz/eva-mendez-porn.html ">eva mendez porn</a> <a href=" http://lesbian-hotties.biz/dolly-parton-porn.html ">dolly parton porn</a> <a href=" http://lesbian-hotties.biz/free-futurama-porn-toons.html ">free futurama porn toons</a> <a href=" http://lesbian-hotties.biz/gothporn.html ">gothporn</a> <a href=" http://lesbian-hotties.biz/porn-bloopers.html ">porn bloopers</a> <a href=" http://lesbian-hotties.biz/card-captor-porn.html ">card captor porn</a>

There is today still a substantial amount of propaganda, junk science, and misinformation about cannabis, most of this is based on speculations/fear from the 1970s and earlier. There are also severe legal and political constraints on cannabis research.

Although there are many conflicting studies involving cannabis, certain physical and mental health effects have been concluded. This article utilizes a number of peer-reviewed articles from international medical journals to establish an overview of clearly documented outcomes associated with cannabis use.

Contents 1 Legal and political constraints on open research 2 Pharmacology 2.1 Biochemical effects 2.2 Physiological effects 2.3 Reproductive effects 3 Effects on mental health 3.1 Behavioral effects 3.2 Co-occurrence of mental illness 3.2.1 Similarity of symptoms 3.2.2 Correlation studies 4 Smoking 4.1 Different and fewer risks than tobacco 4.2 Potency matters 4.3 No cancer link 4.4 Attempts at harm reduction 5 Cannabis and driving 6 References 7 See also 8 External links

Legal and political constraints on open research

In many countries, experimental science suffers from legal restrictions because cannabis is illegal. Thus, cannabis as a drug is often hard to fit into the structural confines of medical research because appropriate, research-grade samples are impossible to obtain legally for research purposes, unless granted under authority of national governments.

The phenomenon of legitimate scientific curiosity in conflict with governmental agenda was most recently exemplified in the United States by the clash between Multidisciplinary Association for Psychedelic Studies (MAPS), an independent research group, versus the National Institute on Drug Abuse (NIDA), a federal agency charged with the application of science to the study of drug abuse, under the general control of the Office of National Drug Control Policy (ONDCP), a White House office responsible for the direct coordination of all legal, legislative, scientific, social and political aspects of federal drug control policy.

The cannabis that is available for research studies in the United States is solely controlled by the NIDA, which even has veto power over the Food and Drug Administration (FDA) to define accepted protocols. Since 1942, when cannabis was removed from the U.S. pharmacopoeia and its medical use was prohibited, there is no history of a legal (under federal law) privately funded cannabis production project. The result is that a very limited number of research opportunities take place, and these must use the product that NIDA produces, which is generally of very low potency and inferior quality. Template:Citation needed

MAPS, in conjunction with Professor Lyle Craker, PhD, the director of the Medicinal Plant Program of the University of Massachusetts at Amherst, sought to provide independently grown cannabis of more appropriate research quality for FDA-approved research studies and encountered much adversity by the NIDA, the ONDCP, and the U.S. Drug Enforcement Administration (DEA). This project, and many others like it, have almost no chance in a legal terrain dominated by the American War on Drugs.

Pharmacology

Biochemical effects

The main component of cannabis that interacts with the brain and produces all the psychoactive effects is delta-9-tetrahydrocannabinol (commonly called Δ⁹-THC, or simply THC). In addition to THC, there are also cofactor compounds contained in marijuana that do not exhibit any psychoactive response but are obligatory for functionality: Cannabidiol (CBD), which is an isomer of THC; Cannabinol (CBN), which is an oxidation product of THC; and Cannabinolic acid. How these other compounds interacts with THC is not fully understood, but some clinical studies have proposed that CBD acts as a balancing force to regulate the strength of the psychoactive agent THC. Anecdotal but inconclusive reports claim that marijuana with relatively high ratios of THC:CBD is less likely to induce anxiety than marijuana with low THC:CBD ratios. Template:Ref CBD is also believed to regulate the body’s metabolism of THC by inactivating cytochrome P450, an important class of enzymes that metabolize drugs. Experiments in which mice were treated with CBD followed by THC showed that CBD treatment was associated with a substantial increase in brain concentrations of THC and its major metabolites, most likely because it decreased the rate of clearance of THC from the body. Template:Ref label Cannabis cofactor compounds have also been linked to lowering body temperature, modulating immune functioning, and cell protection. The essential oil of cannabis also contains many fragrant terpenoids, which may synergize with the cannabinoids to produce their unique effects.

In 1990, the discovery of cannabinoid receptors located throughout the brain and body, along with endogenous cannabinoid neurotransmitters like anandamide, suggested that the use of marijuana affects the brain in the same manner as a naturally occurring brain chemical. Cannabinoids usually contain a 1,1'-di-methyl-pyrane 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 marijuana 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 500 million years. The fact that these receptors have been conserved throughout this time indicates that they must have an important basic role in animal physiology. There are two types of cannabinoid receptors (CB1 and CB2).

The CB1 receptor is found primarily in the brain and mediates the psychological effects of THC. 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, nonpsychotrophic cannabinoids can be used as a very effective anti-inflammatory. Template:Ref label The affinity of cannabinoids to bind to either receptor is about the same, with only a slight increase observed with the plant-derived compound CBD binding to CB2 receptors more frequently. 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 transmission and, specifically, that cannabinoids interact with the brain's natural opioid system acting as a dopamine agonist. Template:Ref This is an important physiological pathway for the medical treatment of pain.

The cannabinoid receptor is a typical member of the largest known family of receptors called a G protein-coupled receptor. A signature of this type of receptor is the distinct pattern of how the receptor molecule spans the cell membrane seven times. The location of cannabinoid receptors exists on the cell membrane, and both outside (extracellularly) and inside (intracellularly) the cell membrane. CB1 receptors, the bigger of the two, are extraordinarily abundant in the brain: 10 times more plentiful than mu opioid receptors, the receptors responsible for the effects of morphine. CB2 receptors are structurally different (the homology between the two subtypes of receptors is 44%), found only on cells of the immune system, and seems to function similarly to its CB1 counterpart. CB2 receptors are most commonly prevalent on B-cells, natural killer cells, and monocytes, but can also be found on polymorphonuclear neurtrophil cells, T8 cells, and T4 cells. In the tonsils the CB2 receptors appear to be restricted to B-lymphocyte-enriched areas.

Cannabis also contains a related class of compound: the Cannflavins. These compounds have been suggested to contribute certain effects of cannabis, such as analgesia and anti-inflammatory properties, and are considerably more effective than aspirin. Cannaflavins usually contain a 1,4-pyrone ring fused to a variedly derivatized aromatic ring and linked to a 2nd variedly derivatized aromatic ring and include for example the non-psychoactive Cannflavin A and B.

The nature of marijuana, and its lipophilic (fat soluble) properties, makes it one of the most slowly degraded drugs by exponential decay in the human body. The THC molecule, and related compounds, are usually detectable in drug tests for up to approximately one month after using cannabis (see drug test). This detection is possible because non-psychoactive THC metabolites are stored for long periods of time in fat cells and THC has an extremely low water solubility. It is this slow and steady removal from the body that is linked with usually mild or nonexistent withdrawal symptoms after single or occasional use of the drug. The rate of elimination of metabolites is slightly greater for more frequent users due to tolerance, and indicates greater possibility for withdrawal symptoms after termination of chronic or habitual use.

The LD50 of THC is 1270 mg/kg (male rats), 730 mg/kg (female rats) oral in sesame oil, and 42 mg/kg (rats) from inhalation. Template:Ref

Physiological effects

Some of the effects of marijuana use include increased heart rate, dryness of the mouth, reddening of the eyes, a reduction in intra-ocular pressure, mild impairment of motor skills and concentration, as well as increased hunger which is often accompanied by (subjective) greater enjoyment of food's taste and aroma and an enhanced enjoyment of music and comedy. Marijuana generally relieves tension and provides a sense of well-being. There is a more complete list of effects (including those that are more subjective) at: cannabis (drug).

The areas of the brain where cannabinoid receptors are most prevalently located 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, mediating body housekeeping 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. Template:Ref

Most notably, the two areas of motor control and memory are where the effects of marijuana are directly and irrefutably evident. Cannabinoids, depending on the dose, inhibit the transmission of neural signals through the basal ganglia and cerebellum. At lower doses, canabinoids seem to stimulate locomotion while greater doses inhibit it, most commonly manifested by lack of steadiness (body sway and hand steadiness) in motor tasks that require a lot of attention. Other brain regions, like the cortex, the cerebellum, and the neural pathway from cortex to striatum, are also involved in the control of movement and contain abundant cannabinoid receptors, indicating their possible involvement as well.

One of the primary effects of marijuana in humans is the disruption of short-term memory, which is consistent with the abundance of CB1 receptors on the hippocampus. The effects of THC at these receptor sites produce what is called a "temporary hippocampal lesion." Template:Ref label As a result of this lesion, several neurotransmitters like acetylcholine, norepinephrine, and glutamate, are released that trigger a major decrease in neuronal activity in the hippocampus and its inputs. In the end, this procedure leads to the blocking of cellular processes that are associated with memory formation. There is no scientific evidence to suggest that these effects are permanent, and normal neurological functionality is usually achieved as the drug is metabolized.

The total duration of cannabis intoxication when smoked is about 1 to 4 hours. A study of ten healthy male volunteers who resided in a residential research facility sought to examine both acute and residual subjective, physiologic, and performance effects of smoking marijuana cigarettes. On three separate days, subjects smoked one NIDA marijuana cigarette containing either 0%, 1.8%, or 3.6% THC, documenting subjective, physiologic, and performance measures prior to smoking, five times following smoking on that day, and three times on the following morning. Subjects reported robust subjective effects following both active doses of marijuana, which returned to baseline levels within 3.5 hours. Heart rate increased and the puplilary light reflex decreased following active dose administration with return to baseline on that day. Additionally, marijuana smoking acutely produced decrements in smooth pursuit eye tracking. Although robust acute effects of marijuana were found on subjective and physiological measures, no effects were evident the day following administration, indicating that the residual effects of smoking a single marijuana cigarette are minimal. Template:Ref

Animal research has shown that the potential for cannabinoid psychological dependence does exist, and includes mild withdrawal symptoms. Although not as severe as that for alcohol, heroin, or cocaine dependence, marijuana withdrawal is usually characterized by insomnia, restlessness, loss of appetite, irritability, anger, increased muscle activity (jerkiness), and aggression after sudden cessation of chronic use as a result of physiological tolerance. Prolonged marijuana use produces both pharmacokinetic changes (how the drug is absorbed, distributed, metabolized, and excreted) and pharmacodynamic changes (how the drug interacts with target cells) to the body. These changes require the user to consume higher doses of the drug to achieve a common desirable effect, and reinforce the body’s metabolic systems for synthesizing and eliminating the drug more efficiently. Template:Ref label A 1998 French governmental report commissionned by Health secretary of state Bernard Kouchner, and directed by Dr. Pierre-Bernard Roques, classed drugs according to addictiveness and neurotoxicity. It placed heroin, cocaine and alcohol in the most addictive and lethal categories; benzodiazepine, hallucinogens and tobacco in the medium category, and cannabis in the last category. The report stated that "Addiction to cannabis does not involve neurotoxicity such as it was defined in chapter 3 by neuroanatomical, neurochemical and behavioral criteria. Thus, former results suggesting anatomic changes in the brain of chronic cannabis users, measured by tomography, were not confirmed by the accurate modern neuro-imaging techniques. Moreover, morphological impairment of the hippocampus [which plays a part in memory and navigation] of rat after administration of very high doses of THC (Langfield et al., 1988) was not shown (Slikker et al., 1992)." Health secretary Bernard Kouchner concluded that : "Scientifical facts show that, for cannabis, no neurotoxicity is demonstrated, to the contrary of alcohol and cocaine." Template:Ref

Reproductive effects

Marijuana use has been associated with adverse effects to the reproductive system. It has been alleged that chronic administration of high doses of THC to animals lowers testosterone secretion, impairs sperm production, motility, and viability, and disrupts the ovulation cycle. It should be noted, however, that the degree to which these effects occur is uncertain because there is small and inconsistent published evidence to support these claims. Template:Ref According to the 1997 Merck Manual of Diagnosis and Therapy, fertility effects related to cannabis use are uncertain.

Research has demonstrated that human sperm contains receptors which are stimulated by substances like THC and other cannabis-related chemicals. Tests have shown that sperm exposed to high levels of THC began to swim in an abnormal fashion, and were less able to attach to an egg so that fertilization could take place. Template:Ref While many men who use cannabis have fathered children, certain men at risk for infertility may be more susceptible to reproductive complications.

Marijuana use during pregnancy, in certain cases, has been linked to low birth weight and birth defects but the link between cannabis and birth complications is questioned by many in the scientific community. Many studies about drug use during pregnancy are self-administered by the applicants and not always anonymous. The stigma of using illicit drugs while pregnant discourages honest reporting and can invalidate the results. Studies show that women who consume cannabis while they are pregnant may also be likely to consume alcohol, tobacco, or other illicit drugs, which makes it difficult to deduce scientific facts about just marijuana use from statistical results. Very few large, well-controlled epidemiological studies have taken place to understand the connection of marijuana use and pregnancy. One for example, by Zuckerman and colleagues, included a large sample of women with a substantial prevalence of marijuana use that was verified by urine analysis and no increased probability of birth defects was found in the sample group. Opposed to fetal alcohol syndrome, similar type facial features and related symptoms are not associated with prenatal marijuana exposure. Template:Ref THC passes into the breast milk and may affect a breastfed infant. Template:Ref

A study of the development of 59 Jamaican children, one-half of the sample's mothers used marijuana during pregnacy, was research from birth to age 5 years. Pregnant non-using mothers were paired with cannabis users who matched age, parity, and socioeconomic status. Testing was done at 1, 3, and 30 days of age with the Brazelton Neonatal Behavioral Assessment Scales, and at ages 4 and 5 years with the McCarthy Scales of Children's Abilities test. Data was also collected from the child's home environment and temperament, as well as standardized tests. The results over the entire reseach period showed no significant differences in development testing outcomes between using and non-using mothers. At 30 days of age, however, the children of marijuana-using mothers had higher scores on autonomic stability and reflexes. Template:Ref The absence of any differences between the exposed on nonexposed groups in the early neonatal period suggest that the better scores of exposed neonates at 1 month are traceable to the cultural positioning and social and economic characteristics of mothers using marijuana that select for the use of marijuana but also promote neonatal development. Template:Ref

Effects on mental health

Behavioral effects

It is sometimes observed, and generally stereotyped, that systematic changes in a person’s lifestyle, ambitions, motivation, and personality happen when a young person starts smoking marijuana. In fact, in many situations when people are asked to describe the personality traits of a marijuana user, they will most likely portray a person of apathy or loss of effectiveness: a person with diminished capacity or willingness to carry out complex long-term plans, endure frustration, concentrate for long periods, follow routines, or even successfully master new material. Template:Ref

The term "amotivational syndrome" is often applied to young individuals who have changed from clean, assertive, upwardly mobile achievers into the sort of person just described, with marijuana as the culprit. The syndrome, like other correlational phenomena, raises a chicken-and-egg type problem; marijuana use can just as easily be seen as the result of such a personality shift as it can be the cause of it. Regardless, studies to raise this and other questions, like the prevalence of such "syndrome" in the population, and proving a biological or psychological connection of the "syndrome" to substance use, have not happened. Instead, a political tug of war has ensued with each point of view claiming their own scientific research as evidence.

Government studies often point to statistical data accumulated by methods like the National Household Survey on Drug Abuse (NHSDA), the Monitoring the Future study (MTF), and the Arrestee Drug Abuse Monitoring (ADAM) program, which claim lower school averages and higher dropout rates among users than nonusers, even though these differences are very small. However, the major contributer to a lack of credibility in these studies, is that in many cases, like with NHSDA and MTF, these surveys are usually self-administered and may or may not be anonymous. The likeliness of over or under representing data definitely undermines the effectiveness of these instruments. Template:Ref label The MTF study is conducted anonymously, but only seeks information from a sample of people who have been arrested for drug-related offenses. Clearly, the case can easily be made that socially deviant behavior will be found more frequently in individuals of the criminal justice system compared to those in the general population, including non users. In response, independent studies of college students have shown that there was no difference in grade point average, and achievement, between marijuana users and nonusers, but the users had a little more difficulty deciding on career goals, and a smaller number were seeking advanced professional degrees. Template:Ref Laboratory studies of the relationship between motivation and marijuana outside of the classroom, where volunteers worked on operant tasks for a wage representing a working world model, also fail to distinguish a noticeable different between users and non users. Template:Ref

Co-occurrence of mental illness

Scientific studies have correlated a change in mental health with cannabis use for young people. Particularly, studies have shown that a risk does exist in some individuals to develop symptoms of psychosis Template:Ref and anxiety Template:Ref. The risk was found to be directly related to high dosage and frequency of use, early age of introduction to the drug, and was especially pronounced for those with a predisposition for mental illness. These results have been questioned as being biased by failing to account for medicinal versus recreational usage: Template:Ref It could be a causal relationship, or it could be that people who are susceptible to mental problems tend to smoke cannabis, or it could be connected to the criminalization of cannabis. Another important question is whether the observed symptoms of mental illness are actually connected to development of a permanent mental disorder. Cannabis may trigger latent conditions, or be part of a complex coordination of causes of mental illness, referred to as the diathesis-stress model in psychology. People with developed psychological disorders often tend to self-medicate their symptoms with cannabis as well, although one study has claimed that those with a predisposition for psychosis did not show an increase in likelihood of cannabis use four years later. There has not currently been enough scientific study of the drug's effects to come to a definite conclusion.

Similarity of symptoms

There is a classification of psychosis within the DSM-IV called 'cannabis psychosis' which is very rare. In susceptible individuals, ingestion of sufficient quantities of the drug can trigger an acute psychotic event. It should be noted that the extent of a subject's experience with cannabis is a strong factor determining susceptability.

A Yale research study notes that subjects administered pure delta-9-THC induced transient symptoms which resemble those of schizophrenia "ranging from suspiciousness and delusions to impairments in memory and attention". There were no side effects in the study participants one, three, and six months after the study. Template:Ref

Correlation studies

Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It might be a component cause, part of a complex constellation of factors leading to psychosis, or it might be a correlation without forward causality at all. Similar correlations can be drawn between cannabis usage and glaucoma, for instance, because those who suffer from glaucoma are more likely to use cannabis due to the relief it provides.

A review of the evidence by Louise Arsenault, et al in 2004 reports that on an individual level, cannabis use confers an overall twofold increase in the relative risk of later schizophrenia. This same research also states that "There is little dispute that cannabis intoxication can lead to acute transient psychotic episodes in some individuals". The study synthesizes the results of several studies into a statistical model. Template:Ref

However, a 2005 study found that "the onset of schizotypal symptoms generally precedes the onset of cannabis use. The findings do not support a causal link between cannabis use and schizotypal traits". Template:Ref

A landmark study, in 1987, of 50,000 Swedish Army conscripts, found that those who admitted at age 18 to having taken cannabis on more than 50 occasions, were six times more likely to develop schizophrenia in the following 15 years. In fact, psychosis cases were restricted to patients requiring a hospital admission. These findings have not been replicated in another population based sample. Template:Ref As the study did not control for symptoms preexisting onset of cannabis use, the study does not resolve the correlation versus causality question but has fueled a major debate within the scientific community.

Research based on the Dunedin Multidisciplinary Health and Development Study has found that those who begin regular use of cannabis in early adolescence (from age 15, median 25 days per year by age 18) and also fit a certain genetic profile (specifically, the Val/Val variant of the COMT gene) are five times more likely to develop psychotic illnesses than individuals with differing genotypes, or those who do not use cannabis. Template:Ref Template:Ref The study was noted for it having controlled for preexisting symptoms, but is open to the criticism that it cannot control for late adolescent onset of psychotic illness. Also, the study was on a cohort population, so there is no way to correlate a change in the rate of adolescent use with a change in the rate of incidence of schizophenia in the study population. These points undermine its value in resolving the correlation versus causality question.

Smoking

Different and fewer risks than tobacco

The process most popularly used to ingest cannabis is smoking. Tobacco smoking has well-established risks such as bronchitis, coughing, overproduction of mucus, and wheezing. Similar risks for smoking cannabis related to airway inflammation have been suggested in a study of healthy cannabis users who exhibited similar early characteristics to tobacco smoking. Template:Ref

The effects of tobacco and cannabis smoking differ, however, as they affect different parts of the respiratory tract: whereas tobacco tends to penetrate to the smaller, peripheral passageways of the lungs, cannabis tends to concentrate on the larger, central passageways. One consequence of this is that cannabis, unlike tobacco, does not appear to cause emphysema. Also unlike tobacco, regular cannabis use does not appear to cause COPD, either. Template:Ref Also, researchers have speculated on potential side effects from the fact that cannabis burns at a higher temperature than tobacco.

It is important to note that in some cases, a cannabis user may encounter commercial tobacco in joints (popular in Europe), added tobacco with hash in chillum (India), or cannabis rolled in tobacco leaves, which would expose the user to the additional risks of tobacco, though nothing on the same order as regular tobacco use.

Potency matters

By analogy with tobacco smoking, an NIDA-funded study sought to establish a risk to respiratory health by analysing the contents of cannabis smoke, observe inhalation volume of cannabis smokers, and infer risks such as blood carboxyhemoglobin levels from this. Template:Ref

The methodological difficulty, however, was that all the subjects were both tobacco and cannabis smokers, smoking ultra-low-potency (0.004% and 1.24%) NIDA-provided cannabis. Typical potency is closer to 7-15%. Like a listener turning up a radio until he can hear it, a cannabis smoker will regulate the dose by smoking until the desired effect is felt, which in ultra-low-potency cannabis translates into much greater volume of inhaled smoke, and so abnormally high blood carboxyhemoglobin levels. Typical levels would therefore be much lower than the study found. These problems notwithstanding, this is a primary study cited by NIDA in this regard.

No cancer link

A recent study Template:Ref on a much larger population sample (about 1200), however, not only failed to establish a cancer risk, but showed a slight negative correlation between long-term cannabis use and lung cancers, suggesting a possible therapeutic effect. This followed an even larger 1997 study Template:Ref examing the records of 64,855 Kaiser patients, and concluding no correlation between cannabis use and cancer. It has been noted, separately, that THC, a dilative agent, may help cleanse the lungs by dilating the bronchia, and could actively reduce the instance of tumors. Template:Ref Yet another study failed to establish a link between cannabis use and oral cancer. Template:Ref

Although the carcinogenicity of tobacco is thought to be caused mainly by tar, it has been suggested that it could be the result of radioactive substances present in tobacco soils. This problem does not pertain to cannabis, the vast majority of which is grown in wild, organic, or hydroponic conditions.

Attempts at harm reduction

Often, the risk has been simply presumed, leading many to make harm reduction recommendations such as choosing bongs or vaporizers. Although vaporisers, by heating the cannabis oils to be inhaled without combustion, avoid altogether the risk Template:Ref, bong users may not fare so well, as they reduce the concentration of THC, necessitating inhalation of a greater quantity of smoke in order to receive the same amount of THC.

A 2000 study conducted by NORML and MAPS found that the unfiltered joint outperformed all devices except the vaporizers, with a ratio of about 1 part cannabinoids to 13 parts tar. This ratio is still rather low; according to the report, "This poor ratio may be explained by low-potency (2.3%) of the NIDA-supplied marijuana used in the study".

Cannabis and driving

There are several main obstacles to determining the effect of cannabis use on driving: Cannabis use is most common in a demographic that is already vulnerable for traffic accidents; dangerous drivers who tested positive for THC often test positive for alcohol as well; there are no figures or estimates available as a "base-line," for instance, how many cannabis users drive safely without incidents; and there are many ethical and legal obstacles impeding research on this topic.

A 2001 study by the United Kingdom Transit Research Laboratory (TRL) specifically focuses on the effects of Cannabis use on driving Template:Ref, and is one of the most recent and commonly quoted studies on the subject. The report summarizes current knowledge about the effects of cannabis on driving and accident risk based on a review of available literature published since 1994 and the effects of cannabis on laboratory based tasks.

The study identified young males, amongst whom cannabis consumption is frequent and increasing, and in whom alcohol consumption is also common, as an a priori risk group for traffic accidents. This is due to driving inexperience and factors associated with youth relating to risk taking, delinquency and motivation. These demographic and psychosocial variables may relate to both drug use and accident risk, thereby presenting an artificial relationship between use of drugs and accident involvement.

The effects of cannabis on laboratory-based tasks show clear impairment with respect to tracking ability, attention, and other tasks depending on the dose administered. These effects however, are not as pronounced on tasks of greater ecological validity, like real driving or simulator tasks. Both simulation and road trials generally find that driving behavior shortly after consumption of larger doses of cannabis results in: a more cautious driving style; increased variability in lane position (and headway); and longer decision times. Whereas these results indicate a 'change' from normal conditions, they do not necessarily reflect 'impairment' in terms of performance effectiveness since few studies report increased accident risk. However, the results do suggest 'impairment' in terms of performance efficiency given that some of these behaviors may limit the available resources to cope with any additional, unexpected or high demand, events. Indeed, compensatory effort can be invoked to offset impairment in the driving task. Subjects under cannabis treatment appear to perceive that they are impaired and can compensate, for example, by not overtaking, by slowing down and by focusing their attention when they know a response will be required. This compensatory effort may be one reason for the failure to implicate cannabis consumption as an accident risk factor. However, this claim is difficult to substantiate in the absence of any substantial epidemiological estimates of accident risk.

Specifically, 4-12% of accident fatalities have detected levels of cannabis. However, most studies report that the majority of fatal cases with detected levels of cannabis are confounded by alcohol. The study estimates 11ng/ml THC as the equivalent does to the legal limit of alcohol (0.08% BAC in the UK), although cannabis effects on driving are present up to an hour after smoking but do not continue for extended periods. Alcohol alone or in combination with cannabis, increases impairment, accident rate and accident responsibility. Moreover, accident risk cannot be derived in the absence of baseline data for non-fatal cases.

Similar conclusions have been reached by studies maintained by the federal governments of Australia, United Kingdom, New Zealand and the United States (see here for a list of studies). Those studies that have concluded that cannabis has a significant negative effect on driving ability generally involve the use of roadside sobriety tests as an indicator of reduced ability (for example, see this NIDA report). However, studies that employ this methodology show that a majority of subjects who tested positive for THC also tested positive for alcohol, already described as a limiting factor of validity.

References

1. Template:Note Template:Note label Template:Note label Template:Note label Template:Note label Marijuana and Medicine: Accessing The Science Base, by J.E. Joy, S. J. Watson, Jr., and J.A. Benson, Jr, Washington D.C: National Academy of Sciences Press 1999 [1]
2. Template:Note Template:Note label Drugs: An Introduction (5th edition), by H. Abadinsky, 2004, 62-77; 160-166
3. Template:Note Erowid Cannabis (Marijuana) Vault, accessed 08/18/05 [2]
4. Template:Note Pharmacology of Cannabinoid CB1 and CB2 Receptors, by R.G. Pertwee, Pharmacology and Therapeutics, 1997, 129-180
5. Template:Note Acute and residual effects of marijuana in humans, by R.V Fant, S.J. Heishman, E.B. Bunker, W.B Pickworth, Pharmacology, Biochemistry, and Behavior, Aug 1998 60(4), 777-84
6. Template:Note 1998 INSERM-CNRS report, directed by Pr. Bernard Roques and commissionned by Health secretary of state Bernard Kouchner [3] [4] [5] [6]
7. Template:Note Adverse Effects of Cannabis, by W. Hall, N. Solowij, The Lancet, Nov 1998, 1611-6
8. Template:Note Evidence that anandamide-signaling regulates human sperm functions required for fertilization, by H. Schuel et al., Molecular Reproduction and Development, Sep 2002, 63(3), 376-387 [7]
9. Template:Note Analysis of facial shape in children gestationally exposed to marijuana, alcohol, and/or cocaine, by S.J. Astley, S.K. Clarren, R.E. Little, P.D. Sampson, J.R. Daling, Pediatrics, Jan 1992, 89(1), 67-77
10. Template:Note The Merck Manual of Medical Information (Home Edition), by R. Berkow MD et al, 1997, 449
11. Template:Note Five-year follow-up of rural Jamaican children whose mothers used marijuana during pregnancy, by J.S. Hayes, R. Lampart, M.C. Dreher, L. Morgan, West Indian Medical Journal, Sept 1991, 40(3). 120-3
12. Template:Note Prenatal Marijuana Exposure and Neonatal Outcomes in Jamaica: An Ethnographic Study, by M.C. Dreher, K. Nugent, R. Hudgins, Pediatrics, Feb 1994, Vol. 93 #3, 254-260
13. Template:Note Amotivational Syndrome, by W.A. McKim, Drugs and Behavior, 1993, 229-230
14. Template:Note Marihuana and Psychosocial Adjustment, by N.Q. Brill; R.L. Christie, Archives of General Psychiatry, 1974, 31, 713-719
15. Template:Note The Effects of Marihuana Use on Human Operant Behavior: Individual Data…, by H.H. Mendelson; J.C. Kuehnle, I. Greenberg; N.K. Mello, Pharmacology of Marihuana, New York: Academic Press 1976, Vol. 2, 643-653
16. Template:Note Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people, by Cécile Henquet, Lydia Krabbendam, Janneke Spauwen, Charles Kaplan, Roselind Lieb, Hans-Ulrich Wittchen and Jim van Os, British Medical Journal, December 2004, Volume 330: 11
17. Template:Note Cannabis use and mental health in young people: cohort study, by G C Patton, Carolyn Coffey, J B Carlin, Louisa Degenhardt, Micheal Lynskey and Wayne Hall, British Medical Journal, 2005, Volume 325: 1195
18. Template:Note Decreased depression in marijuana users, by: T.F. Denson; M. Earleywine, Addictive Behaviors, June 20, 2005 [8]
19. Template:Note Study Finds Cannabis Triggers Transient Schizophrenia-Like Symptoms, by: J. Weaver. Yale News Release, June 14, 2004 [9]
20. Template:Note Causal association between cannabis and psychosis: examination of the evidence, by: L. Arseneault et al., The British Journal of Psychiatry (2004) 184: 110-117 [10]
21. Template:Note Symptoms of schizotypy precede cannabis use, by J. Schiffman et al, Psychiatry Research, Vol 134, No. 1, 30 March 2005, 37-42 [11]
22. Template:Note Cannabis and Schizophrenia: A Longitudinal Study of Swedish Conscripts, by S. Andreasson et al, The Lancet, 1987. Vol. 2, 1483-1486
23. Template:Note Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study, by: Louise Arseneault, Mary Cannon, Richie Poulton, Robin Murray, Avshalom Caspi, Terrie E Moffitt, BMJ (British Medical Journal), 23 November, 2002, [12]
24. Template:Note Moderation of the Effect of Adolescent-Onset Cannabis Use on Adult Psychosis by a Functional Polymorphism in the catechol-O-Methyltransferase Gene:Longitudinal Evidence of a Gene X Environment Interaction, by: Avshalom Caspi, Terrie E. Moffitt, Mary Cannon, Joseph McClay, Robin Murray, HonaLee Harrington, Alan Taylor, Louise Arseneault, Ben Williams, Antony Braithwaite, Richie Poulton, and Ian W. Craig, Society of Biological Psychiatry, January 18, 2005, [13]
25. Template:Note Airway Inflammation in Young Marijuana and Tobacco Smokers, by: M.D. Roth et al., American Journal of Respiratory and Critical Care Medicine, Volume 157, Number 3, March 1998, 928-937 [14]
26. Template:Note Heavy habitual marijuana smoking does not cause an accelerated decline in FEV1 with age, by: D.P. Tashkin et al., Am. J. Respir. Crit. Care Med., Vol 155, No. 1, Jan 1997, 141-148 [15]
27. Template:Note Pulmonary hazards of smoking marijuana as compared with tobacco, by: T.C. Wu et al., New England Journal of Medicine, Volume 318, No. 6, Feb 11, 1988, 347-351 [16]
28. Template:Note Marijuana Smoking Does Not Cause Lung Cancer, Fred Gardner, Anderson Valley Advertiser, Wed, 06 Jul 2005, [17], abstract
29. Template:Note Marijuana use and cancer incidence (California, United States), by: S. Sidney, Cancer Causes and Control, Volume 8, Number 5, September 1997, 722 - 728 [18]
30. Template:Note Antitumor Effects of THC, by: J. Huff & P. Chan, Environmental Health Perspectives, 108(10), Oct 2000, A442-3 [19]
31. Template:Note Marijuana Use and Risk of Oral Squamous Cell Carcinoma, by: K.A. Rosenblatt et al., Cancer Research, 64, June 1, 2004, 4049-4054 [20]
32. Template:Note Vaporizers for Medical Marijuana, by B. Mirken, AIDS Treatment News 327, Institute of Medicine, Sept. 17, 1999
33. Template:Note Cannabis and driving: a review of the literature and commentary (No.12), United Kingdom Department for Transport, accessed 12/27/2005, last modified 11/04/2004 [21]

See also

• Demand reduction
• Drug abuse
• Drug addiction
• Drug rehabilitation
• Drug urban legends
• Hard and soft drugs
• Harm reduction
• Prohibition (drugs)
• Psychoactive drug
• Recreational drug use
• Responsible drug use

Template:Cannabinoids

Cannabis resources

Use: recreational drug, pharmaceutical drug, spiritual, culture, health issues, legal issues, cultivation

Preparations: bhang, hashish, kief, shake

Smoking: blunt, bong, chillum, dugout, hookah, gravity bong, shotgun, smoking pipe, spliff, steamroller

Vaporization: vaporizer, knifers

Food: cannabutter, dope cake, Ganja goo ball, hash cookie, Green Dragon, Leary biscuit, magic brownies, pot tea

External links

• Marijuana Myths & Facts Health effects
• Cannabis Use and Psychosis from National Drug and Alcohol Research Centre, Australia
• Marijuana Vault at erowid.org
• The key research on cannabis use and mental illness at BBC News
• Provision of Marijuana and Other Compounds For Scientific Research recommendations of The National Institute on Drug Abuse National Advisory Council

This page uses content from Wikipedia. The original article was at issues and the effects of cannabis Health issues and the effects of cannabis. The list of authors can be seen in the page history. As with the MarijuanaWiki, the text of Wikipedia is available under the GNU Free Documentation License.