cannabis olympian

Cannabis Sativa and Cannabis Indica

Cannabis Sativa and Cannabis Indica are closely connected with the history and development of some of the oldest cultures on Earth having been cultivated by humans for tens of thousands of years primarily for its strength as a fiber, its medicinal uses and its nutritional value.

Both Cannabis Sativa and Cannabis Indica, originating in the temperate zones of central Asia, played significant roles in the religions and cultures of Africa, the Middle East, India, and China.

Carolus Linnaeus came up with the name for hemp in Latin botanical nomenclature "Cannabis Sativa" in 1753.

Carolus Linnaeus chose the word Cannabis based on the classical Greek word "kannabis" which was originally derived from the Sanskrit word "cana."

The Hebrew word is "kaneh-bosem" (pluralized ; singular is kaneh-bos).

The third syllable "bis" derives from "bosm" or the Aramaic "busma" which translate to fragrant.

Cannabis is fragrant cane.

The word " Sativa" comes from Latin and means "sown" or "cultivated."

Prehistoric teeth show people ate medicinal weeds

legalize cannabis

The Chinese used cannabis for rope, clothing, bowstrings, paper and medicine.

Early Chinese doctoring was based on the concept of demons.

If a person were ill, it was because some demon had invaded his body. The only way to cure him was to drive the demon out.

The priest-doctor did his utmost to find some way of getting the upper hand over the malevolent demon believed responsible for an illness.

Although the Chinese continued to rely on intentional magic in the fight against disease, they also gradually developed an appreciation and knowledge of the curative powers of medicines.

2700 BC Emperor Shen-Nung, the Father of Chinese Medicine, concerned about his suffering subjects looks to plants for cures.

Shen-Nung tried poisons and their antidotes on himself and compiled the medical encyclopedia called, Pen Ts'ao.

The Pen Ts'ao list hundreds of drugs derived from vegetable, animal and mineral sources.

Among these drugs is the plant cannabis, "ma."

Ma was a unique drug because it was both feminine, or yin, and masculine, or yang.

Yin represented the weak, passive, and negative female influence in nature while yang represented the strong, active, and positive male force.

When yin and yang were in balance, the body was in harmony and healthy.

When yin and yang were out of balance, the body was in a state of disequilibrium and ill.

Ma was used to treat absences of yin, such as: female weaknesses (menstruation), gout, rheumatism, malaria, beri-beri, constipation, and absentmindedness.

2000 BC In India bhang is a symbol of hospitality.

A host would offer a cup of bhang to a guest.

Atharvaveda (12:6.15) calls bhang one of the "five kingdoms of herbs which release us from anxiety."

Atharvaveda hymns were compiled in the early Indian Iron Age, c. 1200 to 1000 BC, corresponding to the early Kuru Kingdom.

Taken in early morning, the drug is believed to cleanse the body of sin.

1000 AD Chinese physicians use cannabis in the treatment of "waste diseases and injuries", adding that it "clears blood and cools temperature, it relieves fluxes; it undoes rheumatism; it discharges pus".

Cannabis is used in Japan in ceremonial purification rites for driving away evil spirits.

shiva meets cherokee

"Followers of Shiva have to consume bhang at least once a year.

The drink, which intensifies perceptivity, induces visions and above all leads to extreme mental concentration.

It is widely used by Yogis.

Details concerning its preparation are to be found as early as the Vedic period.

The description of the way soma was prepared and its immediate use without fermentation, can only apply to bhang and is identical to the method employed today."- Alain Danielou

The Persian word bhanga is almost identical to the Indian term bhang.

Mirceau Eliade noted Zoroaster was a user of bhanga and may have relied on its intoxication to bridge the metaphysical gap between Heaven and Earth.

One of the few surviving books of the Zend-Avesta, called the Vendidad, "The Law Against Demons", in fact calls bhanga Zoroaster's "good narcotic."

"Amongst other cannabis initiates can be counted the Zoroastrian heroes Gustap and Ardu Viraf, who after drinking bhang, 'where transported in soul to heaven and had the highest mysteries revealed to them'.

These ancient out of body experiences are classic examples of what is known as 'shamanistic ecstasy'.

And 'shamanistic flight'.

The belief that the soul actually left the body in theses magical rituals, resulted in the belief that this occurred also at the point of death, giving rise to a belief in an afterlife." - Chris Bennet

Modern day Egyptologists agree that cannabis was used by the ancient Egyptians in their medicine.

Mention of cannabis is made in the following Egyptian medical texts:

The Ramesseum III Papyrus (1700 BC)
Eber's Papyrus (1600 BC)
The Berlin Papyrus (1300 BC)
The Chester Beatty VI Papyrus (1300 BC)

Kyphi was used as an offering to the Gods.

As the sun set, Egyptian worshippers would burn this fragrant preparation to the Sun God RA, praying for his return the following morning.

Kyphi was applied on the skin to heal wounds, was a potent relaxant and an aphrodisiac.

Unlike the ointments of the Assyrians the Kyphi was a rather solid and wax like concoction.

Researchers have suggested more than 50 natural ingredients for making the Kyphi, the most popular probably being: Aloeswood, Benzoin, Cannabis Resin, Cardamom Seeds, Cassia, Cedar, Cinnamon, Copal, Frankincense, Galangal Root, Ginger, Honey, Juniper, Lemongrass, Mastic, Mint, Myrrh, Orris, Pistachio, Raisins, Red Wine, Rose Petals, Saffron, Sandalwood, Storax Balsam.

In the temples of the ancient world, the main sacrifice was the inhalation of incense.

Incense is defined as the perfume or smoke from spices and gums when burned in celebrating religious rites or as an offering to a deity.

Bronze and gold incense burners were cast very early in history and their forms were often inspired by cosmological themes representing the harmonious nature of the universe.

"In the Judaic world, the vapors from burnt spices and aromatic gums were considered part of the pleasurable act of worship. In proverbs (27:9) it is said that 'Ointment and perfumes rejoice the heart.' Perfumes were widely used in Egyptian worship. Stone altars have been unearthed in Babylon and Palestine, which have been used for burning incense made of aromatic wood and spices. While the casual readers today may interpret such practices as mere satisfaction of the desire for pleasant odors, this is almost certainly an error; in many or most cases, a psychoactive drug was being inhaled. In the islands of the Mediterranean 2,500 years ago and in Africa hundreds of years ago, for example leaves and flowers of a particular plant were often thrown upon bonfires and the smoke inhaled; the plant was marijuana." - Edward Preble and Gabriel V. Laurey

Kaneh-Bosem, 'Fragrant Cane', played an integral part of healing rituals during the time of Jesus and was considered a holy sacrament.

Jesus of Nazareth used cannabis based oils to heal eye and skin diseases.

The word Christ derives from being anointed with cannabis enriched holy oil.

"There is a classic Greek term, cannabeizein, which means to smoke cannabis. Cannabeizein frequently took the form of inhaling vapors from an incense burner in which these resins were mixed with other resins, such as myrrh, balsam, frankincense, and perfumes." - William A. Embolden, Jr.

The Greek title "Christ" is the translation of the Hebrew word "Messiah", which in English becomes "The Anointed".

The Messiah was recognized as such by his being anointed with the holy anointing oil, the use of which was restricted to the instillation of Hebrew priests and kings.

Anointing was common among kings of Israel.

It was the sign and symbol of royalty.

The word 'Messiah' signifies the 'Anointed One', and none of the kings of Israel were styled the Messiah unless anointed."

The ancient recipe for this anointing oil, recorded in the Septuagint book of Exodus (30: 22-23) included over nine pounds of flowering cannabis tops extracted into a hind (about 6.5 litres) of olive oil, along with a variety of other herbs and spices.

The ancient 'chosen ones' were literally drenched in this potent cannabis holy oil.

one compassion

Every prophet must be initiated.

His higher self must be awakened and made conscious so that his mission can be fulfilled.

Amongst the Essenes' ritual lustrations preceded most liturgical rites, the most important one of which was participation in a sacred meal -- an anticipation of the Messianic banquet.

The central focus of the early Christian church was the Eucharist or the "body and blood" of the Lord.

This was interpreted as a fellowship meal with the resurrected Christ.

In meeting the Resurrected One in the Eucharist meal the Christian community had the expectation of entering the Kingdom of God and, thus, salvation.

In the Biblical story of Creation, God said, "Behold, I have given you every herb bearing seed and to you it will be for meat." (Genesis 1:29)

Cannabis is technically a herb considered a spiritual meat in the ancient world.

"Moreover, brethren, I would not that ye should be ignorant, how that our fathers were under the cloud, and all passed through the sea; And were all baptized unto Moses in the Cloud and in the sea; And did all eat the same spiritual meat: for they drank of that Spiritual Rock that followed them: and that Rock was Christ." - I Corinthians 10:1-3

From this passage in Corinthians we see that the spiritual cloud resulting from the burning of incense was instrumental in the baptism of the Israelites.

This baptism is also compared to the "eating and drinking" of the spirit of Christ.

Throughout the ancient world sacrifice was a sacramental communal meal involving the idea of the god as a participant in the meal or as identical with the food consumed.

The communion sacrifice was one in which the deity indwells the oblation so that the worshippers actually consume the divine.

The original motive of sacrifice was an effort toward communion among the members of a group, on one hand, and between them and their god, on the other.

At its best, sacrifice was a "sacrament" and in one form or another life itself.

Spirit is defined as the active essence of the Deity serving as an invisible and life-giving or inspiring power in motion.

Scripture makes it abundantly clear that the sacrificial cloud or smoke contained the Spirit of God (Christ) and was instrumental in inspiring, sanctifying, and purifying the patriarchs.

Knowledge and healing were two aspects of the same life-force.

To be healed by the 'Holy Plant' was to receive divine knowledge, it was also to be cured of every sickness.

James suggests that anyone of the Christian community who was sick should call to the elders to anoint him with oil in the name of Jesus.

The Twelve are sent out among their fellow-men casting out demons and anointing the sick with oil.

The Ancient Hebrews used cannabis in 12 ways: as paper, cords, clothing, sails, oil, fishnets, sealant, food, incense and in ceremony, relaxation, and medicine.

"And he showed me a river of water of life, clear as crystal, flowing out from the throne of God and of the Lamb, down the middle of its broadway. And on the side of the river and on that side there were trees of life producing twelve crops of fruit, yielding their fruits each month. And the leaves of the trees were for the curing of the nations." - Revelation 22:1-2

Canaan, the ancient home of the Israelites, is a form of "Cana," derived from cannabis and "Cana".

The Three Wise Men who came to usher in the birth of Jesus were Zoroastrians, who believed God gave hemp as a gift to mankind.

jesus cannabis

"The anointing with oil was the introduction of the candidate into unfading bliss, thus becoming a Christ."

"There is water in water, there is fire in chrism." (Gospel of Philip).

In the first few centuries AD, Christian Gnostic groups such as the Archontics, Valentians and Sethians rejected water baptism as superfluous, referring to it as an "incomplete baptism".

In the tractate, the Testimony of Truth, water baptism is rejected with a reference to the fact that Jesus baptized none of his disciples.

Being "anointed with unutterable anointing", the so-called "sealings" recorded in the Gnostic texts, can be seen as a very literal event.

CB receptors

"Christ came into their midst so that he might anoint them with the ointment. The ointment is the mercy of the Father. Those whom he has anointed are the ones who have become perfect." - Gospel of Truth

"Holy oil, given us for sanctification, hidden mystery in which the cross was shown us, you are the unfolder of the hidden parts. You are the humiliator of stubborn deeds. You are the one who shows the hidden treasures. You are the plant of kindness. Let your power come by this [unction]." - Acts of Thomas

Mesopotamian use went far beyond the spiritual.

The medicinal properties of the plant were well known as noted in the groundbreaking paper by cannibinoid expert Dr. Ethan Russo, 'Clinical Cannabis in Ancient Mesopotamia: A Historical Survey with Supporting Scientific Evidence'

Dr. Russo records that numerous topical applications of cannabis for medical purposes can be found throughout ancient Mesopotamian documents.

Interestingly, records of topical ointments used in the treatment of "Hand of Ghost" an ancient malady now thought to be epilepsy, included cannabis as a key ingredient.

Ancient Mesopotamian preparations that included cannabis were also used in the treatment of certain diseases of the chest and lungs, stomach problems, skin lesions, lice, swollen joints and a variety of other maladies.

During the Middle Ages, soldiers often took a drink of bhang before entering battle, just as Amerikans took a swig of whiskey.

The widespread belief in cannabis as a magical herb led to it condemnation as a tool of witchcraft.

The Holy Roman Empire condemned cannabis as a tool of Satan and outlawed it use.

Users were condemned and burned at the stake as heretics.

1600 British Monarchs required all landowners throughout the British Empire to grow cannabis to rig the naval ships.

1700 Cannabis preparations began appearing in medical reference texts as a treatment for coughs, general pain and as an analgesic to soothe allergies.

1800 Various forms of cannabis are available for purchase in a chemist's shop.

A pill form of cannabis is developed and used as an antibiotic and painkiller.

After the Civil War use of cannabis was popular and considered socially acceptable.

1890 The British find the use of cannabis so extensive in colonial India, that they commission a large scale study.

British physicians were concerned that cannabis was endangering the health of the native people and driving them insane.

Over 1,000 standardized interviews were conducted throughout India by eminent British and Indian medical experts.

The commission was systematic and thorough.

It sampled a large and diverse group of people in a range of situations, from farmers to hospital psychiatrists.

After years of detailed work, The Indian Hemp Drugs Commission Report produced six volumes of data and conclusions.

Commissioners were particularly concerned with whether or not cannabis caused psychoses.

CBD cures schizophrenia

After years of through and well conducted research, The Commission concluded that suppressing the use of herbal cannabis (bhang) would be totally unjustifiable:

"To the Hindu the cannabis plant is holy.

A guardian lives in the bhang leaf.

To see in a dream the leaves, plant, or water of bhang is lucky.

No good thing can come to the man who treads underfoot the holy bhang leaf.

A longing for bhang foretells happiness.

Bhang has many medicinal virtues.

It cures dysentry and sunstroke, clears phlegm, quickens digestion, sharpens appetite, makes the tongue of the lisper plain, freshens the intellect, and gives alertness to the body and gaiety to the mind.

Such are the useful and needful ends for which in his goodness the Almighty made bhang.

Bhang is the Joygiver, the Skyflier, the Heavenly-guide, the Poor Man's Heaven, the Soother of Grief.

No god or man is as good as the religious drinker of bhang.

The supporting power of bhang has brought many a Hindu family safe through the miseries of famine."

Bhang is so common in some parts of India that it can be found in government licensed street stands.

THC destroys tumors

1907 Merck Index lists that use of Cannabis seeds for emulsions to be used to relieve the effects of gonorrhea.

1909 "Hemp seed, in infusion, has been found very useful in after-pains, and in the bearing down sensation accompanying prolapsus uteri. - King's American Dispensatory

1927"When (hemp seed oil is) rubbed with water form an emulsion, which may be used advantageously in inflammations of the mucous membrane -US Dispensatory

Today, as in ancient times, cannabis has been used to treat many different ailments including glaucoma, epilepsy, skin afflictions, arthritis, sickness, nausea, headaches and cramps to name a few.

hemp oil cures cancer

The endocannabinoid system is the most important physiologic system involved in establishing and maintaining human health.

Endocannabinoids and their receptors are found throughout the body: in the brain, organs, connective tissues, glands, and immune cells.

In each tissue, the cannabinoid system performs different tasks, but the goal is always the same: homeostasis, the maintenance of a stable internal environment despite fluctuations in the external environment.

Autophagy, a process in which a cell sequesters part of it self to be self-digested and recycled, is mediated by the cannabinoid system.

While this process keeps normal cells alive, allowing them to maintain a balance between the synthesis, degradation, and subsequent recycling of cellular products, it has a deadly effect on malignant tumor cells, causing them to consume themselves in a programmed cellular suicide.

Endocannabinoids and cannabinoids are also found at the intersection of the body's various systems, allowing communication and coordination between different cell types.

At the site of an injury, for example, cannabinoids can be found decreasing the release of activators and sensitizers from the injured tissue, stabilizing the nerve cell to prevent excessive firing, and calming nearby immune cells to prevent release of pro-inflammatory substances.

Three different mechanisms of action on three different cell types for a single purpose: minimize the pain and damage caused by the injury.

The endocannabinoid system, with its complex actions in our immune system, nervous system, and all of the body's organs, is literally a bridge between body and mind.

By understanding this system we begin to see a mechanism that explains how states of consciousness can promote health or disease.

1983 Reagan/Bush administration persuade US universities and researchers to ***DESTROY *** all cannabis research work done between 1966 and 1976, including compendiums in libraries.

Despite common knowledge and widespread scientific support, the federal government has for nearly 30 years kept cannabis in Schedule I as a deliberate way to deny citizens good health and guarantee lifelong dependence on toxic chemical snake oil products from pharmaceutical corporations !

2011 Over 850,000 people in America are arrested for marijuana-related crimes.

Entrenched interest groups have spent and continue to spend huge sums of money to protect their bottom line: Police & Prison Guard Unions ; Private Prisons, Alcohol and Pharmaceutical Corporations.

Kristina Marie
Kristina Marie@Kristina88Marie, January 20, 2014

I haven't said anything in awhile want to say that I am feeling great since starting my ketogenic diet
and I have much hope for the future! Also, Dave and I are getting married!!!
So lots has changed but I'm still chugging along, happier than ever!!!

Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC.

CBD, in particular, is thought to have significant analgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.

Cannabinoids cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis.

Cannabinoids kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in glioma cells.

Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.

Cannabinoids contribute to pain modulation through an anti-inflammatory mechanism.

A CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids.

Delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake.

The endocannabinoid system serves as a regulator of feeding behavior.

CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.

Jesus and his disciples used a healing cannabis ointment.

Jesus did perform his healing miracles magically through the power invested in him by the omnipotent Lord of the Universe with cannabis.

The modern reintroduction of cannabis based medicines becomes, if not a miracle, at least a profound revelation.

"Humanity has had a evolutionary partnership with this plant that stretches back more than 10,000 years." - Chris Bennet

cannabis legal

States NOT engaged in the Eugenics Agenda !

endocannabinoid system

central nervous system



brain injury

spinal injury






conditioned fear


amyotrophic lateral sclerosis

multiple sclerosis




healing cannabis caduceus

immune system








gastrointestinal system

chronic liver disease

kidney fibrosis




respiratory system

lung function

healing cannabis caduceus







bile duct











cannabinoid receptors

endocannabinoid system

Cannabinoids in health and disease.

Conclusion: Numerous diseases, such as anorexia, emesis, pain, inflammation, multiple sclerosis, neurodegenerative disorders (Parkinson's disease, Huntington's disease, Tourette's syndrome, Alzheimer's disease), epilepsy, glaucoma, osteoporosis, schizophrenia, cardiovascular disorders, cancer, obesity, and metabolic syndrome-related disorders, to name just a few, are being treated or have the potential to be treated by cannabinoid agonists/antagonists/cannabinoid-related compounds.

*** In view of the very low toxicity and the generally benign side effects of this group of compounds, neglecting or denying their clinical potential is unacceptable. ***

Pharmacokinetics and pharmacodynamics of cannabinoids.

Conclusion: Properties of cannabis that might be of therapeutic use include analgesia, muscle relaxation, immunosuppression, sedation, improvement of mood, stimulation of appetite, antiemesis, lowering of intraocular pressure, bronchodilation, neuroprotection and induction of apoptosis in cancer cells.

Endocannabinoids in the immune system and cancer.

Conclusion: The experimental evidence reviewed in this article argues in favor of the therapeutic potential of these compounds in immune disorders and cancer.

central nervous system

Control of the cell survival/death decision by cannabinoids.

Cannabinoids and cell fate.Conclusion: Regarding the central nervous system, most of the experimental evidence indicates that cannabinoids may protect neurons from toxic insults such as glutamaergic overstimulation, ischemia and oxidative damage.

Cannabinoids and cell fate.

Conclusion: Most of the experimental evidence indicates that cannabinoids may protect normal neurons from toxic insults.


Neuroprotective antioxidants from marijuana

Conclusion: The psychotropic cannabinoid receptor agonist delta 9-tetrahydrocannabinol (THC) and cannabidiol, (a non-psychoactive constituent of marijuana), both reduced NMDA, AMPA and kainate receptor mediated neurotoxicities.

Delta9-tetrahydrocannabinol protects hippocampal neurons from excitotoxicity.

Conclusion: Excitotoxic neuronal death underlies many neurodegenerative disorders. This study demonstrates the importance of agonist efficacy and the duration of treatment on the neuroprotective effects of cannabinoids.

Neuroprotective Effect of Delta9-Tetrahydrocannabinol and Cannabidiol in N-Methyl-d-Aspartate-Induced Retinal Neurotoxicity

Conclusion: In glaucoma, the increased release of glutamate is the major cause of retinal ganglion cell death. In conclusion, our results indicate that lipid peroxidation and ONOO- formation play an important role in NMDA-induced retinal neurotoxicity and cell loss in the retina, and that THC and CBD, by reducing the formation of these compounds, are effective neuroprotectants.


Neurocognition in college-aged daily marijuana users

Conclusion: Marijuana users were high functioning, demonstrating comparable IQs to controls and relatively better processing speed. Marijuana users demonstrated relative cognitive impairments in verbal memory, spatial working memory, spatial planning, and motivated decision making but comorbid use of alcohol, which was heavier in marijuana users, was unexpectedly found to be associated with better performance in some of these areas.

Is Illicit Drug Use Harmful to Cognitive Functioning in the Midadult Years?

Conclusion: At the population level, it does not appear that current illicit drug use is associated with impaired cognitive functioning in early middle age.

Effects of Smoking Marijuana on Brain Perfusion and Cognition

Smoking marijuana resulted in intoxication, as assessed by a behavioral rating scale, but did not significantly alter mean behavioral performance on the attention task. There was no significant rCBF change in the nucleus accumbens or other reward-related brain regions, nor in basal ganglia or hippocampus, which have a high density of cannabinoid receptors.

Intelligence, cognition unaffected by heavy marijuana use

Conclusion: The researchers conclude that heavy marijuana use produces no irreversible mental deficits.

Preliminary findings of a longitudinal study of effects on IQ in young adults

Conclusion: We conclude that marijuana does not have a long-term negative impact on global intelligence.

Long-term effects of marijuana use on the brain

Conclusion: Compared with controls, marijuana users had significantly less bilateral orbitofrontal gyri volume, higher functional connectivity in the orbitofrontal cortex (OFC) network, and higher structural connectivity in tracts that innervate the OFC (forceps minor) as measured by fractional anisotropy (FA)

brain injury

Cannabinoid agonist rescues learning and memory after a traumatic brain injury

Conclusion: We found that the brain-injured animals treated with the agonist showed a marked recovery.

Endocannabinoids: a new family of lipid mediators involved in the regulation of neural cell development.

Conclusion: Cannabinoids inhibit cortical neuron differentiation and promote glial differentiation. On the other hand, experiments with differentiated neurons have shown that cannabinoids also regulate neuritogenesis, axonal growth and synaptogenesis.

An endogenous cannabinoid (2-AG) is neuroprotective after brain injury.

Conclusion: When 2-AG was administered together with additional inactive 2-acyl-glycerols that are normally present in the brain, functional recovery was significantly enhanced.

Ultralow doses of cannabinoid drugs protect the mouse brain from inflammation-induced cognitive damage

Conclusion: An ultralow dose of THC that lacks any psychotrophic activity protects the brain from neuroinflammation-induced cognitive damage and might be used as an effective drug for the treatment of neuroinflammatory conditions, including neurodegenerative diseases.

The effect of cannabichromene on adult neural stem/progenitor cells

Conclusion: Our results suggest that CBC raises the viability of NSPCs while inhibiting their differentiation into astroglia, possibly through up-regulation of ATP and adenosine signalling.

stimulate brain cell growth

Research Suggests Marijuana Analogue Stimulates Brain Cell Growth

Conclusion: The team found that rats treated with HU-210 on a regular basis showed neurogenesis – the growth of new brain cells in the hippocampus. This region of the brain is associated with learning and memory, as well as anxiety and depression. The effect is the opposite of most legal and illicit drugs such as alcohol, nicotine, Heroin™, and cocaine.

Effect of marijuana use on outcomes in traumatic brain injury.

Conclusion: The THC(+) group was compared with the THC(-) group with respect to injury mechanism, severity, disposition, and mortality. A positive THC screen is associated with decreased mortality in adult patients sustaining TBI.

Mechanisms of cannabidiol neuroprotection

Conclusion: Our findings demonstrate that CBD exerts robust neuroprotective effects in vivo in HI piglets, modulating excitotoxicity, oxidative stress and inflammation, and that both CB2 and 5HT1A receptors are implicated in these effects.

Neuroprotection by Delta9-Tetrahydrocannabinol against Ouabain-Induced In Vivo Excitotoxicity

Conclusion: These results provide evidence that the cannabinoid system can serve to protect the brain against neurodegeneration.

The anxiolytic effect of cannabidiol on chronically stressed mice depends on hippocampal neurogenesis

Conclusion: Cannabidiol (CBD), the main non-psychotomimetic component of the plant Cannabis sativa, exerts therapeutically promising effects on human mental health such as inhibition of psychosis, anxiety and depression. However, the mechanistic bases of CBD action are unclear. Here we investigate the potential involvement of hippocampal neurogenesis in the anxiolytic effect of CBD

Comparison of Cannabidiol, Antioxidants, and Diuretics in Reversing Binge Ethanol-Induced Neurotoxicity

Conclusion: This study provides the first demonstration of CBD as an in vivo neuroprotectant and shows the efficacy of lipophilic antioxidants in preventing binge ethanol induced brain injury.

spinal injury

Cannabinoids to treat spinal cord injury.

Conclusion: The endocannabinoid system is expressed in the intact spinal cord, and it is dramatically upregulated after lesion.

Protective effects of cannabidiol on lesion-induced intervertebral disc degeneration

Conclusion: Considering that cannabidiol presents an extremely safe profile and is currently being used clinically, these results suggest that this compound could be useful in the treatment of intervertebral disc degeneration.


Cannabinoids Can Limit Neurological Stroke Damage

Conclusion: The findings showed that the compounds could reduce the size of stroke and improve neurological function.


Phytocannabinoids and epilepsy

Conclusion: Phytocannabinoids produce anticonvulsant effects through the endocannabinoid system, with few adverse effects.

Analysis in conditional cannabinoid 1 receptor-knockout mice reveals neuronal subpopulation-specific effects on epileptogenesis in the kindling paradigm

Conclusion: The endocannabinoid system plays an active role in seizure termination but does not regulate epileptogenesis.


Cannabis Use and Cognition in Schizophrenia

Conclusion: Our own results confirm the overall impression from the literature review of better cognitive performance in the cannabis user group. A majority of the studies report better cognitive functioning in the cannabis-related schizophrenia and psychosis groups compared to non-drug groups.

A systematic review of the antiPsychotic properties of cannabidiol in humans.

Conclusion: The first small-scale clinical studies with CBD treatment of patients with psychotic symptoms further confirm the potential of CBD as an effective, safe and well-tolerated antiPsychotic compound

Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia

Conclusion: Experimental studies show that cannabidiol reduces psychosis-like effects of Delta9-tetrahydrocannabinol and synthetic analogs.

Decreased glial reactivity could be involved in the antiPsychotic-like effect of cannabidiol.

Conclusion: our data support the view that inhibition of microglial activation may improve schizophrenia symptoms.


A possible role for the endocannabinoid system in the neurobiology of depression

Conclusion: Although data available are sufficient to suggest a possible involvement of the endogenous cannabinoid system in the neurobiology of depression, additional studies should be performed in order to better elucidate the role of this system in the physiopathology of depression.

Antidepressant-like effects of Delta9-tetrahydrocannabinol and rimonabant in the olfactory bulbectomised rat model of depression.

Conclusion: These findings indicate antidepressant-like behavioural properties of both THC and rimonabant in OB rats although additional studies are required to clarify the relationship between the chronic effects of cannabinoids in other pre-clinical models and in human depression.

Antidepressant-like effects of cannabidiol in mice: possible involvement of 5-HT1A receptors.

Conclusion: CBD induces antidepressant-like effects comparable to those of imipramine. These effects of CBD were probably mediated by activation of 5-HT(1A) receptors.


Cannabinoid CB1 receptors in the dorsal hippocampus and prelimbic medial prefrontal cortex modulate anxiety-like behavior

Conclusion: Endocannabinoids (ECBs) such as anandamide (AEA) act by activating cannabinoid type 1 (CB1) or 2 (CB2) receptors. The anxiolytic effect of drugs that facilitate ECB effects is associated with increase in AEA levels in several encephalic areas, including the prefrontal cortex (PFC). We observed that drugs which interfere with ECB reuptake/metabolism in both the PL and in the dentate gyrus of the dHIP induced anxiolytic-like effect, in both the EPM and in the VCT via CB1 receptors, suggesting that CB1 signaling in these brain regions modulates defensive responses to both innate and learned threatening stimuli. This data further strengthens previous results indicating modulation of hippocampal and MPFC activity via CB1 by ECBs, which could be therapeutically targeted to treat anxiety disorders.

Cannabinoid CB1 receptors in the dorsal hippocampus and prelimbic medial prefrontal cortex modulate anxiety-like behavior

Conclusion: Modulation of hippocampal and MPFC activity via CB1 by ECBs, which could be therapeutically targeted to treat anxiety disorders.

conditioned fear

2-AG promotes the expression of conditioned fear via cannabinoid receptor type 1 on GABAergic neurons

The cannabinoid receptor type 1 (CB1) antagonist SR141716 (3 mg/kg) caused an increase in conditioned freezing upon repeated tone presentation on three consecutive days. 2-AG fear-promoting effects depended on CB1 signaling in GABAergic neurons, while an involvement of glutamatergic neurons remained inconclusive due to the high freezing shown by vehicle-treated Glu-CB1-KO.

amyotrophic lateral sclerosis

Cannabis and amyotrophic lateral sclerosis

Conclusion: Based on the currently available scientific data, it is reasonable to think that cannabis might significantly slow the progression of ALS, potentially extending life expectancy and substantially reducing the overall burden of the disease.

Survey of cannabis use in patients with amyotrophic lateral sclerosis

Conclusion: Although the small number of people with ALS that reported using cannabis limits the interpretation of the survey findings, the results indicate that cannabis may be moderately effective at reducing symptoms of appetite loss, depression, pain, spasticity, and drooling.

multiple sclerosis

There is evidence for the use of cannabinoids for symptomatic treatment of multiple sclerosis

Conclusion: There is evidence that nabiximols oromucosal spray may reduce subjective symptoms of spasticity and that dronabinol is effective against neuropathic pain in patients with MS.

Smoked cannabis for spasticity in multiple sclerosis

Conclusion: Smoked cannabis was superior to placebo in symptom and pain reduction in participants with treatment-resistant spasticity.

Cannabinoids inhibit neurodegeneration in models of multiple sclerosis

Conclusion: Cannabinoids inhibit neurodegeneration in models of multiple sclerosis. In addition to symptom management, cannabis may also slow the neurodegenerative processes that ultimately lead to chronic disability in multiple sclerosis

Activation of Cannabinoid CB2 receptors Reduces Hyperalgesia in an Experimental Autoimmune Encephalomyelitis Mouse Model of Multiple Sclerosis

Conclusion: Our results suggest that JWH-133 acts at CB2 receptors, most likely within the dorsal horn of the spinal cord, to suppress the hypersensitivity associated with experimental autoimmune encephalomyelitis.


Effects of cannabidiol in the treatment of patients with Parkinson's disease: an exploratory double-blind trial.

Conclusion: Parkinson's disease (PD) has a progressive course and is characterized by the degeneration of dopaminergic neurons. Although no neuroprotective treatments for PD have been found to date, the endocannabinoid system has emerged as a promising target. Our findings point to a possible effect of CBD in improving quality of life measures in PD patients with no psychiatric comorbidities

Cannabis (medical marijuana) treatment for motor and non-motor symptoms of Parkinson disease

Conclusion: Significant improvement of sleep and pain scores. No significant adverse effects of the drug were observed. The study suggests that cannabis might have a place in the therapeutic armamentarium of PD.

Symptom-relieving and neuroprotective effects of the phytocannabinoid Delta9-THCV

Conclusion: Given its antioxidant properties and its ability to activate CB2 but to block CB1 receptors, Delta9-THCV has a promising pharmacological profile for delaying disease progression in PD and also for ameliorating parkinsonian symptoms.

Cannabinoids provide neuroprotection against 6-hydroxydopamine toxicity

Conclusion: Our results support the view of a potential neuroprotective action of cannabinoids against the in vivo and in vitro toxicity of 6-hydroxydopamine, which might be relevant for PD. Our data indicated that these neuroprotective effects might be due, among others, to the antioxidant properties of certain plant-derived cannabinoids, or exerted through the capability of cannabinoid agonists to modulate glial function, or produced by a combination of both mechanisms.

Delta9-tetrahydrocannabinol (THC) exerts a direct neuroprotective effect in a human cell culture model of Parkinson's disease.

Conclusion: We have demonstrated up-regulation of the CB1 receptor in direct response to neuronal injury in a human PD cell culture model, and a direct neuronal protective effect of ??-THC that may be mediated through PPAR? activation.


The potential therapeutic effects of THC on Alzheimer's disease

Conclusion: These sets of data strongly suggest that THC could be a potential therapeutic treatment option for Alzheimer's disease through multiple functions and pathways.

Neuroprotection Mediated by Blockade of Microglial Activation

Conclusion: Alzheimer's disease (AD) is characterized by enhanced ß-amyloid peptide (ßA) deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits. Cannabinoids are neuroprotective agents against excitotoxicity in vitro and acute brain damage in vivo. Recent studies on therapeutic strategies for neurodegenerative diseases such as Parkinson's disease and AD have focused on the neuroprotective properties (e.g., slowing the ongoing neurodegeneration) rather than just on palliating symptoms of the diseases (Dawson and Dawson, 2002). Because cannabinoids combine both anti-inflammatory and neuroprotective actions, our findings may set the basis for the use of these compounds as a therapeutic approach for AD.

A Molecular Link Between the Active Component of Marijuana and Alzheimer's Disease Pathology

Conclusion: Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years. AChE inhibitors such as THC and its analogues may provide an improved therapeutic for Alzheimer's disease, augmenting acetylcholine levels by preventing neurotransmitter degradation and reducing Aß amalgamation, thereby simultaneously treating both the symptoms and progression of Alzheimer's disease.

Prolonged oral cannabinoid administration prevents neuroinflammation, lowers ß-amyloid levels and improves cognitive performance

Conclusion: Alzheimer's disease (AD) brain shows an ongoing inflammatory condition and non-steroidal anti-inflammatories diminish the risk of suffering the neurologic disease. Cannabinoids are neuroprotective and anti-inflammatory agents with therapeutic potential. We have shown that chronically administered cannabinoid showed marked beneficial effects concomitant with inflammation reduction and increased Aß clearance.


Cannabinoids reduce symptoms of Tourette's syndrome

Conclusion: Currently, the treatment of Tourette's syndrome (TS) is unsatisfactory. A single-dose, cross-over study in 12 patients, as well as a 6-week, randomised trial in 24 patients, demonstrated that Delta9-tetrahydrocannabinol (THC), the most psychoactive ingredient of cannabis, reduces tics in TS patients. No serious adverse effects occurred and no impairment on neuropsychological performance was observed.

gastrointestinal system

Cannabinoids in intestinal inflammation and cancer.

Conclusion: Pharmacological elevation of endocannabinoid levels may be a promising strategy to counteract intestinal inflammation and colon cancer.

chronic liver disease

The role of the endocannabinoid system in liver diseases

Conclusion: The EC system is strongly up-regulated during chronic liver diseases. Until now it has been implicated in the pathogenesis of fatty liver disease associated with obesity, alcohol abuse, and hepatitis C, in the progression of fibrosis to cirrhosis, and in the development of portal hypertension, hyperdynamic circulatory syndrome and its complications, and cirrhotic cardiomyopathy. Furthermore, the EC system can participate in the pathogenesis of acute liver injury by modulating the mechanisms responsible for cell injury and inflammatory response. Thus, targeting the CB1 and CB2 receptors represents a potential therapeutic goal for the treatment of liver diseases.

Cannabinoid receptors as new targets of antifibrosing strategies during chronic liver diseases

Conclusion: Endocannabinoid-based therapies, combining CB2 agonists and CB1 antagonists may open novel therapeutic perspectives for the treatment of chronic liver diseases.

The endocannabinoid system as a key mediator during liver diseases

Conclusion: CB1 receptors have been implicated in the pathogenesis of several lesions such as liver fibrogenesis, alcoholic and metabolic steatosis, or circulatory failure associated with cirrhosis. In contrast, stimulation of hepatic CB2 receptors is emerging as an overall protective pathway with antifibrogenic properties and beneficial effects on liver inflammation, alcoholic fatty liver and hepatocyte survival and regeneration.

Beneficial paracrine effects of cannabinoid receptor 2 on liver injury and regeneration

Conclusion: CB2 receptors reduce liver injury and promote liver regeneration following acute insult, via distinct paracrine mechanisms involving hepatic myofibroblasts.

CB1 cannabinoid receptor antagonism: a new strategy for the treatment of liver fibrosis

Conclusion: Our study shows that CB1 receptor antagonists hold promise for the treatment of liver fibrosis.

Cannabidiol protects liver from binge alcohol-induced steatosis

Conclusion: CBD can alleviate lipid accumulation in both an in vitro HepG2 cell model and an in vivo binge alcohol treatment model by multiple mechanisms.

Cannabinoid CB2 receptors protect against alcoholic liver disease by regulating Kupffer cell polarization

Conclusion: These findings demonstrate that CB2 receptors display beneficial effects on alcohol-induced inflammation by regulating M1/M2 balance in Kupffer cells, thereby reducing hepatocyte steatosis via paracrine interactions between Kupffer cells and hepatocytes.

Two non-psychoactive cannabinoids reduce intra-cellular lipid levels and inhibit hepatosteatosis

Conclusion: Our results suggest that THCV and CBD might be used as new therapeutic agents for the pharmacological treatment of obesity- and metabolic syndrome-related NAFLD/hepatosteatosis


Cannabinoids suppress acute and anticipatory nausea

Conclusion: Cannabinoids have great promise as treatments for nausea and that their anti-nausea effects may be mediated by the interoceptive insular cortex.

Regulation of nausea and vomiting by cannabinoids

Conclusion: This model may be a useful tool for elucidating the neurobiology of nausea and the role that the endocannabinoid system plays in the regulation of this distressing condition.

Regulation of nausea and vomiting by cannabinoids

Conclusion: Future efforts aimed at developing new endocannabinoid-based anti-nausea and anti-emetic therapies are clearly warranted.

kidney fibrosis

Expression of cannabinoid receptors in human kidney

Conclusion: Our data suggest a possible implication of the endocannabinoid system in the physiology and development of the human kidney.

Cannabinoid receptor 1 is a major mediator of renal fibrosis

Conclusion: CB1 has a major role in the activation of myofibroblasts and may be a new target for treating chronic kidney disease.


Cannabidiol, a safe and non-psychotropic ingredient of the marijuana plant Cannabis sativa, is protective in a murine model of colitis

Cannabidiol, a safe and non-psychotropic ingredient of marijuana, exerts pharmacological effects (e.g., antioxidant) and mechanisms (e.g., inhibition of endocannabinoids enzymatic degradation) potentially beneficial for the inflamed gut.


Cannabis induces a clinical response in patients with Crohn's disease

Conclusion: A short course (8 weeks) of THC-rich cannabis produced significant clinical, steroid-free benefits to 10 of 11 patients with active Crohn's disease, compared with placebo, without side effects.

respiratory system

lung function

The effect of phytocannabinoids on airway hyper-responsiveness, airway inflammation, and cough

Conclusion: Cannabis has been demonstrated to have bronchodilator, anti-inflammatory, and antitussive activity in the airways. Only Delta9-THC demonstrated effects on airway hyper-responsiveness, anti-inflammatory activity, and antitussive activity in the airways.

Antitussive effect of WIN 55212-2, a cannabinoid receptor agonist

Conclusion: The antitussive effect of WIN 55212-2 is mediated by the activation of cannabinoid CB(1) receptors and mu(2) (naloxonazine-insensitive)-opioid receptors, but not mu(1) (naloxonazine-sensitive)- or kappa-opioid receptors.

Cannabidiol improves lung function and inflammation in mice submitted to LPS-induced acute lung injury.

Conclusion: We conclude that CBD administered therapeutically, i.e. during an ongoing inflammatory process, has a potent anti-inflammatory effect and also improves the lung function in mice

immune system

Cannabinoids and the immune system

Conclusion: It is likely that the cannabinoid system, along with other neuroimmune systems, has a subtle but significant role in the regulation of immunity and that this role can eventually be exploited in the management of human disease.

Cannabinoid-induced apoptosis in immune cells as a pathway to immunosuppression.

Cannabinoids have been shown to act as potent immunosuppressive and anti-inflammatory agents and have been shown to mediate beneficial effects in a wide range of immune-mediated diseases such as multiple sclerosis, diabetes, septic shock, rheumatoid arthritis, and allergic asthma. In this review, we will focus on apoptotic mechanisms of immunosuppression mediated by cannabinoids on different immune cell populations and discuss how activation of CB2 provides a novel therapeutic modality against inflammatory and autoimmune diseases as well as malignancies of the immune system, without exerting the untoward psychotropic effects.

Cannabinoids as novel anti-inflammatory drugs

Conclusion: The potential use of cannabinoids as a new class of anti-inflammatory agents against a number of inflammatory and autoimmune diseases that are primarily triggered by activated T cells or other cellular immune components.

Inhaled medicinal cannabis and the immunocompromised patient

Conclusion: Medicinal cannabis is an invaluable adjunct therapy for pain relief, nausea, anorexia, and mood modification in cancer patients and is available as cookies or cakes, as sublingual drops, as a vaporized mist, or for smoking.

Cannabinoids and ceramide: two lipids acting hand-by-hand.

Conclusion: Sustained ceramide accumulation in tumor cells mediates cannabinoid-induced apoptosis, as evidenced by in vitro and in vivo studies.

The endocannabinoid anandamide neither impairs in vitro T-cell function nor induces regulatory T-cell generation.

Conclusion: Direct antitumor activity of endogenous cannabinoid anandamide together with the absence of negative effects on T-cell functions.


Efficacy of Inhaled Cannabis on Painful Diabetic Neuropathy

Conclusion: This small, short-term, placebo-controlled trial of inhaled cannabis demonstrated a dose dependent reduction in diabetic peripheral neuropathy pain in patients with treatment-refractory pain. This adds preliminary evidence to support further research on the efficacy of the cannabinoids in neuropathic pain.

Cannabis Use in Patients with Fibromyalgia

Conclusion: The use of cannabis was associated with beneficial effects on some Fibromyalgia symptoms.

Neuropathic orofacial pain: cannabinoids as a therapeutic avenue

Conclusion: Neuropathic orofacial pain (NOP) exists in several forms including pathologies such as burning mouth syndrome (BMS), persistent idiopathic facial pain (PIFP), trigeminal neuralgia (TN) and postherpetic neuralgia (PHN). BMS and PIFP are classically diagnosed by excluding other facial pain syndromes. Analgesia is one the principal therapeutic targets of the cannabinoid system and many studies have demonstrated the efficacy of cannabinoid compounds in the treatment of neuropathic pain.

The effectiveness of cannabinoids in the management of chronic nonmalignant neuropathic pain

Conclusion: Cannabis-based medicinal extracts used in different populations of chronic nonmalignant neuropathic pain patients may provide effective analgesia in conditions that are refractory to other treatments.


Cannabinoid receptor CB2 is involved in tetrahydrocannabinol-induced anti-inflammation against lipopolysaccharide in MG-63 cells

Conclusion: CB2 is involved in the THC-induced anti-inflammation in LPS-stimulated MG-63 cells, and the anti-inflammation may be mediated by cofilin-1.


Antibacterial cannabinoids from Cannabis sativa

Conclusion: These observations suggest that the prenyl moiety of cannabinoids serves mainly as a modulator of lipid affinity for the olivetol core, a per se poorly active antibacterial pharmacophore, while their high potency definitely suggests a specific, but yet elusive, mechanism of activity.

Cannabinoids Delta9-Tetrahydrocannabinol and Cannabidiol Differentially Inhibit the Lipopolysaccharide-activated NF-?B and Interferon-ß/STAT Proinflammatory Pathways in BV-2 Microglial Cells

Conclusion: Cannabinoids have been shown to exert anti-inflammatory activities in various in vivo and in vitro experimental models as well as ameliorate various inflammatory degenerative diseases.


Involvement of the endocannabinoid system in osteoarthritis pain

Conclusion: This review summarizes the promising results that have been recently obtained in support of the therapeutic value of cannabinoids for osteoarthritis management.

Characterisation of the cannabinoid receptor system in synovial tissue and fluid in patients with osteoarthritis and rheumatoid arthritis

Conclusion: Our data predict that the cannabinoid receptor system present in the synovium may be an important therapeutic target for the treatment of pain and inflammation associated with OA and RA.

The endocannabinoid system and its therapeutic implications in rheumatoid arthritis.

Conclusion: We discuss the possible functions of the endocannabinoid system in the modulation of RA, which may be a potential target for treatment.

Efficacy, tolerability and safety of a cannabis-based medicine (Sativex) in the treatment of pain caused by rheumatoid arthritis

Conclusion: Significant analgesic effect was observed and disease activity was significantly suppressed following Sativex treatment.

Peripheral cannabinoid receptor, CB2, regulates bone mass

Conclusion: CB2 offers a molecular target for the diagnosis and treatment of osteoporosis, the most prevalent degenerative disease in developed countries.


Autism-Associated Neuroligin-3 Mutations Commonly Disrupt Tonic Endocannabinoid Signaling

Conclusion: Our data thus suggest that neuroligin-3 is specifically required for tonic endocannabinoid signaling, raising the possibility that alterations in endocannabinoid signaling may contribute to autism pathophysiology.

Modeling an autism risk factor in mice leads to permanent immune dysregulation.

Conclusion: These studies support a link between cellular immune dysregulation and ASD-related behavioral deficits in a mouse model of an autism risk factor.


The endocannabinoid system of the skin in health and disease

Conclusion: The newly discovered endocannabinoid system (ECS; comprising the endogenous lipid mediators endocannabinoids present in virtually all tissues, their G-protein-coupled cannabinoid receptors, biosynthetic pathways and metabolizing enzymes) has been implicated in multiple regulatory functions both in health and disease. It seems that the main physiological function of the cutaneous ECS is to constitutively control the proper and well-balanced proliferation, differentiation and survival, as well as immune competence and/or tolerance, of skin cells. Pathological alterations in the activity of the fine-tuned cutaneous ECS might promote or lead to the development of certain skin diseases.

Anti-inflammatory activity of topical THC

Conclusion: This has important implications for the future development of strategies to harness cannabinoids for the treatment of inflammatory skin diseases.


Delta-9 tetrahydrocannabinol (THC) inhibits lytic replication of gamma oncogenic herpesviruses in vitro

Conclusion: THC specifically targets viral and/or cellular mechanisms required for replication and possibly shared by these gamma herpesviruses, and the endocannabinoid system is possibly involved in regulating gamma herpesvirus latency and lytic replication.

Cannabis May Help Combat Cancer-causing Herpes Viruses

Conclusion: Small concentrations of THC were more potent and selective against gamma herpes viruses than the commonly used antiviral drugs acyclovir, gancicyclovir and foscamet.


Cannabidiol increases survival and promotes rescue of cognitive function in a murine model of cerebral malaria.

Conclusion: Cerebral malaria (CM) is a severe complication resulting from Plasmodium falciparum infection that might cause permanent neurological deficits. Our results indicate that CBD exhibits neuroprotective effects in CM model and might be useful as an adjunctive therapy to prevent neurological symptoms following this disease.


Cannabis in painful HIV-associated sensory neuropathy

Conclusion: Smoked cannabis was well tolerated and effectively relieved chronic neuropathic pain from HIV-associated sensory neuropathy. The findings are comparable to oral drugs used for chronic neuropathic pain.

Cannabinoids inhibit migration of microglial-like cells to the HIV protein Tat

Conclusion: These results indicate that cannabinoid-mediated inhibition of BV-2 microglial-like cell migration to Tat is linked functionally to the CB2R. Furthermore, the results indicate that activation of the CB2R leads to altered expression and compartmentation of the ß-chemokine receptor CCR-3.

Cannabinoid inhibits HIV-1 Tat-stimulated adhesion of human monocyte-like cells to extracellular matrix proteins

Conclusion: The blood-brain barrier (BBB) is a complex structure that is composed of cellular elements and an extracellular matrix (ECM). HIV-1 Tat promotes transmigration of monocytes across this barrier, a process that includes interaction with ECM proteins. The results indicate that cannabinoids that activate the CB2R inhibit the ECM adhesion process. Thus, this receptor has potential to serve as a therapeutic agent for ablating neuroinflammation associated with HIV-elicited influx of monocytes across the BBB.


Many scientific studies have reported that various cannabinoids (both natural and synthetic) exert a wide range of growth-inhibiting effects on cancer cells, including:

- Triggering cell death, through a mechanism called apoptosis.
- Stopping cells from dividing.
- Preventing new blood vessels from growing into tumours –a process termed angiogenesis.
- Reducing the chances of cancer cells to metastasize through the body, by stopping cells from moving or invading neighbouring tissue.
- Speeding up the cell's internal 'waste disposal machine' –a process known as autophagy – which can lead to cell death.

Cannabinoids and cancer.

Conclusion: In 1975, Munson discovered that cannabinoids suppress Lewis lung carcinoma cell growth. The mechanism of this action was shown to be inhibition of DNA synthesis. Antiproliferative action on some other cancer cells was also found.

Cannabinoids in the treatment of cancer.

Conclusion: This review will summarize the anti-cancer properties of the cannabinoids.

The association between cannabinoids and cancer

Conclusion: The results of the newest study focused on the association between cannabinoids use and cancer risk showed no significant association between increased cancer incidence and cannabinoids use and it does not depend on the amount of used cannabis.

Endocannabinoids in the immune system and cancer.

Conclusion: The experimental evidence reviewed in this article argues in favor of the therapeutic potential of these compounds in immune disorders and cancer.

Involvement of cannabinoids in cellular proliferation.

Conclusion: Control of the cellular proliferation has become a focus of major attention as opening new therapeutic possibilities for the use of cannabinoids as potential antitumor agents. The capacity of endogenous and synthetic cannabinoids to induce apoptosis of different tumoral cells in culture and in vivo, the mechanism underlying and the potential therapeutic applications are discussed in this review.

Cannabinoid receptor ligands as potential anticancer agents

Conclusion: The development of CB(2)-selective anticancer agents could be advantageous in light of the unwanted central effects exerted by CB(1) receptor ligands.

Antineoplastic and apoptotic effects of N-acylethanolamines cannabinoids.

Conclusion: Cannabinoids are potential anticancer agents.

HU-331, a novel cannabinoid-based anticancer topoisomerase II inhibitor.

Conclusion: The cannabinoid quinone HU-331 is a highly specific inhibitor of topoisomerase II, compared with most known anticancer quinones. It might represent a new potent anticancer drug.

A cannabinoid quinone inhibits angiogenesis by targeting vascular endothelial cells.

Conclusion: These data lead us to consider cannabidiol hydroxyquinone (HU-331) to have high potential as a new antiangiogenic and anticancer drug.

Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1.

Conclusion: These findings provide a novel mechanism underlying the anti-invasive action of cannabidiol and imply its use as a therapeutic option for the treatment of highly invasive cancers.

Plant-derived cannabinoids modulate the activity of transient receptor potential channels of ankyrin type-1 and melastatin type-8

Conclusion: Phytocannabinoids and cannabis extracts exert some of their pharmacological actions also by interacting with TRPA1 and TRPM8 channels, with potential implications for the treatment of pain and cancer.

p38 MAPK is involved in CB2 receptor-induced apoptosis of human leukaemia cells.

Conclusion: These findings support a role for p38 MAPK in CB2 receptor-induced apoptosis of human leukaemia cells.

The CB2 cannabinoid receptor signals apoptosis via ceramide-dependent activation of the mitochondrial intrinsic pathway.

Conclusion: CB2 receptor activation signals apoptosis via a ceramide-dependent stimulation of the mitochondrial intrinsic pathway.

Cannabinoids protect astrocytes from ceramide-induced apoptosis through the phosphatidylinositol 3-kinase/protein kinase B pathway.

Conclusion: These findings constitute the first evidence for an "astroprotective" role of cannabinoids: (i) cannabinoids rescue primary astrocytes from C(2)-ceramide-induced apoptosis in a dose- and time-dependent manner; (ii) triggering of this anti-apoptotic signal depends on the phosphatidylinositol 3-kinase/protein kinase B pathway; (iii) ERK and its downstream target p90 ribosomal S6 kinase might be also involved in the protective effect of cannabinoids; and (iv) cannabinoids protect astrocytes from the cytotoxic effects of focal C(2)-ceramide administration in vivo.


Antitumorigenic effects of cannabinoids beyond apoptosis.

Conclusion: Apart from their proapoptotic and antiproliferative action, recent research has shown that cannabinoids may likewise affect tumor cell angiogenesis, migration, invasion, adhesion, and metastasization.

Endocannabinoids as emerging suppressors of angiogenesis and tumor invasion

Conclusion: The potential use of cannabinoids to retard tumor growth and spreading is even more appealing considering that they show a good safety profile, regarding toxicity, and are already used in cancer patients as palliatives to stimulate appetite and to prevent devastating effects such as nausea, vomiting and pain.

Predominant CB2 receptor expression in endothelial cells of glioblastoma in humans.

Conclusion: The abundant expression and distribution of CB2 receptors in glioblastoma and particularly endothelial cells of glioblastoma indicate that impaired tumor growth in presence of CB may be associated with CB2 activation. Selective CB2 agonists might become important targets attenuating vascular endothelial growth factor (VEGF) signalling and thereby diminishing neoangiogenesis and glioblastoma growth.

The stress-regulated protein p8 mediates cannabinoid-induced apoptosis of tumor cells.

Conclusion: Here, we describe the signaling pathway that mediates cannabinoid-induced apoptosis of tumor cells.

Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors.

Conclusion: Cannabinoid-treated tumors showed an increased number of apoptotic cells. This was accompanied by impairment of tumor vascularization, as determined by altered blood vessel morphology and decreased expression of proangiogenic factors


Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells

Conclusion: CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.

Cannabinoid receptor 1 is a potential drug target for treatment of translocation-positive rhabdomyosarcoma

Cannabinoid receptor agonists are capable of reducing proliferation and inducing apoptosis in diverse cancer cells such as glioma, breast cancer, and melanoma, we evaluated whether CB1 is a potential drug target in rhabdomyosarcoma. Conclusion: These results support the notion that cannabinoid receptor agonists could represent a novel targeted approach for treatment of translocation-positive rhabdomyosarcoma.

The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation

Conclusion: Anandamide was the first brain metabolite shown to act as a ligand of "central" CB1 cannabinoid receptors. Anandamide blocks human breast cancer cell proliferation through CB1-like receptor-mediated inhibition of endogenous prolactin action at the level of prolactin receptor.

Antitumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma.

Conclusion: Results obtained in a panel of tumor cell lines clearly indicate that, of the five natural compounds tested, cannabidiol is the most potent inhibitor of cancer cell growth (IC(50) between 6.0 and 10.6 microM), with significantly lower potency in noncancer cells.

JunD is involved in the antiproliferative effect of Delta9-tetrahydrocannabinol on human breast cancer cells.

Conclusion: The first report showing not only that cannabinoids regulate JunD but, more generally, that JunD activation reduces the proliferation of cancer cells, which points to a new target to inhibit breast cancer progression.

Delta9-tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation.

Conclusion: We found a correlation between CB(2) expression and histologic grade of the tumors. There was also an association between CB(2) expression and other markers of prognostic and predictive value, such as estrogen receptor, progesterone receptor, and ERBB2/HER-2 oncogene. Importantly, no significant CB(2) expression was detected in nontumor breast tissue. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.

Delta9-tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation.

Conclusion: We found a correlation between CB(2) expression and histologic grade of the tumors. There was also an association between CB(2) expression and other markers of prognostic and predictive value, such as estrogen receptor, progesterone receptor, and ERBB2/HER-2 oncogene. Importantly, no significant CB(2) expression was detected in nontumor breast tissue. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.

Delta9-tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation.

Conclusion: We found a correlation between CB(2) expression and histologic grade of the tumors. There was also an association between CB(2) expression and other markers of prognostic and predictive value, such as estrogen receptor, progesterone receptor, and ERBB2/HER-2 oncogene. Importantly, no significant CB(2) expression was detected in nontumor breast tissue. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.


Cannabinoid receptor as a novel target for the treatment of prostate cancer.

Conclusion: WIN-55,212-2 or other non-habit-forming cannabinoid receptor agonists could be developed as novel therapeutic agents for the treatment of prostate cancer.

Inhibition of human tumour prostate PC-3 cell growth by cannabinoids R(+)-Methanandamide and JWH-015: involvement of CB2.

Conclusion: This study defines the involvement of CB(2)-mediated signalling in the in vivo and in vitro growth inhibition of prostate cancer cells and suggests that CB(2) agonists have potential therapeutic interest and deserve to be explored in the management of prostate cancer.

Delta9-tetrahydrocannabinol induces apoptosis in human prostate PC-3 cells via a receptor-independent mechanism.

Conclusion: THC caused apoptosis in a dose-dependent manner. Morphological and biochemical changes induced by THC in prostate PC-3 cells shared the characteristics of an apoptotic phenomenon.


Cannabinoid 2 receptor induction by IL-12 and its potential as a therapeutic target for the treatment of anaplastic thyroid carcinoma.

Conclusion: Cannabinoids have shown antitumor effects in many types of cancer models, CB2 may be a viable therapeutic target for the treatment of anaplastic thyroid carcinoma.

A metabolically stable analogue of anandamide, Met-F-AEA, inhibits human thyroid carcinoma cell lines by activation of apoptosis.

Conclusion: New insights into the mechanism of Met-F-AEA action, and could have significance in providing a basis for the management of thyroid carcinoma.

A metabolically stable analogue of anandamide, Met-F-AEA, inhibits human thyroid carcinoma cell lines by activation of apoptosis.

Conclusion: New insights into the mechanism of Met-F-AEA action, and could have significance in providing a basis for the management of thyroid carcinoma.


Cannabinoid derivatives induce cell death in pancreatic MIA PaCa-2 cells via a receptor-independent mechanism.

Conclusion: Our results demonstrate that Cannabinoids produce a significant cytotoxic effect via a receptor-independent mechanism.

Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes.

Conclusion: Results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB(2) receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress-related genes ATF-4 and TRB3.


Potentiation of cannabinoid-induced cytotoxicity in mantle cell lymphoma through modulation of ceramide metabolism.

Conclusion: The cytotoxic effect of a cannabinoid is enhanced by modulation of ceramide metabolism.

Cannabinoid receptor ligands mediate growth inhibition and cell death in mantle cell lymphoma.

Conclusion: Induction of apoptosis in mantle cell lymphoma.

Cannabinoid receptor-mediated apoptosis induced by R(+)-methanandamide and Win55,212-2 is associated with ceramide accumulation and p38 activation in mantle cell lymphoma.

Conclusion: Cannabinoids induce growth inhibition and apoptosis in mantle cell lymphoma.

Expression of cannabinoid receptors type 1 and type 2 in non-Hodgkin lymphoma:
growth inhibition by receptor activation.

Conclusion: Cannabinoid receptor ligands will have efficiency in reducing tumor burden in malignant lymphoma overexpressing CB1 and CB2.

Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease.

Conclusion: Culture of primary acute lymphoblastic leukemia cells with THC in vitro reduced cell viability and induced apoptosis.


Cannabinoids and gliomas

Conclusion: Cannabinoids seem to be selective antitumoral compounds, as they kill glioma cells, but not their non-transformed astroglial counterparts.

Cannabinoids as potential new therapy for the treatment of gliomas.

Conclusion: A pilot clinical trial on patients with glioblastoma multiforme demonstrated their good safety profile together and remarkable antitumor effects.

Arachidonylethanolamide induces apoptosis of human glioma cells through vanilloid receptor-1.

Conclusion: In contrast with their role in THC-mediated death, both CB1 and CB2 partially protected glioma against Arachidonylethanolamide-induced apoptosis.

Up-regulation of cyclooxygenase-2 expression is involved in R(+)-methanandamide-induced apoptotic death of human neuroglioma cells.

Conclusion: This study defines COX-2 as a hitherto unknown target by which a cannabinoid induces apoptotic death of glioma cells.

Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines.

Conclusion: The nonpsychoactive CBD was able to produce a significant antitumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an antineoplastic agent.

Down-regulation of tissue inhibitor of metalloproteinases-1 in gliomas

Conclusion: TIMP-1 down-regulation may be a hallmark of cannabinoid-induced inhibition of glioma progression.

Cannabinoids induce glioma stem-like cell differentiation and inhibit gliomagenesis.

Conclusion: Results demonstrate that cannabinoids target glioma stem-like cells, promote their differentiation, and inhibit gliomagenesis, thus giving further support to their potential use in the management of malignant gliomas.

Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells.

Conclusion: THC can promote the autophagic death of human cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.

Cannabinoids inhibit glioma cell invasion by down-regulating matrix metalloproteinase-2 expression.

Conclusion: Cannabinoid-induced inhibition of MMP-2 expression and cell invasion was prevented by blocking ceramide biosynthesis and by knocking-down the expression of the stress protein p8.

Delta9-tetrahydrocannabinol induces apoptosis in C6 glioma cells.

Conclusion: THC-induced apoptosis in glioma C6.9 cells relys on a CBI receptor-independent stimulation of sphingomyelin breakdown.

Cannabinoids down-regulate PI3K/Akt and Erk signalling pathways and activate proapoptotic function of Bad protein.

Conclusion: Cannabinoids were shown to induce apoptosis of glioma cells in vitro and tumor regression in vivo.

Delta 9-tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells.

Conclusion: Delta(9)-THC is shown to significantly affect viability of GBM cells via a mechanism that appears to elicit G(1) arrest due to downregulation of E2F1 and Cyclin A.

Cannabis extract can have dramatic effect on brain cancer

Conclusion: Tumours growing in the brains of mice were drastically slowed down when THC/CBD was used with irradiation.


Estrogenic induction of cannabinoid CB1 receptor in human colon cancer cell lines.

Conclusion: The CB1 receptor can be considered an estrogen-responsive gene.

Cannabinoid receptor activation induces apoptosis through tumor necrosis factor alpha-mediated ceramide de novo synthesis in colon cancer cells.

Conclusion: The present study shows that either CB1 or CB2 receptor activation induces apoptosis through ceramide de novo synthesis in colon cancer cells.

The cannabinoid delta(9)-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells.

Conclusion: These data suggest an important role for CB1 receptors and BAD in the regulation of apoptosis in colorectal cancer cells. The use of THC, or selective targeting of the CB1 receptor, may represent a novel strategy for colorectal cancer therapy.


Effect of a synthetic cannabinoid agonist on the proliferation and invasion of gastric cancer cells.

Conclusion: Cannabinoids as a new gastric cancer therapy.

Pharmacological synergism between cannabinoids and paclitaxel in gastric cancer cell lines

Conclusion: Cannabinoids as a good palliative agent for cancer patients receiving paclitaxel.


Delta9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemia T cells is regulated by translocation of Bad to mitochondria.

Conclusion: Raf-1/MEK/ERK/RSK-mediated Bad translocation played a critical role in THC-induced apoptosis in Jurkat cells.

Cannabidiol-induced apoptosis in human leukemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression

Conclusion: The results from this study reveal that cannabidiol, acting through CB2 and regulation of Nox4 and p22(phox) expression, may be a novel and highly selective treatment for leukemia.

Targeting cannabinoid receptors to treat leukemia: role of cross-talk between extrinsic and intrinsic pathways in Delta9-tetrahydrocannabinol (THC)-induced apoptosis of Jurkat cells

Conclusion: These data suggest that the intrinsic pathway plays a more critical role in THC-induced apoptosis while the extrinsic pathway may facilitate apoptosis via cross-talk with the intrinsic pathway.

Cannabis-induced cytotoxicity in leukemic cell lines: the role of the cannabinoid receptors and the MAPK pathway

Conclusion: One of the most intriguing findings was that THC-induced cell death was preceded by significant changes in the expression of genes involved in the mitogen-activated protein kinase (MAPK) signal transduction pathways.


R(+)-methanandamide-induced apoptosis of human cervical carcinoma cells involves a cyclooxygenase-2-dependent pathway.

Conclusion: A role of COX-2 and PPARgamma in MA-induced apoptosis was confirmed in another human cervical cancer cell line (C33A) and in human lung carcinoma cells (A549).

Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1

Conclusion: Using Matrigel invasion assays we found a cannabidiol-driven impaired invasion of human cervical cancer (HeLa, C33A) and human lung cancer cells (A549) that was reversed by antagonists to both CB(1) and CB(2) receptors as well as to transient receptor potential vanilloid 1 (TRPV1). These findings provide a novel mechanism underlying the anti-invasive action of cannabidiol and imply its use as a therapeutic option for the treatment of highly invasive cancers.


A comparative study on cannabidiol-induced apoptosis in murine thymocytes and EL-4 thymoma cells.

Conclusion: Both thymocytes and EL-4 thymoma cells are susceptible to CBD-induced apoptosis.

Delta(9)-tetrahydrocannabinol-induced apoptosis in the thymus and spleen as a mechanism of immunosuppression in vitro and in vivo.

Conclusion: Thymocytes and splenocytes exposed to THC in vivo exhibited apoptosis upon in vitro culture. Together, these results suggest that in vivo exposure to THC can lead to significant suppression of the immune response by induction of apoptosis.

bile duct

The dual effects of delta(9)-tetrahydrocannabinol on cholangiocarcinoma cells:
anti-invasion activity at low concentration and apoptosis induction at high concentration.

Conclusion: THC retards cholangiocarcinoma cell growth and metastasis.


Cannabinoid receptors as novel targets for the treatment of melanoma.

Conclusion: Cannabinoid antiproliferative action on melanoma cells was due, at least in part, to cell cycle arrest at the G1-S transition via inhibition of the prosurvival protein Akt and hypophosphorylation of the pRb retinoblastoma protein tumor suppressor.

Revisiting CB1 receptor as drug target in human melanoma

Conclusion: Previous studies have indicated the antitumoral effect of human melanocytes, human melanoma cell lines expressing CB1 receptor (CB1), and of the peritumoral administration of endocannabinoids. Our studies revealed that systemic administration of a stable CB1 agonist, ACEA, into SCID mice specifically inhibited liver colonization of human melanoma cells.

Exploiting Cannabinoid-Induced Cytotoxic Autophagy to Drive Melanoma Cell Death

Conclusion: Although the global incidence of cutaneous melanoma is increasing, survival rates for patients with metastatic disease remain <10%. our findings suggest that THC activates noncanonical autophagy-mediated apoptosis of melanoma cells, suggesting that cytotoxic autophagy induction with Sativex warrants clinical evaluation for metastatic disease.


The expression level of CB1 and CB2 receptors determines their efficacy at inducing apoptosis in astrocytomas

Conclusion: The high expression level of CB(1) and CB(2) receptors commonly found in malignant astrocytomas precludes the use of cannabinoids as therapeutics, unless AKT is concomitantly inhibited, or cannabinoids are applied at concentrations that bypass CB(1) and CB(2) receptors, yet still activate ERK1/2.


Cannabis smoking and lung cancer risk

Conclusion:Our pooled results showed no significant association between the intensity, duration, or cumulative consumption of cannabis smoke and the risk of lung cancer overall or in never smokers.

Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo.

Conclusion: There was significant inhibition of the subcutaneous tumor growth and lung metastasis of A549 cells in THC-treated animals as compared to vehicle-treated controls. Tumor samples from THC-treated animals revealed antiproliferative and antiangiogenic effects of THC.

Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1

Conclusion: Our data indicate that cannabinoids induce ICAM-1, thereby conferring TIMP-1 induction and subsequent decreased cancer cell invasiveness


unique library index

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