Prison abolition movement

From Wikipedia, the free encyclopedia

The prison abolition movement is a loose network of groups and activists that seek to reduce or eliminate prisons and the prison system, and replace them with systems of rehabilitation that do not place a focus on punishment and government institutionalization. The prison abolitionist movement is distinct from conventional prison reform, which is the attempt to improve conditions inside prisons.

Supporters of prison abolition also work to end solitary confinement, the death penalty, and the construction of new prisons. Others support book to prisoner projects and defend the rights of prisoners to have access to information and library services. Some organizations such as the Anarchist Black Cross seek total abolishment of the prison system, without any intention to replace it with other government-controlled systems. Many anarchist organizations believe that the best form of justice arises naturally out of social contracts or restorative justice.

Advocates of prison abolition

Prominent social activist Angela Davis, outspoken critic of the prison-industrial complex (PIC), openly supports prison abolition. In her work, she writes: "Mass incarceration is not a solution to unemployment, nor is it a solution to the vast array of social problems that are hidden away in a rapidly growing network of prisons and jails. However, the great majority of people have been tricked into believing in the efficacy of imprisonment, even though the historical record clearly demonstrates that prisons do not work."

Angela Davis and Ruth Wilson Gilmore co-founded Critical Resistance, which is an organization working to "build an international movement to end the Prison Industrial Complex by challenging the belief that caging and controlling people makes us safe." Other similarly motivated groups such as the Prison Activist Resource Center (PARC), a group "committed to exposing and challenging all forms of institutionalized racism, sexism, able-ism, heterosexism, and classism, specifically within the Prison Industrial Complex," and Black & Pink, an abolitionist organization that focuses around LGBTQ rights, all broadly advocate for prison abolition. Furthermore, the Human Rights Coalition, a 2001 group that aims to abolish prisons, and the California Coalition for Women Prisoners, a grassroots organization dedicated to dismantling the PIC, can all be added to the long list of organizations that desire a different form of justice system.

Since 1983, the International Conference on Penal Abolition (ICOPA) gathers activists, academics, journalists, and "others from across the world who are working towards the abolition of imprisonment, the penal system, carceral controls and the prison industrial complex (PIC)," to discuss three important questions surrounding the reality of prison abolition ICOPA was one of the first penal abolitionist conference movements, similar to Critical Resistance in America, but "with an explicitly international scope and agenda-setting ambition."

Anarchists wish to eliminate all forms of state control, of which imprisonment is seen as one of the more obvious examples. Anarchists also oppose prisons given that statistics show incarceration rates affect mainly poor people and ethnic minorities, and do not generally rehabilitate criminals, in many cases making them worse. As a result, the prison abolition movement often is associated with humanistic socialism, anarchism and anti-authoritarianism. 

In October 2015, members at a plenary session of the National Lawyers Guild (NLG) released and adopted a resolution in favor of prison abolition.

Proposed reforms and alternatives

Proposals for prison reform and alternatives to prisons differ significantly depending on the political beliefs behind them. Proposals and tactics often include:

• Penal system reforms:
  • Substituting, for incarceration, supervised release, probation, restitution to victims, and/or community work.
  • Decreasing terms of imprisonment by abolishing mandatory minimum sentencing
  • Decreasing ethnic disparity in prison populations
• Prison condition reforms
• Crime prevention rather than punishment
• Abolition of specific programs which increase prison population, such as the prohibition of drugs (e.g., the American War on Drugs), gun control, prohibition of sex work, and alcohol restrictions.
• Education programs to inform people who have never been in prison about the problems
• Fighting individual cases of wrongful conviction

The United Nations Office on Drugs and Crime published a series of handbooks on criminal justice. Among them is Alternatives to Imprisonment which identifies how the overuse of imprisonment impacts fundamental human rights, especially those convicted for lesser crimes. 

Social justice and advocacy organizations such as Students Against Mass Incarceration (SAMI) at the University of California, San Diego often look to Scandinavian countries Sweden and Norway for guidance in regards to successful prison reform because both countries have an emphasis on rehabilitation rather than punishment. According to Sweden's Prison and Probation Service Director-General, Nils Öberg, this emphasis is made popular among the Swedish because the act of imprisonment is considered punishment enough. This focus on rehabilitation includes an emphasis on promoting normalcy for inmates, a charge lead by experienced criminologists and psychologists. In Norway a focus on preparation for societal re-entry has yielded "one of the lowest recidivism rates in the world at 20%, [while] the US has one of the highest: 76.6% of [Americans] prisoners are re-arrested within five years". The Scandinavian method of incarceration seems to be successful: the Swedish incarceration rate decreased by 6% between 2011 and 2012.

Abolitionist views

Many prison reform organizations and abolitionists in the United States advocate community accountability practices, such as community-controlled courts, councils, or assemblies as an alternative to the criminal justice system.

Organizations such as INCITE! and Sista II Sista that support women of color who are survivors of interpersonal violence argue that the criminal justice system does not protect marginalized people who are victims in violent relationships. Instead, victims, especially those who are poor, minorities, transgender or gender non-conforming can experience additional violence at the hands of the state. Instead of relying on the criminal justice system, these organizations work to implement community accountability practices, which often involve collectively-run processes of intervention initiated by a survivor of violence to try to hold the person who committed violence accountable by working to meet a set of demands. For organizations outside the United States see, e.g. Justice Action, Australia.

Some anarchists and socialists contend that a large part of the problem is the way the judicial system deals with prisoners, people, and capital. According to Marxists, in capitalist economies incentives are in place to expand the prison system and increase the prison population. This is evidenced by the creation of private prisons in America and corporations like CoreCivic, formerly known as Correction Corporation of America (CCA). http://www.cca.com/  Its shareholders benefit from the expansion of prisons and tougher laws on crime. More prisoners is seen as beneficial for business. Some anarchists contend that with the destruction of capitalism, and the development of social structures that would allow for the self-management of communities, property crimes would largely vanish. There would be fewer prisoners, they assert, if society treated people more fairly, regardless of gender, color, ethnic background, sexual orientation, education, etc.

Mental illness and prison

Prison abolitionists such as Amanda Pustilnik take issue with the fact that prisons are used as a "default asylum" for many individuals with mental illness.

"Why do governmental units choose to spend billions of dollars a year to concentrate people with serious illnesses in a system designed to punish intentional lawbreaking, when doing so matches neither the putative purposes of that system nor most effectively addresses the issues posed by that population?"

To rephrase, if the whole point of the penal system is to rehabilitate and reform individuals who have willingly transgressed, then those transgress the law who for reasons outside there cognitive control transgress don't belong in prison since prisoners were never designed nor intended to rehabilitate this population. 

In the United States, there are more people with mental illness in prisons than in psychiatric hospitals. This statistic is one of the major pieces of evidence that prison abolitionists claim highlights the depravity of the penal system.

Prison abolitionists contend that prisons violate the Constitutional rights (5th and 6th Amendment rights) of mentally ill prisoners on the grounds that these individuals will not be receiving the same potential for rehabilitation as the non-mentally ill prison population. This injustice is sufficient grounds to argue for the abolishment of prisons. Prisons were not designed to be used to house the mentally ill, and prison practices like solitary confinement are awful for mmental health. Additionally, individuals with mental illnesses have a much higher chance of committing suicide while in prison.

1973 Walpole Prison Uprising

In 1973, two years after the Attica Prison uprising, the inmates of Walpole prison formed a prisoners' union to protect themselves from guards, end behavioral modification programs, advocate for the prisoner's right for education and healthcare, gain more visitation rights, work assignments, and to be able to send money to their families. 

The union also created a general truce within the prison and race-related violence sharply declined. During the Kwanzaa celebration, black prisoners were placed under lockdown, angering the whole facility and leading to a general strike. Prisoners refused to work or leave their cells for three months, leading to the guards beating prisoners, putting prisoners in solitary confinement, denying prisoners medical care and food.

The strike ended in the prisoners' favour as the superintendent of the prison resigned. The prisoners were granted more visitation rights and work programs. Angered by this, the prison guards went on strike and abandoned the prison, hoping that this would create chaos and violence throughout the prison. But the prisoners were able to create an anarchist community where recidivism dropped dramatically and murders and rapes fell to zero. Prisoners volunteered to cook meals. Vietnam veterans who'd been trained as medics took charge of the pharmacy and distribution of meds. Decisions were made in community assemblies. 

Guards retook the prison after two months, leading to many prison administrators and bureaucrats quitting their jobs and embracing the prison abolition movement.

Arguments made for prison abolition

• Lack of proper legal representation

"Eighty percent of people accused of crimes [in the United States] are unable to afford a lawyer to defend them." The US Supreme Court held in 1963 that a poor person facing felony charges "cannot be assured a fair trial unless counsel is provided for him."

"Long Term Neglect and underfunding of indigent defense have created a crisis of extra ordinary proportions in many states throughout the country."

• War on drugs conceals racial tension

(2005) "The United States leads the world in the number of people incarcerated in federal and state correctional facilities. There are currently more than 2 million people in American prisons or jails. Approximately one-quarter of those people held in U.S. prisons or jails have been convicted of a drug offense. The United States incarcerates more people for drug offenses than any other country. With an estimated 6.8 million Americans struggling with drug abuse or dependence, the growth of the prison population continues to be driven largely by incarceration for drug offenses."

"The so-called drug war was started in the 1980s and it was aimed directly at the black population. None of this has anything to do with drugs. It has to do with controlling and criminalizing dangerous populations."

"Blacks are 12.3 percent of the U.S. population (2001) but they comprise fully half of the roughly 2 million Americans currently behind Bars. On any given day, 30 percent of African-American males aged 20–29 are "under correctional supervision".

Blacks constitute 13 percent of all drug users, but 35 percent of those arrested for drug possession, 55 percent of persons convicted, and 74 percent of people sent to prison.

• Incarceration is socially and economically crippling to the convicted and the community.

"Each Prisoner represents an economic asset that has been removed from that community and placed elsewhere. As an economic being, the person would spend money at or near his or her area of residence—typically, an inner city. Imprisonment displaces that economic activity: Instead of buying snacks in a local deli, the prisoner makes those purchases in a prison commissary. The removal may represent a loss of economic value to the home community, but it is a boon to the prison [host] community. Each prisoner represents as much as $25,000 in income for the community in which the prison is located, not to mention the value of constructing the prison facility in the first place. This can be a massive transfer of value: a young male worth a few thousand dollars of support to children and local purchases is transformed into a $25,000 financial asset to a rural prison community. The economy of the rural community is artificially amplified, the local city economy is artificially deflated."

Unfortunately, there are no definitive national statistics on the employment status of felons. But both anecdotal evidence and fragmentary data confirm what common sense would predict: individuals who have been incarcerated have great difficulty securing employment when they return to society. Except for a short period in the late 1990s, when the labor market was so tight that the Wall Street Journal reported on employer efforts to reach out to felons, those leaving prison have faced formidable obstacles to employment. Some of these difficulties are related to company policies or procedures and others are the result of employer perceptions of felons' job skills or trustworthiness. Felons are also barred from public employment in a number of states, including three with a high proportion of African American residents (Alabama, Mississippi, and South Carolina). Occupations that are licensed by states also have restrictions on allowing felons to work in them.

• It is argued by the Massachusetts Statewide Harm Reduction Coalition that the prison system is in violation of the Universal Declaration of Human Rights, which was adopted by the United Nations General Assembly in 1948, and which is prescribing life, liberty, equality and justice to all people without discrimination of any sort as an inalienable right. The Universal Declaration of Human Rights has also abolished all forms of slavery and genocide, including torture, repression and oppression that prisons thrive upon.
• Imprisonment is seen by some as a form of violent behavior which legitimizes violence and cruelty, producing a "boomerang effect of dehumanization" on the society which dehumanizes itself and limits its potential for a peaceful future by resorting to the use of such repressive and cruel institutions.
• Prisons may be less effective at discouraging crimes and/or compensating victims than other forms of punishment.
• Degree and quality of access to justice depends on the financial resources of the accused.
• Prisons alienate people from their communities.
• In the U.S., people of color and from the lower class are much more likely to be imprisoned than people of European descent or people who are wealthy.
• People who are put in prison for what are arguably crimes motivated by need, such as some minor theft (food, etc.) or prostitution, find it much harder to obtain legal employment once convicted of a crime. Arguably, this difficulty makes it more likely they will find themselves back in the prison system, having had few other options or resources available to support themselves and/or their families. Many prison abolitionists argue that we should "legalize survival" and provide help to those who need it instead of making it even harder to find work and perpetuating the non-violent crimes.
• Prisons are not proven to make people less violent. In fact, there is evidence that they may instead promote violence in individuals by surrounding them with other violent criminals, which can lead to predictable negative/violent results.
• Drug-related offenders are being ushered in and out of the prison system like a revolving door. Rather than educate, and rehabilitate the offender to a clean path of sobriety and increased stature, the state ignores them.

Arguments made against prison abolition

Opponents of the abolition argue that none of the arguments above address the protection of non-criminal population from the effects of crime, and from particularly violent criminals.

• Individuals who have committed crimes, especially crimes violent in nature, must repay society. Retributive philosophy argues that punishment is necessary in order for an individual who has done wrong to pay for their crime
• Utilitarian ethics argues that the unhappiness of few is good or right if it leads to the happiness of the majority. The ethical argument in this case is that keeping 1% of the population incarcerated is worth it for the safety of the majority
• Deterrence theory makes the case that prison discourages citizens from committing a crime, because they would not want to end up in prison

Effects of cannabis

From Wikipedia, the free encyclopedia

A gram of cannabis

 

Chemical compounds in the Cannabis plant, including 400 different cannabinoids such as tetrahydrocannabinol (THC), allow its drug to have various psychological and physiological effects on the human body. Different plants of the genus Cannabis contain different and often unpredictable concentrations of THC and other cannabinoids and hundreds of other molecules that have a pharmacological effect, so that the final net effect cannot reliably be foreseen. 

Acute effects while under the influence can include euphoria and anxiety. Although some assert that Cannabidiol (CBD), another cannabinoid found in cannabis in varying amounts, may alleviate the adverse effects of THC that some users experience, little is known about CBD's effects on humans. The well-controlled studies with humans have a hard time showing that CBD can be distinguished from a placebo, or that it has any systematic effect on the adverse effects of cannabis. When ingested orally, THC can produce stronger psychotropic effects than when inhaled. At doses exceeding the psychotropic threshold, users may experience adverse side effects such as anxiety and panic attacks that can result in increased heart rate and changes in blood pressure.

In the United States research about medical cannabis has been hindered by federal law. Smoking any substance could possibly carry similar risks as smoking tobacco due to carcinogens in all smoke, and the ultimate conclusions on these factors are disputed.

Cannabis use disorder is defined as a medical diagnosis in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).

Effects

The structural formula of tetrahydrocannabinol

 

Tetrahydrocannabivarin

 

Cannabidiol

 

Cannabinol

 

Cannabivarin

 

Cannabidivarin

Cannabinoids and cannabinoid receptors

The most prevalent psychoactive substances in cannabis are cannabinoids, particularly THC. Some varieties, having undergone careful selection and growing techniques, can yield as much as 34% THC. Another psychoactive cannabinoid present in Cannabis sativa is tetrahydrocannabivarin (THCV), but it is only found in small amounts and is a cannabinoid antagonist.

There are similar compounds in cannabis that do not exhibit psychoactive response but are obligatory for functionality: cannabidiol (CBD), an isomer of THC; cannabivarin (CBV), an analog of cannabinol (CBN) with a different side chain, cannabidivarin (CBDV), an analog of CBD with a different side chain, and cannabinolic acid. How these other compounds interact with THC is not fully understood. Some clinical studies have proposed that CBD acts as a balancing agent to regulate the strength of the psychoactive agent THC. CBD is believed to regulate the metabolism of THC by inactivating cytochrome P450, an important class of enzymes that metabolize drugs. Experiments in which babies were treated with CBD followed by THC showed that CBD 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. Cannabis cofactors have also been linked to lowering body temperature, modulating immune function, and cell protection. The essential oil of cannabis contains many fragrant terpenoids which may synergize with the cannabinoids to produce their unique effects. THC is converted rapidly to 11-hydroxy-THC, which is also pharmacologically active, so the euphoria outlasts measurable THC levels in blood.

THC and cannabidiol are neuroprotective antioxidants. Research on rats has demonstrated that THC prevents hydroperoxide-induced oxidative damage as well as or better than other antioxidants in a chemical (Fenton reaction) system and neuronal cultures. Cannabidiol was significantly more protective than either vitamin E or vitamin C.

The cannabinoid receptor is a typical G protein-coupled receptor. A characteristic of this type of receptor is the distinct pattern of how the molecule spans the cell membrane seven times. Cannabinoid receptors are located 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 the μ-opioid receptors responsible for the effects of morphine. CB2 receptors are structurally different (the sequence similarity 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 prevalent on B-cells, natural killer cells, and monocytes, but can also be found on polymorphonuclear neutrophil cells, T8 cells, and T4 cells. 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.

Biochemical mechanisms in the brain

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 500 million years. The binding of cannabinoids to cannabinoid receptors decrease adenylyl cyclase activity, inhibit calcium N channels, and disinhibit K⁺_A channels. There are at least 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, nonpsychotropic cannabinoids can be used as a very effective anti-inflammatory. 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 endogenous opioid system and may affect dopamine transmission.

Sustainability in the body

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.

Toxicities

Related to cannabinoids

No fatal overdoses with cannabis use have been reported. A review published in the British Journal of Psychiatry in February 2008 said that "no deaths directly due to acute cannabis use have ever 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. In dogs, the minimum lethal dose of THC is over 3 g/kg.

According to the Merck Index, the LD₅₀ of THC (the dose which causes the death of 50% of individuals) is 1270 mg/kg for male rats and 730 mg/kg for female rats from oral consumption in sesame oil, and 42 mg/kg for rats from inhalation.

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 CYP450, thus leading to drug toxicities by medications that the person consuming cannabis may be taking.

Related to smoking

A 2007 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). This study found that directly inhaled cannabis smoke contained as much as 20 times as much ammonia and 5 times as much hydrogen cyanide as tobacco smoke and compared the properties of both mainstream and sidestream (smoke emitted from a smouldering 'joint' or 'cone') smoke. Mainstream cannabis smoke was found to contain higher concentrations of selected polycyclic aromatic hydrocarbons (PAHs) than sidestream tobacco smoke. However, other studies have found much lower disparities in ammonia and hydrogen cyanide between cannabis and tobacco, and that some other constituents (such as polonium-210, lead, arsenic, nicotine, and tobacco-specific nitrosamines) are either lower or non-existent in cannabis smoke.

Cannabis smoke contains thousands of organic and inorganic chemical compounds. This tar is chemically similar to that found in tobacco smoke or cigars. Over fifty known carcinogens have been identified in cannabis smoke. These include nitrosamines, reactive aldehydes, and polycylic hydrocarbons, including benz[a]pyrene. Marijuana smoke was listed as a cancer agent in California in 2009. A study by the British Lung Foundation published in 2012 identifies cannabis smoke as a carcinogen and also finds awareness of the danger is low compared with the high awareness of the dangers of smoking tobacco particularly among younger users. 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. Professor David Nutt, a UK drug expert, points out that the study cited by the British Lung Foundation has been accused of both "false reasoning" and "incorrect methodology". Further, he notes that other studies have failed to connect cannabis with lung cancer, and accuses the BLF of "scaremongering over cannabis".

Short-term effects

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. After oral ingestion of cannabis, the onset of effect is delayed relative to smoking, taking 30 minutes to 2 hours, but the duration is prolonged due to continued slow absorption. The duration of noticeable effects has been observed to diminish after prolonged, repeated use and the development of increased tolerance to cannabinoids.

Psychological effects

A Hindu man smoking cannabis in Kolkata, India.

 

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. Some effects may include a general alteration of conscious perception, euphoria, feelings of well-being, relaxation or stress reduction, increased appreciation of the arts, including humor and music (especially discerning its various components/instruments), joviality, metacognition and introspection, enhanced recollection (episodic memory), increased sensuality, increased awareness of sensation, increased libido, and creativity. 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. Between 20 and 30 percent of recreational users experience intense anxiety and/or panic attacks after smoking cannabis, however, some report anxiety only after not smoking cannabis for a prolonged period of time. Inexperience and use in an unfamiliar environment are major contributing factors to this anxiety. 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 effects, including an increased enjoyment of food taste and aroma, and marked distortions in the perception of time (where experiencing a "rush" of ideas can create the subjective impression of much time passing). At higher doses, effects can include altered body image, auditory and/or visual illusions, pseudohallucinations, and ataxia from selective impairment of polysynaptic reflexes. In some cases, cannabis can lead to acute psychosis and 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. If the episode is accompanied by aggression or sedation, physical restraint may be necessary.

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.

Somatic effects

Bloodshot eye

 

Some of the short-term physical effects of cannabis use include increased heart rate, dry mouth, reddening of the eyes (congestion of the conjunctival blood vessels), a reduction in intra-ocular pressure, muscle relaxation and a sensation of cold or hot hands and feet and / or flushed face.

Electroencephalography or EEG shows somewhat more persistent alpha waves of slightly lower frequency than usual. Cannabinoids produce a "marked depression of motor activity" via activation of neuronal cannabinoid receptors belonging to the CB1 subtype.

Duration

Peak levels of cannabis-associated intoxication occur approximately 30 minutes after smoking it and last for several hours.

Smoked

The total short-term duration of cannabis use when smoked depends on the potency, method of smoking – e.g. whether pure or in conjunction with tobacco – and how much is smoked. Peak levels of intoxication typically last an average of three to four hours.

Oral

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. Very high doses may last even longer. 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.

Neurological effects

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. 

In in-vitro experiments THC at extremely high concentrations, which could not be reached with commonly consumed doses, caused competitive inhibition of the AChE enzyme and inhibition of β-amyloid peptide aggregation, implicated in the development of Alzheimer's disease. 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.

Effects on driving

While several studies have shown increased risk associated with cannabis use by drivers, other studies have not found increased risk. Cannabis usage has been shown in some studies to have a negative effect on driving ability. The British Medical Journal indicated that "drivers who consume cannabis within three hours of driving are nearly twice as likely to cause a vehicle collision as those who are not under the influence of drugs or alcohol".

In Cannabis and driving: a review of the literature and commentary, the United Kingdom's Department for Transport reviewed data on cannabis and driving, finding although impaired, "subjects under cannabis treatment appear to perceive that they are indeed impaired. Where they can compensate, they do...". In a review of driving simulator studies, researchers note that "even in those who learn to compensate for a drug's impairing effects, substantial impairment in performance can still be observed under conditions of general task performance (i.e. when no contingencies are present to maintain compensated performance)."

A 2012 meta-analysis found that acute cannabis use increased the risk of an automobile crash. An extensive 2013 review of 66 studies regarding crash risk and drug use found that cannabis was associated with minor, but not statistically significant increased odds of injury or fatal accident.

In the largest and most precisely controlled study of its kind carried out by the U.S. Department of Transportation’s National Highway Traffic Safety Administration, it was found that other "studies that measure the presence of THC in the drivers' blood or oral fluid, rather than relying on self-report tend to have much lower (or no) elevated crash risk estimates. Likewise better controlled studies have found lower (or no) elevated crash risk estimates". The study found that "after adjusting for age, gender, race and alcohol use, drivers who tested positive for marijuana were no more likely to crash than those who had not used any drugs or alcohol prior to driving".

On the other hand, a recent study of Journal of Transport & Health indicated that the numbers of fatal crashes involving marijuana after the recreational marijuana legalization or decriminalization have significantly increased in Colorado, Washington, and Massachusetts.

Cardiovascular effects

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. There are medical reports of occasional heart attacks or myocardial infarction, stroke and other cardiovascular side effects. Marijuana's cardiovascular effects are not associated with serious health problems for most young, healthy users. Researchers reported in the International Journal of Cardiology, "Marijuana use by older people, particularly those with some degree of coronary artery or cerebrovascular disease, poses greater risks due to the resulting increase in catecholamines, cardiac workload, and carboxyhemoglobin levels, and concurrent episodes of profound postural hypotension. 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 2013 analysis of 3,886 myocardial infarction survivors over an 18-year period showed "no statistically significant association between marijuana use and mortality".

A 2008 study by the National Institutes of Health Biomedical Research Centre in Baltimore found that heavy, chronic smoking of marijuana (138 joints per week) changed blood proteins associated with heart disease and stroke.

A 2000 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 1960 to 2008, all of which occurred in Europe.

Combination with other drugs

A confounding factor in cannabis research is the prevalent usage of other recreational drugs, especially alcohol and nicotine. Such complications demonstrate the need for studies on cannabis that have stronger controls, and investigations into alleged symptoms of cannabis use that may also be caused by tobacco. 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 2001 showed that cannabis in Australia is rarely used without other drugs. 95% of cannabis users also drank alcohol; 26% took amphetamines; 19% took ecstasy and only 2.7% reported not having used any other drug with cannabis. While research has been undertaken on the combined effects of alcohol and cannabis on performing certain tasks, little research has been conducted on the reasons why this combination is so popular. 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.

Memory and learning

Studies on cannabis and memory are hindered by small sample sizes, confounding drug use, and other factors. The strongest evidence regarding cannabis and memory focuses on its temporary negative effects on short-term and working memory.

In a 2001 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". On his studies regarding cannabis use, lead researcher and Harvard professor Harrison Pope said he found marijuana is not dangerous over the long term, but there are short-term effects. 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". Researchers from the University of California, San Diego School of Medicine failed to show substantial, systemic neurological effects from long-term recreational use of cannabis. Their findings were published in the July 2003 issue of the Journal of the International Neuropsychological Society. The research team, headed by Dr Igor Grant, found that cannabis use did affect perception, but did not cause permanent brain damage. Researchers looked at data from 15 previously published controlled studies involving 704 long-term cannabis users and 484 nonusers. The results showed long-term cannabis use was only marginally harmful on the memory and learning. Other functions such as reaction time, attention, language, reasoning ability, perceptual and motor skills were unaffected. The observed effects on memory and learning, they said, showed long-term cannabis use caused "selective memory defects", but that the impact was "of a very small magnitude". A study at Johns Hopkins University School of Medicine showed that very heavy use of marijuana is associated with decrements in neurocognitive performance even after 28 days of abstinence.

Appetite

The feeling of increased appetite following the use of cannabis has been documented for hundreds of years, and is known colloquially as "the munchies" in the English-speaking world. Clinical studies and survey data have found that cannabis increases food enjoyment and interest in food. A 2015 study suggests that cannabis triggers uncharacteristic behaviour in POMC neurons, which are usually associated with decreasing hunger. Rarely, chronic users experience a severe vomiting disorder, cannabinoid hyperemesis syndrome, after smoking and find relief by taking hot baths.

Endogenous cannabinoids ("endocannabinoids") were discovered in cow's milk and soft cheeses. Endocannabinoids are also found in human breast milk. It is widely accepted that the neonatal survival of many species "is largely dependent upon their suckling behavior, or appetite for breast milk" and recent research has identified the endogenous cannabinoid system to be the first neural system to display complete control over milk ingestion and neonatal survival. It is possible that "cannabinoid receptors in our body interact with the cannabinoids in milk to stimulate a suckling response in newborns so as to prevent growth failure".

Pathogens and microtoxins

Most microorganisms found in cannabis only affect plants and not humans, but some microorganisms, especially those that proliferate when the herb is not correctly dried and stored, can be harmful to humans. Some users may store marijuana in an airtight bag or jar in a refrigerator to prevent fungal and bacterial growth.

Fungi

Aspergillus fumigatus

 

The fungi Aspergillus flavus, Aspergillus fumigatus, Aspergillus niger, Aspergillus parasiticus, Aspergillus tamarii, Aspergillus sulphureus, Aspergillus repens, Mucor hiemalis (not a human pathogen), Penicillium chrysogenum, Penicillium italicum and Rhizopus nigrans have been found in moldy cannabis. Aspergillus mold species can infect the lungs via smoking or handling of infected cannabis and cause opportunistic and sometimes deadly aspergillosis. Some of the microorganisms found create aflatoxins, which are toxic and carcinogenic. Researchers suggest that moldy cannabis should thus be discarded to avoid these serious risks.

Mold is also found in smoke from mold-infected cannabis, and the lungs and nasal passages are a major means of contracting fungal infections. Levitz and Diamond (1991) suggested baking marijuana in home ovens at 150 °C [302 °F], for five minutes before smoking. Oven treatment killed conidia of A. fumigatus, A. flavus and A. niger, and did not degrade the active component of marijuana, tetrahydrocannabinol (THC)."

Bacteria

Cannabis contaminated with Salmonella muenchen was positively correlated with dozens of cases of salmonellosis in 1981. "Thermophilic actinomycetes" were also found in cannabis.

Long-term effects

Exposure to marijuana may have biologically-based physical, mental, behavioral and social health consequences and is "associated with diseases of the liver (particularly with co-existing hepatitis C), lungs, heart, eyesight and vasculature" according to a 2013 literature review by Gordon and colleagues. The association with these diseases has only been reported in cases where people have smoked cannabis. The authors cautioned that "evidence is needed, and further research should be considered, to prove causal associations of marijuana with many physical health conditions".

Cannabis use disorder is defined in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) as a condition requiring treatment. Several drugs have been investigated in an attempt to ameliorate the symptoms of stopping cannabis use. Such drugs include bupropion, divalproex, nefazodone, lofexidine, and dronabinol. Of these, dronabinol has proven the most effective.

Effects in pregnancy

Cannabis consumption in pregnancy might be associated with restrictions in growth of the fetus, miscarriage, and cognitive deficits in offspring based on animal studies, although there is limited evidence for this in humans at this time. A 2012 systematic review found although it was difficult to draw firm conclusions, there was some evidence that prenatal exposure to cannabis was associated with "deficits in language, attention, areas of cognitive performance, and delinquent behavior in adolescence". A report prepared for the Australian National Council on Drugs concluded cannabis and other cannabinoids are contraindicated in pregnancy as it may interact with the endocannabinoid system.

Cannabinoid receptor

From Wikipedia, the free encyclopedia

CB₁ and CB₂ structures.

Cannabinoid receptors, located throughout the body, are part of the endocannabinoid system, which is involved in a variety of physiological processes including appetite, pain-sensation, mood, and memory.

Cannabinoid receptors are of a class of cell membrane receptors in the G protein-coupled receptor superfamily. As is typical of G protein-coupled receptors, the cannabinoid receptors contain seven transmembrane spanning domains. Cannabinoid receptors are activated by three major groups of ligands: endocannabinoids, produced by the mammillary body; plant cannabinoids (such as cannabidiol, produced by the cannabis plant); and synthetic cannabinoids (such as HU-210). All of the endocannabinoids and phytocannabinoids (plant based cannabinoids) are lipophilic, such as fat soluble compounds.

There are currently two known subtypes of cannabinoid receptors, termed CB₁ and CB₂. The CB₁ receptor is expressed mainly in the brain (central nervous system or "CNS"), but also in the lungs, liver and kidneys. The CB₂ receptor is expressed mainly in the immune system and in hematopoietic cells. Mounting evidence suggests that there are novel cannabinoid receptors that is, non-CB₁ and non-CB₂, which are expressed in endothelial cells and in the CNS. In 2007, the binding of several cannabinoids to the G protein-coupled receptor GPR55 in the brain was described.

The protein sequences of CB₁ and CB₂ receptors are about 44% similar. When only the transmembrane regions of the receptors are considered, amino acid similarity between the two receptor subtypes is approximately 68%. In addition, minor variations in each receptor have been identified. Cannabinoids bind reversibly and stereo-selectively to the cannabinoid receptors. Subtype selective cannabinoids have been developed which theoretically may have advantages for treatment of certain diseases such as obesity.

It appears that cannabinoid receptors are unique to the phylum Chordata and, as such, they have a rather restricted phylogenetic distribution in the animal kingdom. However, enzymes involved in biosynthesis/inactivation of endocannabinoids and endocannabinoid signalling in general (involving targets other than CB1/2-type receptors) occur throughout the animal kingdom. Although the cannabinoid receptors are unique to Chordates, other organisms are still able to process the endocannabinoids through other techniques.

CB₁

Cannabinoid receptor type 1 (CB₁) receptors are thought to be one of the most widely expressed G_αi protein-coupled receptors in the brain. One mechanism through which they function is endocannabinoid-mediated depolarization-induced suppression of inhibition, a very common form of retrograde signaling, in which the depolarization of a single neuron induces a reduction in GABA-mediated neurotransmission. Endocannabinoids released from the depolarized post-synaptic neuron bind to CB₁ receptors in the pre-synaptic neuron and cause a reduction in GABA release due to limited presynaptic calcium ions entry.

They are also found in other parts of the body. For instance, in the liver, activation of the CB₁ receptor is known to increase de novo lipogenesis.

Prenatal cannabis exposure (PCE) perturbs the fetal endogenous cannabinoid signaling system (ECSS) which affects neurodevelopment and results in abnormalities in cognition and neuropsychiatric disorders.

CB₂

CB₂ receptors are mainly expressed on T cells of the immune system, on macrophages and B cells, and in hematopoietic cells. They also have a function in keratinocytes. They are also expressed on peripheral nerve terminals. These receptors play a role in antinociception, or the relief of pain. In the brain, they are mainly expressed by microglial cells, where their role remains unclear. While the most likely cellular targets and executors of the CB₂ receptor-mediated effects of endocannabinoids or synthetic agonists are the immune and immune-derived cells (e.g. leukocytes, various populations of T and B lymphocytes, monocytes/macrophages, dendritic cells, mast cells, microglia in the brain, Kupffer cells in the liver, astrocytes, etc.), the number of other potential cellular targets is expanding, now including endothelial and smooth muscle cells, fibroblasts of various origins, cardiomyocytes, and certain neuronal elements of the peripheral or central nervous systems.

Other cannabinoid receptors

The existence of additional cannabinoid receptors has long been suspected, due to the actions of compounds such as abnormal cannabidiol that produce cannabinoid-like effects on blood pressure and inflammation, yet do not activate either CB₁ or CB₂.^[18][19] Recent research strongly supports the hypothesis that the N-arachidonoyl glycine (NAGly) receptor GPR18 is the molecular identity of the abnormal cannabidiol receptor and additionally suggests that NAGly, the endogenous lipid metabolite of anandamide (also known as arachidonoylethanolamide or AEA), initiates directed microglial migration in the CNS through activation of GPR18. Other molecular biology studies have suggested that the orphan receptor GPR55 should in fact be characterised as a cannabinoid receptor, on the basis of sequence homology at the binding site. Subsequent studies showed that GPR55 does indeed respond to cannabinoid ligands. This profile as a distinct non-CB₁/CB₂ receptor that responds to a variety of both endogenous and exogenous cannabinoid ligands, has led some groups to suggest GPR55 should be categorized as the CB₃ receptor, and this re-classification may follow in time. However this is complicated by the fact that another possible cannabinoid receptor has been discovered in the hippocampus, although its gene has not yet been cloned, suggesting that there may be at least two more cannabinoid receptors to be discovered, in addition to the two that are already known. GPR119 has been suggested as a fifth possible cannabinoid receptor, while the PPAR family of nuclear hormone receptors can also respond to certain types of cannabinoid.

Signaling

Cannabinoid receptors are activated by cannabinoids, generated naturally inside the body (endocannabinoids) or introduced into the body as cannabis or a related synthetic compound. Similar responses are produced when introduced in alternative methods, only in a more concentrated form than what is naturally occurring. 

After the receptor is engaged, multiple intracellular signal transduction pathways are activated. At first, it was thought that cannabinoid receptors mainly inhibited the enzyme adenylate cyclase (and thereby the production of the second messenger molecule cyclic AMP), and positively influenced inwardly rectifying potassium channels (=Kir or IRK). However, a much more complex picture has appeared in different cell types, implicating other potassium ion channels, calcium channels, protein kinase A and C, Raf-1, ERK, JNK, p38, c-fos, c-jun and many more.

Separation between the therapeutically undesirable psychotropic effects, and the clinically desirable ones, however, has not been reported with agonists that bind to cannabinoid receptors. THC, as well as the two major endogenous compounds identified so far that bind to the cannabinoid receptors —anandamide and 2-arachidonylglycerol (2-AG)— produce most of their effects by binding to both the CB₁ and CB₂ cannabinoid receptors. While the effects mediated by CB₁, mostly in the central nervous system, have been thoroughly investigated, those mediated by CB₂ are not equally well defined.

Cannabinoid treatments

Synthetic tetrahydrocannabinol (THC) is prescribed under the INN dronabinol or the brand name Marinol, to treat vomiting and for enhancement of appetite, mainly in people with AIDS as well as for refractory nausea and vomiting in people undergoing chemotherapy. Use of synthetic THC is becoming more common as the known benefits become more prominent within the medical industry. THC is also an active ingredient in nabiximols, a specific extract of Cannabis that was approved as a botanical drug in the United Kingdom in 2010 as a mouth spray for people with multiple sclerosis to alleviate neuropathic pain, spasticity, overactive bladder, and other symptoms.