Marijuana is a commonly ingested drug with a variety of health 'effects', some beneficial and some not so desirable. The smoke per se from joints is not healthy, but activation of the cannabinoid system (via THC) can confer beneficial effects if used wisely
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Cannabis is a herb with a wide range of uses, but is most notably known currently for its use as a recreational drug (for which it is commonly referred to as marijuana or weed). It is typically smoked, but can also be cooked into foods or inhaled through a vaporizer.
It works on a unique set of receptors known as the 'endocannabinoid' (internal cannabinoid) system, named after the plant name (Cannabis). It is the only known plant that can activate these receptors, although our bodies do regulate them without the plant through dietary fats.
It can benefit health in a myriad of ways through the endocannabinoid system. It does seem to suppress acute changes in the body - and could potentially be an ultimate long term regulator of many body systems, as it can prevent a fair bit of changes that would result in metabolic abnormalities.
In general, Cannabis stays in the body for a long time after initial ingestion as excretion rates are slow
It is currently illegal to buy on its own in many countries and regions, and can usually be acquired only with a prescription in these areas for medical purposes.
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Cannabis Sativa, Weed, Medical Marijuana, Marihuana, dope, ganja
Hemp Protein (same plant, but this term tends to refer to a food product without THC)
Marijuana is highly neuroactive, but is generally classified as an anxiolytic.
Marijuana, without a prescription, is illegal in various countries. Consult your region's legal statutes before attempting to smoke up.
It does seem to suppress acute changes in the body, so during any intense fat loss or muscle building phases it should be avoided for the most part. Over the long-term (of which health is ultimate, rather than ego) then it seems that it can prevent a fair bit of changes that would result in metabolic abnormalities, although it may be classified as a pro-obesogen via its suppression of fat lipolysis and habit of giving some people the munchies.
Examine.com Medical DisclaimerAny dose which provides a neurological sensation is enough to saturate the body for a prolonged time, an 'ideal' dose has not been established.
Frequent toking is not required due to the ability of the cannabinoids to saturate the body for 1-2 weeks, or possibly more, depending on dose.
Although I cannot really recommend this (legality issues and all that), I find it incredibly interesting for cannabinoids to have such a long half-life.
Having a 'supplement' once every two weeks and getting benefit from it everyday between each bimonthly toking session is pretty cool. That being said, the immense 'modulatory' potency of marijuana makes it hard to manipulate as a supplement for acute changes. If you deviate too far from homeostasis (which is the goal of fat loss and muscle building) then it seems to then work opposite your goals.
Kurtis Frank
The plant Cannabis sativa or Cannabis indica (otherwise known as Hemp) is a plant from Traditional Chinese Medicine that also has a history of usage for various non-nutritional and non-medical purposes, such as fibers and textile manufacturing. Preparations of any Cannabis plant used for pharmacological reasons (smoking, vaporizing, or otherwise ingestion) is typically referred to as Marijuana, and is distinct from Hemp Protein supplements (meal replacements or oils made from the same plant, but without the primary psychoactive ingredient. Marijuana is, at the moment, the most widely used illicit substance in the world, according to the UN[1] but can legally be given as a medical treatment for various forms of cancer, AIDS/HIV, and neurological impairments.[2][3]
Cannabis Sativa leaves and flowers have been used in a preparation called Bhang to then be used in beverages or sometimes smoked; usually in Bangladesh and northern India.
Marijuana is a traditional chinese medicine that has been used in some surrounding cultures, and currently is classified as an illicit compound in various (but not all) western nations
As a plant, marijuana (or the family of cannabis plants) contains various phytochemicals. The primary active ingredient is seen as Delta-9-TetraHydroCannabinol (THC), others including cannabidiol (CBD) cannabigerol (CBG)[4] and cannabidivarin.[5] These phytochemicals are collectively known as 'phytocannabinoids' and act on the endocannabinoid system in the body.[6][7] They are the only known naturally produced cannabinoids that can be ingested, and the typical agonists for these ubiquitous receptors in the human body are anandamide and 2-arachidonoyl glycerol, both derivatives of the omega-6 fatty acid 'Arachidonic Acid'.[6]
When ingested in a gaseous state (toking) pulmonary (lung) assimilation causes a maximum plasma value and the onset of psychotropic effects in a few minutes, a maximum of said psychotropic effects is noted 15-30 minutes after initial ingestion to taper off 2-3 hours after exposure.[8] Systemic bioavailability ranges from 10+/-7%[9] to 27+/-10%[10], with habitual users absorbing more of the active THC. The reason for the low bioavailability is due to a hypothesized (up to) 30% loss from pyrolysis, poor lung absorption, and losses to sidestream smoke not being ingested.[8] Toking in the form of a pipe seems to eliminate sidestream losses, and absorption rates of up to 45% have been recorded.[11]
After oral ingestion (brownies) peak serum levels are achieved at a variable 60-120 minutes after ingestion, due to varying digestive potencies inter-person.[8][12] Some studies have noted delays of peak values up to 4-6 hours post ingestion[13] and some showing multiple plasma peaks.[14] With a fatty acid vehicle, intestinal uptake of radiolabelled THC (of which includes both the active Delta-9 form and its acid hydrolysis Delta-8[15]) exceeds 90% in most cases[12], although after extensive hepatic first-pass metabolism the amount available to systemic circulation varies from 2-14%, with high interindividual differences.[16][8]
Ophthalmic (eye) administration has only been researched in rabbits, in which a light mineral solution resulted in 6-40% systemic bioavailability and a peak serum level 1 hour after application, which remained high for several hours.[17]
Tissue distribution of THC is assumed to be due to the molecule's physicochemical properties (traits denotes by the structure's shape), as there exists no THC-specific transport or barriers that affect tissue concentration.[18][8] Approximately 10% of assimilated THC is bound to red blood cells[19] while the otehr 90% floats freely in the blood. Of this 90%, 95-99% are bound to plasma proteins such as lipoproteins and, to a lesser extent, albumin.[20][21] Due to THC's lipophilicity (fat-solubility), it can diffuse through cell membranes.
THC, at times correlated near peak plasma levels or shortly after, rapidly enters highly vascularized (good blood supply) tissues and organs such as; muscle, spleen, heart, lungs, liver, and kidneys.[22] Due to its lipophilicity, it eventually almost exclusively settles into adipose tissue (body fat) and can be stored in the long-term.[23][24]
THC can easily cross the placental barrier, and can appear in a child's blood if a mother ingests marijuana. This is seen across all species to varying degrees.[25][26][27] Human breastmilk can contain levels of THC up to 8.4 times that found in plasma, and thus a mother smoking 1-2 joints a day can expose their child to values ranging from 0.01-0.1mg active THC through breastmilk.[28]
THC may also accumulate in the testicles, where it may influence reproductive function.[22]
Although metabolism exists in the lungs and heart tissue, Tetrahydrocannabinoids are metabolized primarily in the liver through the P450 enzyme system, via hydroxylation and oxidation reactions.[29][30] A member of the CYP2C subfamily seems to be the most active in humans.[31]
Although over 100 separate metabolites of THC have been identified[32], the major one is hydroxylation of THC at the C-11 (eleventh carbon) site to form 11-OH-THC, and further oxidation results in THC-COOH.[33] All mediated by liver P450 enzymes, the rate limiting step of which seems to be hepatic blood flow.[8][34]
THC metabolites are commonly excreted in the urine through the acid metabolite 11-nor-9-carboxy-THC glucuronide, a glucuronidated form of THC-COOH.[35] A proposed mechanism of long-term storage is when 11-OH-THC conjugates with fatty acids in the adipocyte.[36]
Excretion of THC compounds in the urine and feces begins after a pseudoequilibrium is met between tissues and plasma. The time of equilibrium changes based on dosage, with low dosage (16mg THC) tokes taking 3-12 hours, and high dosage (34mg) tokes taking 6-27 hours.[37] The carboxylated metabolite (THC-COOH) can be detected in the plasma for up to 7 days after both dosages.[37] This long duration metabolism is partially explained by the slow release of THC conjugates from adipose and other body tissue into the bloodstream[18] and partially due to the half-life of various THC conjugates, which although not accurately known ranges from 12-36 hours for 11-OH-THC and 25-55 hours for THC-COOH; typically values in the 20-30 hour range are reported for the THC molecule itself.[38][10] Typically the metabolites have longer half-lives than the parent THC molecules. Complications arise in measuring the half-life of Delta-9-THC due to interpersonal and interspecies differences, and some complications in distinguishing THC from its metabolites in vivo.
Excretion of THC occurs primarily as acid metabolites rather than the parent molecule, with 20-35% being excreted in the urine and 65-80% excreted in the feces.[12][34] Most being excreted in the feces due to the molecule's fat-solubility, extensive enterohepatic recirculation, and resorption from the renal tubules (which minimizes urine excretion)[12][39] Roughly 65% of THC and THC metabolites are excreted after 72 hours from both routes.[8][12] Full elimination of THC from the body may take up to two weeks to occur.[13] There also seems to be differences between chronic and first-time users, with chronic users taking much longer to fully metabolize all THC from the body; in some cases under urine analysis metabolites can be traced in the urine up to 46-77 days after administration[40] although averages were 12.9 days for light users and 31.5 days for chronic users.
The endocannabinoid system is a regulatory system in the body which comprises of Cannabinoid 1 (CB1) and Cannabinoid 2 (CB2) receptors, of which THC and endocannabinoids (such as anandamide) act as agonists.[41][42][43] CB1 receptors are prominent in neural tissue but are also found in the pituitary and peripheral tissue such as the thyroid, adrenals, gastrointestinal tract, and reproductive organs.[44] CB2 receptors are found almost exclusively in immune cells[45], although some are found in keratinocytes as well.[46] There is suspected to be a third (or more) class(es) of cannabinoid receptors beyond CB1 and CB2; although they have yet to be identified officially[47] the receptor GPR55 looks to be a promising addition.[48]
The endocannabinoid system is a system regulating homeostasis in the body[44], and has implications in nocioreception[49], regulation of motor activity[50], neuroprotection against inflammation[51] injury[52] and excitotoxicity[53], certain phases of memory encoding[54][55] and general neurohomeostatic mechanisms related to stress prevention.[56] It can also modulate immune and inflammation responses[57] and parameters of cardiac health.[58] Cannabinoid agonists also have benefit in tumor anti-proliferation[59] as well as alleviating chemotherapy induced nausea.[60]
Beyond the endocannabinoid system and the cannabinoid receptors, marijuana has been noted to act on Vallinoid Receptor 1 (VR1) as an agonist,[61] 5-HT type 3 receptors,[62] and alpha7-nicotinic acetylcholine receptors.[63]
Cannabinoids are known as modulators, or of having the ability to suppress and induce effects that are counter to each other, of which significant is titrated towards homeostasis (ie. will induce effects in those deficient in the effects, will inhibit those with a surplus of the effects).
This is shown through cannabinoid agonism possessing the ability to both inhibit[64] and induce Adenyl Cyclate (AC) activity,[65] possessing the ability to promote cellular survival[66] via Akt/PI3K phosphorylation and also induce cell apoptosis (death) via ceramide synthesis,[67] and also mediate a balance between neurogenesis and neurodegeneration.[68][69] Marijuana (as a whole plant) has also been involved in both pro-estrogenic reactions[70] and anti-estrogenic reactions.[71]
The agonistic effects of Delta-9-Tetrahydrocannabinoid can also be mediated by the antagonistic effects of another component of marijuana, Delta8 & 9-tetrahydrocannabivarin[72] and the inverse-agonistic properties of cannabidiol.[73]
The endocannabinoid system is thought to be related to longevity due to its involvement in food and appetite regulation[74] and the relationship between longevity and caloric restriction.[75] It appears that endogenous N-acylethanolamines that mediate the cannabinoid system are reduced under caloric restriction (and the enzyme that mediates catabolism, FAAH,[76] appears to be upregulated[77] which is not dependent on DAF-16 but dependent on PHA-4 which is the downstream target of FOX01[78]), and that supplementation of one of these fatty amides (eicosapentaenoyl ethanolamide) abolishes the effects of caloric restriction (nematodes).[75] It has been noted in mice that abolishing the FAAH enzymes fails to modify lifespan despite an increase in anandamide, but abolishing the CB1 receptor promotes lifespan.[79]
Increasing the activity of FAAH appears to be able to increase lifespan via mechanisms related to caloric restriction, and preventing signalling via the CB1 receptor appears to promote lifespan; this has not yet been applied to mammals ingesting marijuana, so practical relevance of this information is unknown
The CB1 receptor was initially known as the 'brain-active' receptor as it was initially isolated only in neural tissue but has since been found systemically,[80] while the CB2 receptor appears to be more related to the immune system (and is the target of some Immune Booster supplements such as Echinacea) It is highly expressed on the basal ganglia and the hippocampus in the brain.[80]
In the forebrain, CB1 expression by axons of GABAergic interneurones with cholecystokinin basket cells is dominant.[81]
There appears to be a correlation between anxiety in adulthood and previous heavy (daily) usage of marijuana during adolescence, where adults who used marijuana during youth and not adulthood were at a slight but significantly elevated risk (RR of 2.2; 95% CI 1.1-4.4) and those who continued usage were at a slightly higher risk (RR of 3.2; 95% CI 1.1-9.1).[82]
In heavy adolescent users of marijuana (approximately daily usage), there does not appear to be any higher risk of depression in adulthood when compared to non-smokers.[82]
In marijuana users who have since abstained, at least one twin study has failed to find a long-term impairment to cognition (with a median 20 years of marijuana cessation)[83] and a meta-analysis assessing shorter term studies suggested that possible impairment is limited to 25 days as it failed to find any impairment for periods longer than that.[84]
Marijuana may help artherosclerosis and artery plaque formation via CB2 agonism.[85] Anandamide inhibits inflammatory gene expression while THC can inhibit artherosclerotic plaque formation by inhibiting macrophage recruitment, both of which negatively influence monocyte adhesion.[86]
A marijuana phytocannabinoid known as 'Cannabigerol' has the properties of being an Alpha-2 Adrenergic agonist (the opposite action of Yohimbine) and thus may preserve fat mass.[87] Activation of hepatic CB1 receptors can also induce cellular changes which can be seen as 'pro-obesogenic' such as expression of the gene SREBP-1c which mediates downstream fat synthesis, such as the enzyme fatty acid synthase[88][89]
The enzyme Carnitine Palmitoyltransferase 1 (COMT1), the rate limiting enzyme of fatty acid Beta-oxidation, is suppressed under the influence of marijuana in the liver[90] yet seems to be elevated in some brain cells, which results in neuronal ketogenesis.[91] Adipose (body fat) cells seem to mimic the liver cell's pro-obesogenic actions more than the neurons actions.[92]
Cannabinoids can be seen and modulators of the immune system, with both influencing and inhibiting effects on various forms of inflammation via CB2 receptor agonism/antagonism, as well as other mechanisms of action.[93] This receptor seems to be heavily involved in neuroinflammation, or more specifically immune function mediated by the CNS.[94]
Marijuana is seen as a treatment for glaucoma via acting on retinal cannabinoid (CB1) receptors, which induced numerous effects in the retina. Of most clinical importance is a reduction in Intra-Ocular pressure (IOP), but also noted are anti-oxidant and anti-inflammatory effects as well as suppression of apoptosis and NMDA-mediated hyperexcitability.[95][96] There appears to be a nonresponse rate for marijuana usage, indicated that it is not a reliable treatment for all.[97]
Marijuana can also be seen as anti-diabetic by preserving islet integrity (synthesizers of insulin) by downregulating inflammatory signals[98], and is a diabetic treatment for alleviating nerve pains.[99]
It can aid gut/intestinal disorders by direct suppression of proinflammatory mediators, inhibition of intestinal motility and diarrhoea, and attenuation of visceral sensitivity.[93][100]
Opposite of the beneficial effects of Marijuana listed above, marijuana seems to be a contributing factor to the development of non-alcoholic fatty liver disease.[90] The pro-steatogenic actions of marijuana seem to be via agonism of hepatic CB1 receptors[88] and perhaps CB2 receptors if non-alcoholic fatty liver disease is present.[101] Via pro-obesogenic transcription factors such as SREBP-1c, an increase in hepatic de novo fatty acid synthesis also occurs.[88] These effects are almost exclusively mediated through the CB1 receptor.[102]
In a study on rats fed 3-6mg/kg Cannabis Sativa as aqueous Bhang solution (at 6mg/mL), 36 days of administration saw a decrease in testosterone by almost half at 3mg/kg bodyweight and further decreases at 6mg/kg bodyweight.[103] It was suggest this was due to inhibitory effects on 3βHSD, the final enzyme in testosterone synthesis; as rats also saw decreases in 3βHSD activity and 3βHSD showed a negative correlation (-0.82) with CB2 receptor expression (of which Marijuana increases)[103] and other studies indicate that THC can inhibit gonadotropin-induced testosterone synthesis even in abundance of gonadotropins; suggesting inhibition at the level of the testicle.[104]
Additionally, THC and cannabis molecules do not prevent gonadotropins from binding to receptors[105] yet still inhibited testosterone synthesis (in this study, via inhibition of cholesterol esterase). Progresterone synthesis has also been shown to be hindered in rat testicles associated with THC.[106] These effects are also seen with Cannabidiol and Cannabinol, and are more effective than THC.[107]
In research animals, Cannabis Sativa and THC appear to be able to potently suppress testosterone levels and may do this via testicular means (cholesterol esterase, 3βHSD) and pituitary mediated means
In humans, infusion of 10mg THC over 50 minutes (as 0.02% solution), compared against a placebo injection at an alternate time, showed a time-dependent decrease in testosterone over the subsequent 6 hours measured; whereas control fluctuated at around 5.5+/-0.5ng/mL and the THC group dropped to around 3.5+/-0.5ng/mL at 4-6 hours (values obtained via graph) despite THC concentrations in the blood disappearing by 1 hour post-test.[108] This relationship appeared to hold true after subjects smoked a 2% marijuana in which testosterone levels appeared to reach about 66% of baseline values after 3 hours (time after not recorded).[108] Other studies using marijuana suggest nonsignificant reductions in testosterone levels after 1-2 2.8% THC joints[109] and another a very slight (8%) transient decreased in testosterone after 20mg THC as a joint.[110] The study showing non-significant changes and the study noting slight decreases controlled for marijuana usage prior to the studies[109], whereas the former (noting larger decreases) did not.[108] Interestingly, a study using isolated THC did not find these same results; suggesting that other compounds in the Cannabis Sativa plant may be causative.[111]
Chronic users of marijuana do not display significantly different baseline levels of testosterone (either gender, tested under non-smoking conditions) up to daily smoking sessions, or 7 joints weekly.[112][113] One study noted depressed testosterone levels are seen with 4+ weekly tokes compared to a control that does not smoke Marijuana.[114] This latter study may be biased (funding from US department of safety).
It has been noted[110] that all human studies on the subject matter showing decreases in testosterone, regardless of statistical significance, show declines still within the normal biological range and are unlikely to influence behavioral effects secondary to testosterone.
In human interventions, the results are somewhat mixed. All studies are noting decreases in testosterone yet the significance of the result spans from a 'minor, statistically insignificant' drop to 1/3rd suppression of testosterone levels acutely. Overall, it seems that there is a suppression of circulating testosterone levels in males and females after smoking marijuana but this may not influence testosterone levels for the long term
Infrequent toking should not significantly influence long-term effects of testosterone, and frequent (7 weekly joints) might for as long as it is continued; there doesn't seem to be long-term adverse effects on testosterone after cessationIt is possible the mechnanism by which testosterone is depressed is through reducing hypothalamic and pituitary output of gonadotropin hormones, as administration of hCG (Human chorionic gonadotropin) in one study that noted marijuana-induced testosterone suppression also noted hCG's ability to reverse it.[114]
This is not to rule out decreased testosterone synthesis in the testes (extrapolated from mouse studies), increased liver conjugation and metabolism of testosterone,[115] or direct antagonism at the level of the androgen receptor,[116][117] with the ability to prevent DHT from binding to the androgen receptor.[118] At least the last mechanism shows clinical relevance, as castrated rats still experience anti-androgenic effects from THC and this effect in independent of circulating testosterone levels.[117] Many of the testosterone-related effects are secondary to the pituitary, as endocannabinoids cannot suppress testosterone in rats lacking a CB1 receptor.[119]
The mechanisms by which marijuana can suppress testosterone synthesis are quite numerous, but mostly due to decreased synthesis in the testicles (both from lack of pituitary input, and inhibiting testicular enzymes involved in testosterone synthesis) and interfering with binding of androgens to their receptors (this would not affect circulating levels of testosterone, but would reduce their effects)
The possibility of THC and Marijuana suppressing testosterone-like effects (through the androgen receptor) even without a drop in testosterone is possible, and cannot be ruled outIt is suspected to suppress testosterone levels for up to 48 hours, as based on a mathematical simulation using the graphs obtained previously with a gradually ascending curve up to 2 days post smoking.[108] Most time curves, however, indicate suppression of testosterone to reach its highest 4-6 hours after consumption; well after THC has been cleared from circulation.[108][109][108]
Acute smoking of two 2.8% joints is associated with a slight increase in circulating growth hormone levels 2 hours after smoking, from about 1ng/mL to 2ng/mL when compared to control (smoking placebo).[109]
Luteinizing Hormone appears to take an instantaneous drop in males smoking marijuana. [109] Chronic usage is not associated with depressed LH levels, although moderate usage (5-6 tokes weekly) is associated with a nonsignificant increase in baseline LH levels.[113]
Chronic usage of marijuana, when tested under non-smoking conditions, is not associated with any significant changes in FSH levels at rest.[113]
Marijuana smoking is able to acutely increase circulating cortisol levels.[109]
Leptin is an adipokine that serves as a nutrient sensor, being increased in states of caloric surplus (to increase metabolic rate) and decreasing itself in states of starvation to reduce metabolic rate.
At least one human study has noted increases in circulating leptin.[120] This study was data-analysis of a previous study on neuropathic pain in HIV infected men[121] and over 5 days of smoking cannabis at 2% THC (doses ranging between 1-8%, based on reports of pain reduction) was able to increase leptin by approximately 67.1% (44.6-93.1% range) relative to their baseline levels whereas smoking a placebo cigarette raises leptin by 12% with a range between a 4.4% reduction and 30.4% increase.[120]
As leptin increases cause a suppression of hunger, these results are somewhat contradictory and emphasis should be placed that it is a pilot study.
One study noted an increase, which is opposite in logic to what is seen with the 'munchies'. Insufficient evidence to draw conclusions from
Smoking marijuana is associated with a 42% increase in circulating Ghrelin levels (relative to baseline) in a study where the placebo group had their levels decrease by 12% (relative to baseline) after smoking a THC-free placebo cigarette.[120]
Oral ingestion of 3-6mg/kg bodyweight liquid Bhang (aqueous Cannabis Sativa) is able to dose-dependently decrease testicle weight in rats over 36 days, by 17% at 3mg/kg and 33% at 6mg/kg.[103]
Histologically, an absence of spermatozoa has been seen after oral administration of 3-6mg/kg Bhang ingestion in up to 40% of tubules observed.[103] Spermatozoa apoptosis (sperm death) appeared to increase as observed via staining.[103]
Those exposed to a high fat diet may be less sensitive to the effects of Delta-9-THC.[122] Possibly through diet-induced desensitization of the cannabinoid receptors via the fatty acid metabolites of anandamide and 2-arachidonoylglycerol (in vivo agonists).
Theoretically, there could be interactions with drugs that are metabolized extensively by the CYP1A2 enzyme that primarily metabolizes marijuana. Interactions could also occur with protein carries as Delta-9-THC and other cannabinoids strongly bind to proteins.[8][39]
Cessation of marijuana during treatment with anti-psychotics has been shown to increase levels of anti-psychotic medication in the blood due to cessation of induction of the CYP1A2 enzyme which degrades both (ie. its activity was induced during marijuana presence, and was not as active in degrading the medications clozapine, olanzapine without the extra induction)[123][124]
Marijuana usage can also increase the effects of sedatives such as alcohol or benzodiazepines[125][126] and can synergistically work with muscle relaxants, bronchodilators, and anti-glaucoma medication.[127] It can also work with the anti-epileptic effects of benzodiazepines.[128]flunitrazepam binding and analgesic activity of synthetic cannabimimetics]
NSAIDS such as indomethacin or acetylsalicyclic acid (aspirin) can inhibit some aspects of marijuana such as the perceived 'high' and tachycardia, as some effects of THC are mediated through prostaglandins (of which NSAIDS inhibit synthesis of).[129][130]
(Common misspellings for Marijuana include mariwana, mariwhana, mariwanna, mariwhanna, canabis, cannibis, canibis)
(Common phrases used by users for this page include what is thc in depth, what is marijuana in-depth, supplementing with fats to boost marijuana high, marijuana's effects on internal organs, endocannabinoids suppliment, cholesterol medication effects on thc)
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