Cannabis is a flowering plant that is best known for the intoxicating flowers produced. Cannabis flowers can be eaten, or smoked, to produce analgesia, euphoria, depersonalization, tachycardia, fragmented thought, and bronchodilation.
Introduction to Cannabis
Cannabis Sativa and its related genera is a flowering, annual, dioecious herb with psychoactive components effecting motor-coordination, memory, pleasure and neural activity.
General effects of Cannabis intoxication include analgesia, euphoria, depersonalization, tachycardia, fragmented thought, and bronchodilation.
Cannabis has been employed historically as a medicine, a shamanic and meditative catalyst, and as a recreational intoxicant since roughly 2500 BC. More recently it has been dissected and pharmacokinetically enhanced for implementation in modern medicine for the treatment of pain, spastic and movement disorders, anorexia and cachexia, glaucoma, and mood disorders.
The major active constituents of Cannabis are the cannabinoids, most notably Δ9-THC and its oxidized analogues CBN (Cannabinol) and CBD (Cannabidol). Other notable cannabinoids (of 66 known) include CBG (Cannabigerol), CBC (Cannabichromene), and Δ8-THC.Using Cannabis
Cannabis can be consumed in many different ways, from ingestion of the raw plant matter to digitally-controlled vaporization. Traditional methods that remain popular today include pipes, cannabis cigarettes, commonly referred to as "joints," and bongs, also known as "water pipes." Portable and stationary vaporizers have been marketed, offering a healthier smoke-free technique of ingestion. Approaches using oral administration include bhang, a traditional Indian beverage, along with THC/CBD pills and food infused with marijuana. Intravenous cannabinoid use has also been noted, though this is mostly confined to research settings and can be highly dangerous if performed incorrectly.[1][2][3]Routes of administration:
Inhalation: The efficiency of inhalation is largely determined by the process by which the cannabinoids are vaporized. With an efficient vaporization process, inhalation proves a most efficient mode of ingestion. Doses of 18-40mg[4] THC reveal the gamut of effect, from medicinal to recreational. Primary sources test using single cigarette doses of 1.75-3.25% potency cannabis.[5]-[6][7][8] Peak detectable levels of THC in plasma occur within 3 minutes[9]. Bioavailability of THC increases two-fold to ~38% with prolonged exposure to inhaled cannabinoids, supporting the observed evidence that frequent multiple-dose application increases potential plasma content.[10][11][12][13] A marijuana cigarette containing 9mg THC results in a maximum plasma concentration of 50ng/ml. Maxima ranges of 200-250ng/ml are achieved smoking a single cigarette of 3.25% potency.[14][15][16][17]
Dry Pipe:
1/16.2 C/T
~30% of THC in sample
Single Percolation Waterpipe or Bong:
1/16.9 C/T
Small waterpipe ~25%, Bong ~15% of THC in sample
Unfiltered joint:
1/13 Cannabanoid/Tar
~20% THC in sample
Filtered joint:
1/16.9 C/T
<20% of THC in sample
Hotplate Vaporizer:
1/9.75 C/T
~10% of THC in sample
Modern Hot Air Vaporizer:
~9/1 C/T
~60% of THC in sample
*[18][19][20][21][22][23]
Oral Digestion:
Oral digestion is normally performed through bonding of THC to food-based lipids such as butter, canola oil, or (in the case of medicinal administration) sesame oil.[24][25][26] Dosages of 20mg THC[27] in lipid suspension are threshold recreational, medicinally effective doses. Oral ingestion of THC has been widely turned down as erratic, unpredictable, and slow, and thus not favored in medicinal treatment[28][29]. Efficacy can be heightened by ingestion of an additional lipophilic vehicle such as milk. First-pass liver metabolism provides a bioavailability of approximately 10% over a prolonged period, though more than 90% of available THC indigested sample is absorbed.[30][31] Degradation of THC occurs in stomach acids and in the gastrointestinal tract, resulting in over 100 metabolites, including most notably the pharmacologically active analogue, 11-OH-THC. Digestion of 20mg THC in sesame oil resulted in peak plasma concentrations of 9ng/ml, with higher immediate concentrations of THC-COOH (185ng/ml) due to first-pass hepatic metabolism.[32][33][34]
Rectal Ingestion:
Absorption of THC through rectal capillaries in ester (hemisuccinate) suppositories is more consistent, though slightly less efficient than oral ingestion.[35] Average doses of 15-30mg provide a breadth of effects from basic analgesia to recreational.[36] Bio-availability as compared to oral ingestion is ~50%.[37] After several 5mg THC hemisuccinate suppositories 3.3ng/ml plasma concentration was reached, with corresponding THC-COOH concentrations of 32.7ng/ml max.[38]
Intravenous Injection:
Intravenous THC administration results closely correlate with inhalation both in efficiency of metabolism and distribution of cannabinoids. Comparative models of metabolism between IV and Inhalation are within +-10% equality.[39][40][41] Effective doses from medicinal to recreational range from 25-150µg/kg, though IV THC is rarely reported for recreational use.[42][43]
Sublingual and Transdermal Induction:
Though both have been proposed and sparse anecdotal evidence supports their potential, little scientific evidence pertaining to dose or pharmacokinetics is available.[44][45]
Metabolism:
Basic metabolism of THC (and similarly, CBN/CBD) occurs as a result of the liver, though to a lesser extent, the lungs and intestines act in the biotransformation of mono-, di-, and tri-hydroxy metabolites. Cytochrome P-450 isoenzyme CYP2C9 is responsible for the hydroxylation to 11-OH-THC, and then the oxidation to 8-B-hydroxy-THC. 11-OH-THC is oxidized to nonpsychoactive 11-nor-9-carboxy-THC (THC-COOH).[46][47][48][49][50]Effects of Cannabis
Altered Perception of Time (distortion of length and intensity of passage), Anxiety, Anxiety Reduction, Anti-Inflammation (muscular and cellular), Analgesia, Appetite Stimulation, Ataxia (acute episodes, see also "Movement Disorders"), Brochodilation, Decreased Body Temperature, Decreased Occular Pressure, Dysphoria (acute episodes), Depersonalization, Dry Mouth, Euphoria, Enhanced Creativity (accompanied and catalyzed by heightened audio acuity), Enhanced Well-Being, Fatigue, Fragmented Thought, Hallucinations, Hypertension, Hyposalivation, Memory Inhibition (short-term interference, minor long-term inhibition), Motor Inhibition, Neuroprotection, Reddend Conjunctive, Relaxation, Tachycardia, Vasodilation. [51][52][53][54][55][56][57][58][59]Combinations with Cannabis
Alcohol- Enhanced CNS impairment. [60][61][62][63]
Amphetamine- Enhanced tachycardia.[64][65][66][67]
Antochlinergenics- Resperpine and Scopolamine may agonize increased THC related tachycardia, as well as hypokinesia. [68]
Benzodiazepines- Antiepileptic action, CNS and respiratory depression increased.[69][70][71]
Barbiturates- Enhanced CNS depressant and tachycardic qualities of THC. Note: Clearance of Barbituates may vary with chronic THC use.[72][73][74]
Cocaine- Enhanced tachycardia and increased nasal uptake readiness due to dilation.[75][76][77][78]
Dextromethorphan- Amplified dissociative intoxication.[79][80][81][82] Dissociatives downregulate THC receptors and decrease all response to Cannabinoids.[83]
See: https://drugs-forum.com/forum/sho...na+Combination for discussion.
Dopamine Agonists- Dopamine D2 receptor agonists increase analgesic effects of THC.[84]
Glaucoma Drugs- Additive relief of intraocular pressure.[85]
Ketamine- Additive CNS depression. [86][87][88]
Nicotine- THC uptake is reduced during nicotine consumption, while nicotine uptake is increased by THC ingestion. [89][90]
NSAIDs- NSAIDs antagonize THC analgesia and motor-coordination impairment. Indomethacin reportedly reduces “high” of THC ingestion in patients. [91]
Opiates- Enhancemend of analgesia and fatigue/sedation. [92][93][94][95]
SSRIs- Increased effect of fluoxetine.[96]
Tricyclic Antidepressants- Inflamation of tachycardic, hypotensive, and sedating actions of amitriptyline.[97]Different Uses for Cannabis
Shamanism, Spirituality, and Meditation-
This chapter needs creation. See https://drugs-forum.com/forum/sh...ad.php?t=32131.
Recreation-
Recreational Cannabis intoxication spans a wide breadth of both time and employment, currently reining as the most commonly used illicit substance in the United States. Recreational methods vary with a near equal spectrum of medicinal, from ‘joints’ and ‘bongs’ to sophisticated vaporizers and edible concoctions.
This chapter needs expansion. See https://drugs-forum.com/forum/sh...ad.php?t=32131.
Medicine-
Medicinal Cannabis treatments have been historically relied upon by countless civilizations on varying continents. Most recently, an assimilation of Cannabis to western medicine has been approached with scientific reason and current partial-employment. [98][99][100][101][102][103][104][105][106]
Anorexia & Appetite:
Small doses of 5-20mg[107] ingested several times daily has shown reasonable efficacy in stimulating appetite with minimal cognitive effect. In a 6-month study, Δ9-THC doubled appetite as compared to placebo in AIDS patients.[108][109][110] Primary Anorexia Nervosa seems untainted by Cannabinoid treatment, perhaps due to the root consisting of a psychological rather than physiological nature.[111][112]
Asthma:
Bronchodialation occurs as a result of Cannabinoid stimulation, primarily from Δ9-THC and CBD, both following vaporization/inhalation and oral ingestion for approximately 1.5 and 2 hours respectively.[113][114][115] Approximately equal in effect to isoprenaline, the orally ingested Δ9-THC (15mg) proved most effective.[116] Smoked Cannabis, though effective, is not recommended nor is it being considered widely for administration due to the high potential for irritation of mucous membranes.[117][118][119][120][121][122][123]
Glaucoma:
Cannabis treatment has been widely shown to decrease intraocular pressure up to 30% for 6 hours, effectively reducing impact of pain and damage resulting from Glaucoma.[124][125][126][127][128]
Migraine:
Perhaps the oldest treatment for Migraine relief dates back to 7th century India where intranasal cannabis was noted by a primary physician.[129][130] It is also notably common in many parts of Asia, and North Africa.[131] More recently noted by clinical physicians in the United States, Δ9-THC’s effect on serotonin (5-HT3) release may explain the underlying reduction in frequency and intensity of Migraine headaches.[132][133][134] Treatments studies of Cannabis and others of Anandamide have shown significant similarities, reinforcing the 5-HT3 receptor agonist theory.[135]
Mood Disorders:
Longstanding reports (Moreau 1845) and anecdotal studies have claimed efficiency of treatment for both mania and depression.[136][137][138][139] Cannabis in combination with SSRI medications has been shown to decrease tension, nervousness, and nausea normally associated with treatment of SSRIs alone.[140] ‘Wakefulness’ and Insomnia Cannabis-treatment studies have proved efficient and favorable when compared to prescription sleep-aids.[141]
Movement Disorders:
Spacticity and ataxia have shown the most positive consistent symptom reductions under Δ9-THC administration.[142][143][144] Tourette’s syndrome is currently under study with positive results favoring near-complete remission of effects under Cannabis treatment, though some studies have shown only moderate results.[145] Dystonia treatments with CBD have shown partial reductions of 15-50%.[146][147][148] In Multiple Sclerosis, as well as Parkinson and Huntington’s diseases, positive conclusions have been drawn without unanimous consent, though the potential for neuroprotective properties seems a boon to accessibility of cannabinoid treatments for neurodegenerative movement disorders.[149] The antiepileptic effects of Cannabis (specifically CBD), for which there is no direct tolerance, are among the primary self-employments of the medicine also under study for prescription treatment.[150][151]
Pain-Management- Cannabis and Cannabinoids have been employed in pain-reduction for cannabis and chemotherapy related pain, and prospectively researched for employment in other fields of analgesia.[152][153][154] A reduction in pain response-stimuli, as well as anti-inflammatory and long-term reduction, has been shown been shown as a direct manifestation of Cannabinoid treatments in both animal and terminal-patient studies. Over a 7-hour period, 20mg Δ9-THC outperformed and outlasted Codeine 120mg.[155]Cannabis and the brain
Cannabis Anxiety
We have a separate wiki page about Cannabis Anxiety:
https://drugs-forum.com/forum/showwiki.php?title=Cannabis_AnxietyThe dangers of Cannabis
Overdose and Side-Effects:
Cannabis overdoses may result in vomiting, increased tachycardia, and temporary bipolar mood cycling. Intense sedation, decreased coordination and mild hallucinations may also occur.[156][157][158]
A Cannabis Bad Trip (sometimes called a 'whitey')
On rare occasions a user can take too much Cannabis. This results in a rough, painful and sometimes disturbing experience. The most common reaction is to remain very still, communicate very little and feel nauseous and anxious- a semi catatonic state. This could be described as being submerged in a black cloud through which you can't see, hear or even think much. Other reactions are the complete opposite of this- a full blown panic attack can happen which is when the user experiences a sudden rush of anxiety, almost like they can feel burning poison rushing through their veins to their heart which begins to feel like it is being squeezed. Breathing can become difficult, sudden burst of energy and intensely weird feelings in the body. This can cause a freakout where the user can run around, scream, think they are having a heart attack or seeing the devil. There can be hallucinations. In such situations, they must be looked after and reassured that it is a temporary experience caused by the drug and that it will pass soon. They may be in shock for a while after the experience.
Toxicity:
No death has ever been reported or observed by Δ9-THC overdose, due to its extremely low acute toxicity.[159][160][161][162] [163][164][165][166]The currently unachieved (in human studies or recreation on record) LD50 for Δ9-THC is above 9,000mg/kg.[167]
Though oral use elicits no long nor short-term damage, the more common mode of ingestion however is combustion, smoking from a pipe or cigarette, which in itself creates many nefarious toxins (400+ Chemical constituents in Cannabis vapor[168]) for metabolism. Vinyl chlorides, phenols, nitrosamines and other known carcinogens and hydrocarbons have been detected in Cannabis smoke at 25%+ as compared to tobacco.[169] Prolonged breatholding (more than normal seated breathing rate) results in 40% increased tar ingestion with less than 10% increased THC.[170][171][172] Cannabis tar has been shown also to increase mutations in microsomal analysis, aiding validity to malignancy as a result of long-term smoked cannabis.[173] Though no direct cases of Cannabis resulting in lung cancer have been reported, higher incidences of lung cancer patients have at some time smoked Cannabis, perhaps due to the increase in CYP1A1 (PAH->carcinogen enzyme) reported as a result of THC ingestion.[174][175]
Tolerance:
Due to its common use as a recreational intoxicant and its employment in medicine, cannabis has been widely examined for its therapeutic potential and side effects. Among these side effects is tolerance, the regulation of cannabinoid uptake as a result of over stimulation. Tolerance is indicated by the requirement of larger doses to achieve a consistent desired effect, or when a given dose no longer provides it. Higher doses commonly result in the indication of higher impact of undesirable effects though, as with cannabinoids, tolerance can be achieved for many of these as well. Tolerance to cannabinoid stimulation results in withdrawal, most notably marked at 12 hours after cessation of “heavy” use by inner-unrest, increased activity and irritability.[176] During a flushing period of 4 weeks following a 4 week daily ingestion period of 210 mg smoked THC, determined by Georgotas and Zeidenberg[177] (comprehensive psychology), mild-withdrawal symptoms were reported to last between 5-7 days, with no inflammation or indication of desire for THC in the remaining 3 weeks.[178][179][180]
Unlike the mythic ‘street-knowledge’ assay, which implies cannabinoid re-absorption through lipid deposits resulting in ‘occupied’ receptors due to constant stimulation, modern neuroassays have concluded tolerance to be based solely in receptor regulation.[181][182][183] The cannabinoid content of endogenous lipid deposits has been shown to be less than active physiologically and psychologically.
A non-tolerant ingestion of smoked marijuana results in peak plasma concentrations of 90-95 ng/ml and peak effects lasting 75-90 minutes at which time plasma levels drop below psychoactive concentrations at 10 ng/ml.[184][185][186] Plasma concentrations are unaltered by tolerance, indicating no change in endocannabinoid signaling, however cannabinoid stimulation, especially in ligand activation, decreases as a result of receptor based regulation. As has been widely explained and explored, availability of bonding-sites is reduced by down-tolerance and phosphorylation after prolonged or extreme exposure to cannabinoid agonists, resulting in a notable decrease in efficacy of stimulation and effects.[187][188][189][190]
Down Regulation and Phosphorylation:
Importunate exposure of receptors to agonist behavior, both with respect to time and dose, results in the endogenous desensitization of Cannabinoid receptors. G protein receptors CB1 and CB2, the primary sites of action for Cannabinoid stimulation, recede from their bonding heights into the cell-membrane after prolonged agonist action.[191][192] This recession, known as downregulation, is coupled with phosphorylation in the desensitization of overestimated receptors in the mechanistic action of Cannabinoid tolerance.[193][194][195] Phosphorylation creates ‘rapid-tolerance’, or the tolerance normally experienced during a single smoke session, normally receding at an equally rapid rate.
Specific Activation:
Various Cannabanoids are active at different receptors, both by their affinity for CB1 or CB2 or their digested distribution. As a result, specific tolerance occurs effecting specific site of action.
-Tolerance to the pharmacological effects of ataxia, analgesia, motor inhibition, and anticonvulsant activity usually occurs within 3-7 days of administration, depending on dose and frequency, as a result of cerebellum based CB1receptor-binding and WIN55,212-2 stimulation. [196][197]
-Long-term memory inhibition, as well as certain neuroendocrine actions (including neuroprotective), take several weeks to develop tolerance desensitization, the former in part due to anandamide’s relatively high endogenous availability. Anandamide levels in the striatum show reduction after prolonged exposure to cannabinoid receptor agonists, though the availability of the precursors was not diminished, suggesting a superficial alteration of productivity. [198][199][200][201]
-More resistant populations of CB1 receptors, primarily located in the limbic regions responsible for emotional stimulation, were uniquely resilient in prolonging the onset of tolerance regulation. Tolerance to immunosuppressive effects of CP-55,940 through stimulation of CB2 receptors is largely insignificant even over extended periods of exposure.[202]
-CB1 activation in Hipocampal neuron populations responsible for short-term memory develops down-tolerance within 24 hours of Δ9-THC administration and showed no impact (positive or negative) from increased anadamide availability or administration.[203][204]
-Cannabinoid analogues WIN55,212-2, CP-55,940 and 11-hydroxy-Δ8-THC, more infinitively specific cannabinoid agonists take 7-9 days to develop normal tolerance shown to take 3-7 days in administration of less-specific agonists. Due to their specific affinity for bonding efficiently with CB1 receptors (predominant site of CNS stimulant and psychoactive activity), tolerance develops more slowly than with less accurately coupled agonists such as Δ9-THC, CBN and CBD.[205]
-In vitro cultures of neuroblastoma cell line (N18TG2) exhibited rapid-tolerance to chronic exposure to cannabinoid agonist stimulation, showing a natural cellular response.[206][207]
Tolerance as Dependence Indication:
Though tolerance and dependence often develop concomitantly, in the case of cannabinoid stimulation, since the primary actions of tolerance are neuroreceptive as opposed to adaptive endocannabinoid signaling, tolerance and dependence are independently significant. There is no scientific consensus on the implications of cannabinoid dependence and withdrawal.[208][209][210][211][212][213][214][215] As there is no indication of somatic and/or neurovegetative periods after abrupt cessation of high-dose cannabinoid therapy, the criteria for physical dependence remain unfulfilled as defined by worldwide health ministries. Psychological withdrawal implications failed to appear in any animal study, though have occurred in human and some non-human primates, to a notably lesser degree than opiods.[216][217][218][219] Primary indicated factors of “heavy” marijuana use behavioral withdrawal include irritability, sleep deficits, attentional deficits, and anxiety, and have been shown to noticeably recede within a 3-day period of cessation, dissipating completely within 1 week.[220][221][222][223][224][225]
Tolerance Reduction:
Recreational tolerance is relatively minute, if existent, in occasional users. Daily consumption for medicinal or recreational purposes however is likely to cause minor tolerance. Allowing receptor recuperation every 90 minutes could greatly decrease the impact of downregulation, and ingestion of appropriate doses rather than the commonly high recreational dose could aid in the resistance of phosphorylation tolerance.[226][227][228] A recent{{when?}} study employing capsaicim antagonists and markers during Δ9-THC administration for analgesic property showed a low ceiling of consumption efficiency, followed by a rapid phosphorylation at high doses, implying a ‘sweet-spot’ theory, in which an exact dose is exponentially more efficient than an overdose.[229]
Forecasting scientific developments imply that through integration of specific agonists at specific bonding sites could reduce selective tolerance while achieving reasonable effects.[230][231][232] The application of esoteric agonists could potentially alleviate tolerance based dosing and the complications it implies. Additionally, dosing with cannabinoid antagonists, such as CBD and CBG, can combat downregulation of receptors and expose increased availability.[233][234]
Pregnancy:
Cannabis is the most commonly used illicit drug among women of childbearing age.{{in where?}} [235][236][237][238][239] Self reported use during pregnancy (NIDA 1992) was 2.9%.[240] Longitudinal studies have concluded use rates of 10 to 16% in middle-class samples and 23 to 30% in inner-city populations.[241][242] These statistics propose cannabis as being one of the most highly used intoxicants during pregnancy, and thus an interesting and important prospect for investigation. Surprisingly, only a handful of studies have actually been completed on prenatal cannabis exposure, but their results are relatively convergent. While the concept of prenatal cannabninoid exposure resulting in a "stoned baby" has been widely disproved and disregarded, impacts on the birthing process (a consistent 1-week delay in gestation period, as well as increased incidence of labor-inducing but non-harmful contractions) and development (specifically cognitive and visuoperceptual) have been examined and debated due to their potential significance.[243][244][245][246]
The following complications have been reported as potential results of marijuana consumption on early baby-hood (Altered Cry Acoustics, Poor Visual Habituation, Minutely Decreased Skull Growth)[247][248][249][250][251], though none of them have been reported in a high enough incidence to "reach statistical significance"[252], meaning that their rate of incidence could not justify blame in exclusion of other factors. Initial complications have been shown to recede completely within 30 days of growth (Fried et al.[253]) Several tests employing The Bayley Scales of Infant Development have "reported no effect of cannabis use during pregnancy on infant mental or motor development" at 1 year growth (Astley S. Little R).[254][255][256] Use during pregnancy has never been linked to IQ or Stanford-Binnet Intelligence evaluations[257][258], but has been linked to poor short term visual memory (Griffith et al.[259]). One report showed that at 6 years, offspring of marijuana users (during pregnancy) display a slightly increased error of omission on a vigilance task, possibly indicated a deficit in sustained attention (Fried et al[260]). Higher ratings of inattention, impulsively, and activity, are also reported (Richardson et al.[261][262]) Impairment of Executive Function has been shown in several studies as a result of prenatal cannabis exposure at 10 years of development [263][264] however, behavioral neuroscientists and developmental psychologists regularly agree that development of Executive Functions is an ongoing process reaching ages beyond the scope of any current or past studies, making the results at age 10 potentially misleading. [265][266][267][268][269]Growing Cannabis
Introduction & Basic Life Cycle:
Natural outdoor growth of Cannabis has existed in Africa, Eastern and Central Europe, North and South America, and Asia for many thousand years[270], and much of the basic and advanced cultivation wisdom is derived from an understanding of the natural systems of nutrients, light and moisture, in which Cannabis naturally exhibits healthy growth.[271][272] Cultivation of Cannabis has been widely adapted and evolved from basic agricultural self-propagation to genetic engineering and advanced nutrient/light delivery systems. Outdoor and indoor soil-based propagation is still widely employed, though the use of hydroponic/aeroponic nutrient and moisture delivery systems and advanced HPS lighting regiments has gained legitimate popularity in medical and recreational based grow-operations.[273] Cannabis is a hearty, annual, seed propagating herb ranging in height from 1-5 meters. Seed germination occurs over a 5-7 day period (usually beginning in April or May in the Northern hemisphere), followed by a 2-3 month vegetative growth period of 8-10 hours of light per day.[274][275] During this period, the stalk develops nodes, bearing leaf petioles and flower-bearing limbs. Late season rises in CO2, coupled with decreased temperature and length of sunlight, elicit a flowering period during which the Cannabis plant will produce seed-pod carrying 'buds' that develop over the course of 2 weeks, or in the case of Sinsemilla, rapidly developing flowers without seeds.[276][277] Both male and female plants create flowers and psychoactive cannabinoids, though several factors alight females for selective reproductivity and flowering.[278] Male flowers require currents for transportation of pollen, and as a result their flowers are 'puffy' and hang low.[279][280] Female flowers are more commonly bunched, upright and dense. The presence of male pollen can elicit up to 1 kg of seeds per female plant, greatly reducing the efficacy of cannabinoid production (though males can be kept vegetative in wait for selective pollination).[281] Male plants produce approximately 50-65% THC as compared to female plants, with higher densities of fibrous content in main stalks.[282] The vast majority of cannabinoids present at the time of harvest (usually at the cessation of flower development) are THC-acids and pre-psychoactive.[283][284][285] Oxidation over the initial 'curing' period of 72 hours, results in the primary psychoactive components, Δ9-THC, CBN, CBD, 11-OH-THC.[286][287]
This chapter needs expansion. See https://drugs-forum.com/forum/sh...ad.php?t=32131.Forms of Cannabis
The once basic gene pool of Cannabis began with Cannabis Sativa and Cannabis Afghanica (originating in Afghanistan and Pakistan), more commonly known as Cannabis Sativa Var. Indica.[288][289] The lesser bred C. Sativa var. Kafiristanica (modern day 'Diesel'), originating in India, has considerably low levels of CBD but high levels of both CBN and THC. Cannabis Ruderalis shows the lowest (~.09%) levels of THC and is rarely bred for uses other than hemp fiber and oil production.[290][291][292] C. Sativa’s traditionally high-levels of THC as compared to natural levels of CBD contrast C. Afghanica’s higher CBD content.[293][294] The contents of Cannabis traditionally used vary by region, though modern use mainly relies on Sensimilla, the process in which female plants are sequestered from male pollination, thus avoiding seed pods and maximizing resin and flower production (therefore THC production).[295][296] When C. Afghanica and variations of C. Sativa are bred, phenotypes occur, producing favorable anomalies such as aesthetically pleasing scent and color mutations, shortened growth periods, and most desirable, controlled (high) levels of THC and CBD.[297][298][299] From these phenotypes are bred colloquial ‘strains’, selectively reproduced for desired traits.[300][301] Endless amalgamations of breeding have created a virtually incomprehensible amount of strains due to the Sensimilla phenotype flaw of eventual hermaphrodidation, requiring stabilization through consistent generational breeding.[302] Cannabinoid production commences with resin production towards the middle of the Cannabis plant's life in resistance of environmental afflictions. Resin glands containing terpenoids and cannabinoids commonly form towards the tip of trichomal stalks, segregated from secretory cells.[303] Small abcission layers below the glandular developments provide easy removal of trichomal bodies for Hash or Charas production.[304][305] Concentrated versions of the active constituents exist in the form of Hashish, Kif, Hash-Oil, and more recently, synthetic esoteric cannabinoid stimulators such as WIN55,212-2 and CP-55,940.[306][307][308][309]Legal status of Cannabis
United Nations
The United Nations unilaterally (as of 1961) considers the possession, cultivation, ingestion, and distribution of Cannabis an illicit act.[310] Active pursuit of Cannabis grow-operations yielded 1416 'labs' of 100,000kg in the 2003-2004 fiscal season. [311][312]USA
Cannabis is Federally regulated as a Schedule I substance (high abuse-potential and no accepted medical value), prohibited for any use.[313][314] Dronabinol and nabilone are synthetic cannabinoids approved by the FDA as Schedule III (low abuse-potential and accepted medical value).[315][316] Twelve states permit Cannabis use for medical purposes and one state provides a defense of medical necessity.[317] Employer sympathy for patients is unregulated and use as a basis for termination is valid.[318]
As the Supreme Court has yet to rule on the constitutionality of state-legalized medicinal Cannabis, the disparity between Federal and State laws agitates treatment, distribution, and law-enforcement/prison populations.[319][320][321]
Alaska, Ballot Measure #8
California, Proposition 215 & Senate Bill 420
Colorado, Amendment 20
Florida, Amendment 2
Hawaii, Senate Bill 862
Maine
Montana, Initiative 148
Nevada
New Mexico, Senate Bill 523
Oregon, Measure 67
Rhode Island, The Edward O. Hawkins and Thomas C. Slater Medical Marijuana Act
Vermont, Senate Bill 76
Washington, Measure 692[322]EU
This chapter needs to be written. See https://drugs-forum.com/forum/s...ad.php?t=32131.History of Cannabis
This is a summary of the history of cannabis. The actual detailed history of cannabis is very complex, please see Detailed Timeline for more information. For this reason it has been summarized into two sections, one on the ancient history and the other on the more modern history, broken up in year 1937 with the passing of the Marijuana Tax Act, which effectively criminalized cannabis. The modern history pertains more to what events caused cannabis’ immediate illegal status, whereas the more historical history envelopes the first case of misinterpretation, leading to a tarnishing of cannabis’ reputation.Detailed Timeline
Pre-1937 History
A now slightly infamous character from Venice named Marco Polo first brought back tails of hashish and its use to Europe, where knowledge of it eventually spread outward in 1271. This was part of the high middle-ages, when the Europeans would have never associated hemp, a very useful source of fiber, with the powerful, corrupting, and otherwise evil drug known as hashish that Marco wrote about. With it came the story of the Hashshashin, highly skilled murderers, and users of this intoxicating drug. From their name came the term ‘assassins’, and the truth is, that is not clear whether or not they even used hashish, cannabis, or any other intoxicant. The simple etymology of the two words came together when Marco encountered them at the same time, thus he classified them together. It was a big misinterpretation and quite unfortunate event which indefinitely led to the global wide presumption that cannabis; in some innate way; triggers violence in the user.
Fast track to 1500, where there was an increase in travel and merchants began to bring spices, fruits, metals, timber, and drugs – primarily hashish and opium. As an intoxicant, cannabis was widely unknown to Europeans, and only a few individuals knew of the connection between hash, hemp, and cannabis. Hemp was needed to produce rope and textiles for the navy, and consequently King Henry VIII issued a royal proclamation which imposed a fine on any farmer that did not set aside some of his land for hemp production.
For the next two centuries hemp was still only a source of fiber for Europe and America. In 1790, Cannabis and derivatives were taxed in Britain, to produce revenue for the debt of the East India Company. Alcohol and tobacco were taxed as well. There was some debate as to whether or not ban bhang, ganja, and charas, as they were seen as Indian hemp drugs. The Governor-General wanted all drugs banned, but the British declined, cannabis was too good of a source for tax revenue. Then finally in 1800 a ban was imposed on hash for the French troops in Egypt, but it was ineffective. When the British blockade was lifted, troops were allowed to go back home, and with them they brought hash. It became well known in France. This was Europe’s first real taste of cannabis.
In 1809, an Arabic scholar identified the word ‘assasin’ with hashish and Hashshashin, and published his findings to the Institute of France on May 19. He was correct in his etymology, but did not assert that it was a derogatory word and that the Hashshashin (Assassins) were not actual hash users. He brought into modern times the belief that the Assassins were hash users, and it evoked their brutal ways. In the 1840’s, cannabis and opium tinctures became widely available in pharmacies and were used for many common ailments. In the 1850’s, cannabis began to appear in dispensatories (physicians textbooks) and was listed as an antibiotic and analgesic. Doctors still preferred opiates because they were water-soluble, and could readily be injected as a painkiller. A large amount of research was being done on cannabis in the mid and late nineteenth century, and it was being praised by doctors all around. Over the next century, this would change.
At around the same time drug consumption was rather rare in Britain. There were no hashish houses in London, and no literature on the subject as in America and France. Alcohol was overly popular, unlike America’s somewhat puritanical take towards it in the 1850’s.
The first laws against cannabis were enacted in America in 1870, because it was thought that it made the Indian coolies ill and indigent. The laws were ignored, as mine operators found that their workers were more productive if they were allowed smoke breaks periodically. In 1877, Cannabis was officially blamed by Indian administrators as the cause of a lazy work force. In fact, it was poor nutrition, housing, medical care, and hygiene, but this was ignored. The British began to agree.
In the 1880’s, many cannabis medications and tinctures were being produced by pharmaceutical companies. Hashish painkillers, marijuana and tobacco snuff, and even marijuana cigarettes were advertised as remedies for all sorts of ailments. It was very difficult to assess a proper dose though, as cannabis tinctures were not pure and settled quickly – this resulted in many documentations of cannabis poisoning. As a recreational drug, cannabis was never as popular as opium because it didn’t act right away, and opium was available as laudanum or other mixtures ready for consumption. Then in 1887, aspirin emerged onto the scene along with other synthetic drugs. It was easier to standardize, and control. In an age of optimism and faith in scientific potential, this was big news. The British Medical Association began to campaign for these new synthetic drugs, and doctors became more aware of them. Around this time, recreational cannabis use hit Britain as it had hit France fifty years earlier, but as a medicine, cannabis had seen its time.
In the 1890’s, hashish use had gained widespread popularity in Britain, and many people were publicizing its use. It was a time of freedom of expression and personal liberty, but this didn’t last. Concern began to rise about drug-taking, and attitudes began to change, with concern came fear. Cannabis use was largely unseen in America, but a ‘new’ way of consuming it appeared as smoking the dried leaves and flowers. Drug use was identified with ethnic minorities and foreigners, and it was deemed ‘un-American’. As with the Chinese and opium, cocaine use by African slaves was prevalent in the southern states, and it was said that it endangered the white population as they would rise up and attack white folks. Now came along cannabis. Hemp had been grown for its fiber, but its psychoactive potential was unknown to the white population. The black slaves knew of it from their experience with dagga, and consumed it just the same. It was, however, the Spanish and Portuguese that brought it into the main stream. Cannabis was popular in Mexico by now, and it slowly crept up into Texas and the southern states.
Then in 1914, a catalytic event occurred which started the crackdown on cannabis. A city by-law was put in place in El Paso banning the sale or possession of marijuana after a serious fight broke out between a marijuana user – a Mexican – and someone else. Other cities followed suit, and soon southern state legislatures began to lobby Washington for federal action. The Harrison Narcotic Act was enacted this year, forcing doctors, pharmacists, and licensed dealers to maintain records of drug transactions. Cannabis was seen as a low priority because it was a common medicine, so it was excluded in the later drafts of the act. However, states began passing their own cannabis laws. From here on, attitudes continued to stiffer towards this new Mexican drug, which also soon became popular among Jazz musicians as well.
In 1930, the Federal Bureau of Narcotics (later to become the DEA) came into existence to enforce drugs laws, and Harry J. Anslinger was assigned first commissioner. At first, he only targeted cocaine and opium, but the FBN was soon in trouble. As the Depression caused a major budget cut, Anslinger needed a new target, and it was marijuana. He began to demonize it, with the un-acclaimed help of William Radolf Hearst who popularized the word marijuana in his newspaper, then spelled with an ‘h’, as a criminal substance undermining American culture. His sensationalism worked extremely well in selling newspapers and attracting the attention of the white population.
Finally, in 1937 the Marijuana Tax Act was passed, effectively controlling the social use of marijuana. It imposed a heavy tax on cannabis, including hemp, and destroyed the slowly fading hemp industry. New funding for the FBN was allocated, and Anslinger had accomplished his goal.[323]Post-1937 History
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