Unfortunately, the lousy weather and finishing up prerequisites for graduate school has reduced my time to post. To continue to add content here, are some of my past grows. Two grows are done in a propriety blend of super soil, one in no-till and one grown hydroponically in coco. All were raised last year around this time.
One benefit of growing your cannabis is knowing what goes into your plant. Although, Massachusetts forbids dispensaries using insecticides when growing cannabis there are ways dispensaries can circumvent this regulation. Silly enough, Massachusetts list the names of prohibited pesticides the state tests for when inspecting cannabis. This means that there are a large number of commonly used insecticides that will fail to show on state inspections. Given the history of making money and people’s greed, it is only a matter of time that a dispensary in Massachusetts will try to use a prohibited insecticide
Azadirachtin is a natural insecticide found in the Neem tree. The Reader may already be familiar using a neem oil/dish soap solution as a foliar spray to control for insects. Producers of Neem oil, press the plant to extract the oil. However, not all the active ingredient in neem is isolated. Neem cake is a product leftover from the pressing of neem for oil. Neem cake has approximately one third to half the strength of Azadirachtin in it compared to neem oil. Neem cake elicits a defense through many anti-insect, and anti-fungal agents contained in the cake resulting in a systemic resistance against evasive insects and problems such as powdery mildew.
Neem cake has a wide variety uses for the organic grower. Neem has an estimated NPK value of 6-1-2. Additionally, the cake is full of micro-nutrients as well as trace elements, growth hormones, and Vitamin C.
A gardener can either use the cake as a soil amendment, top dressing or tea. One popular method for neem cake is a tea mixture including kelp and silica. Kelp is full of beneficial macro and micronutrients. Also, silica has insecticide properties as well as it strengthens the plant structure.
5 gallons of reverse osmosis water
- ½ cup of neem cake/meal
- ¼ cup of kelp meal
- 1 tsp of silica
For a small 1-gallon mixture
- 2 tbsp of neem cake/meal
- 1 tbsp of neem cake
- ¼ tsp or 1 mL of silica
Mix in a bucket of water and bubble for 24 to 48 hours. Feed it to the plants for routine pest management.
Just discovered this news article.
Thank you to the community of dank growers out there that share evidence-based information!
When smoking cannabis, how a person inhales is a significant contributor to the amount of the desired cannabinoid that enters the bloodstream. Bioavailability is the amount of an administered drug that is absorbed by the body. It is the consensus that the bioavailability of cannabis when inhaled is approximately 25%; where the bioavailability of ingested cannabis is 6% (more on increasing the bioavailability of edibles in a later blog). Through controlled experiment, scientists discovered six variables affecting the availability of smoked cannabis:
Smoking dynamics (most significant)
Smoking dynamics is the method, and biological mechanics of an individual’s inhalation while smoking.
- Puff volume is a part of smoking dynamics; it is the number of inhalations a person takes from a joint. In a study examining blood THC levels in cannabis smokers, researchers discovered, puff volume affects the amount of THC available in the bloodstream.
- Reduced puffs per minute will increase the time it takes to reach peak THC blood levels. Additionally, slower puff volume increases the time it takes for the body to return to baseline after smoking. However, THC does not reach the same peak plasma levels compared to increased puff volume.
- Peak THC blood plasma levels are higher with increased puff volume. Also, peak THC levels are achieved early in the smoking session compared to a lower volume. Nevertheless, the body returns to baseline significantly faster with increase puff volume once smoking stops.
The smoking dynamic of a water-pipe is similar to accelerated puff volume of a joint.
Generally, THC plasma concentrations increased progressively for as long as puffs were taken. As a result, peak THC concentrations does not occur until the end of the smoking session. Finding suggests that increased volume of smoke (approximately 200 ml) every 2.5 minutes delivers adequate THC to the blood to balance the drug’s rate of disappearance into the extravascular compartment.
A higher percentage of the cannabinoid desired increases the amount of the cannabinoid in the bloodstream.
Amount of cannabinoid left after pyrolytic destruction
Pyrolytic destruction is the decomposition brought about by high temperatures. Pyrolysis destroys a portion of cannabinoid desired when smoking cannabis. Researchers found 20% to 30% of THC is lost to pyrolysis when smoking from a joint or water-pipe.
Amount of cannabis lost in the side-stream smoke
When a person smokes a joint, smoke produced is either inhaled when puffs are taking (main-stream) or escapes to the surrounding environment (side-stream). Initial findings studying the amount of THC lost in side-stream concluded 40%-50% of THC is lost. However, researchers may have overestimated these findings. The study used a two puff per minute protocol. Others have commented that most individuals take more than two puffs per minute. Nevertheless, THC lost to side-stream while smoking a joint increase the more it is idle. Researchers noted that 90% of the total smoke time is idle; therefore, a significant amount of THC still escapes through side-stream.
Method used (joint or water-pipe)
- ~20% lost in bowl residue
- ~8% lost in stem and pipe residue
- ~3.5% product lost in water from pipe
- ~8% lost in plant material from water
- ~40% main-stream smoke (usable product)
- up-to 40-50% lost to side-stream (if
- 20 to 30% lost to pyrolytic destruction
- 20 to 30% In mainstream smoke (usable product)
Note: No side-stream was reported for the water-pipe because the protocol used only enough cannabis for one complete inhalation (hit).
Amount of marijuana trapped in the mucosa of the upper respiratory tract
While smoking cannabis, the upper respiratory tract traps a small amount of THC in the mucosa thereby reducing bioavailability. Studies found the amounts of THC lost is considered of minor importance.
In closing, despite the listed variables above, there are still reports of wide fluctuations in the bioavailability of cannabis among individuals. Variations in bioavailability are because of unique biological differences people have between each other. Biological uniqueness means a significant amount of people can either feel the effects of cannabis at lower doses or may need higher doses to feel any effect. If a person is new to cannabis, it will benefit them to start with decrease potency and increase potency if required. Additionally, individuals can also increase puff volume to increase the availability of the desired cannabinoid. Following these procedures will reduce the incidents of a temporary psychotic episode from a significant one-time dose when using cannabis.
Marijuana smoking: Factors that influence the bioavailability of tetrahydrocannabinol. (1990). In N. C. Chiang, & R. L. Hawks (Eds.), Research findings on smoking of abused substances (pp. 42-62). Rockville, Maryland: National Institute on Drug Abuse.
Cannabinoid hyperemesis syndrome (CHS) is said to be brought on by chronic heavy use of cannabis. Symptoms include recurrent episodes of nausea, vomiting, and abdominal pain. Sufferers of CHS can find temporary relief of symptoms by taking either a hot bath or shower. Case studies show that CHS resolves itself when cannabis use stops. CHS often gets misdiagnosed and can lead to costly ineffective treatments. A recent study examining the prevalence of CHS in urban cannabis smokers estimate that between 2.13 to 3.38 million may suffer symptoms similar to CHS. All cases seem to come from excessive smoking of cannabis and not edibles.
The author of this post would like to see more studies examining the nutritional choices and physical activity levels of individuals suffering from cannabinoid hyperemesis syndrome. Nutrition and physical activity are modifiable risk factors that can resolve a multitude of health issues. It would not be a big surprise if exercise and proper diet would reduce CHS symptoms. Nevertheless, futures studies will hold the answers.
Habboushe, J., Rubin, A., Liu, H., & Hoffman, R. S.The prevalence of cannabinoid hyperemesis syndrome among regular marijuana smokers in an urban public hospital. Basic & Clinical Pharmacology & Toxicology, , n/a-n/a. doi:10.1111/bcpt.12962
Sullivan, S. (2009). Cannabinoid hyperemesis. Canadian Journal of Gastroenterology, 24(5), 284-285. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886568/
In America more than 30 percent of adults are considered overweight; likewise, the prevalence of obesity in America also tops one third. Obesity is any adult with a body mass index (BMI) greater than 30. Obesity is associated with multiple comorbidities significantly contributing to disease and early death.
Similar to the endocrine system; the endocannabinoid system is known to help regulate much of the body’s functions. The endocannabinoid system consists of CB1 and CB2 receptors spread throughout the body. Scientists discovered that using antagonist drugs on CB1 receptors would be a promising intervention for reducing the weight of obese people. However, early human trials of an antagonist drug under the name “Rimonabant” produced unfavorable mental side effects and was later discontinued.
In light of new hope, recent studies found CB2 antagonists also reduce weight but did not come with the same adverse side-effects as CB1 antagonist stimulation. Delta9-tetrahydrocannabivarin (THCV), one of many cannabinoids in cannabis, is known to have an antagonist effect on CB2 receptors. THCV shows promise that one day it may help people control weight and save countless lives.
Centers of Disease Control and Prevention.Adult obesity facts. Retrieved from https://www.cdc.gov/obesity/data/adult.html
Deveaux, V., Cadoudal, T., Ichigotani, Y., Teixeira-Clerc, F., Louvet, A., Manin, S., . . . Lotersztajn, S. (2009). Cannabinoid CB2 receptor potentiates obesity-associated inflammation, insulin resistance and hepatic steatosis. Plos One, 4(6), e5844. doi:10.1371/journal.pone.0005844
Hillard, C. J. (2015). Endocannabinoids and the endocrine system in health and disease. In R. G. Pertwee (Ed.), Endocannabinoids (pp. 317-339). Cham: Springer International Publishing. doi:10.1007/978-3-319-20825-1_11
Leite, C. E., Mocelin, C. A., Petersen, G. O., Leal, M. B., & Thiesen, F. V. (2009). Rimonabant: An antagonist drug of the endocannabinoid system for the treatment of obesity. Pharmacological Reports, 61(2), 217-224. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/19443932
Pagotto, U., Marsicano, G., Cota, D., Lutz, B., & Pasquali, R. (2006). The emerging role of the endocannabinoid system in endocrine regulation and energy balance. Endocrine Reviews, 27(1), 73-100. Retrieved from http://dx.doi.org/10.1210/er.2005-0009
Pertwee, R. G. (2007). The diverse CB(1) and CB(2) receptor pharmacology of three plant cannabinoids: Î”(9)-tetrahydrocannabinol, cannabidiol and Î”(9)-tetrahydrocannabivarin. British Journal of Pharmacology, 153(2), 199-215. doi:10.1038/sj.bjp.0707442
Pertwee, R. G., Thomas, A., Stevenson, L. A., Ross, R. A., Varvel, S. A., Lichtman, A. H., . . . Razdan, R. K. (2006). The psychoactive plant cannabinoid, Î”(9)-tetrahydrocannabinol, is antagonized by Î”(8)- and Î”(9)-tetrahydrocannabivarin in mice in vivo. British Journal of Pharmacology, 150(5), 586-594. doi:10.1038/sj.bjp.0707124
Thomas, A., Stevenson, L. A., Wease, K. N., Price, M. R., Baillie, G., Ross, R. A., & Pertwee, R. G. (2005). Evidence that the plant cannabinoid Δ9-tetrahydrocannabivarin is a cannabinoid CB1 and CB2 receptor antagonist. British Journal of Pharmacology, 146(7), 917-926. doi:10.1038/sj.bjp.0706414
The prevalence of any population having a psychotic disorder is approximately 3.5%; additionally, the incidence of schizophrenia is ~1%. Just as there are an infinite number studies on ways predicting psychotic disorders, there are an equal amount of studies attempting to reduce the number of cases among the population. Nevertheless, without any background in research methods, one may not know what to make of all these studies.
Before we start, the following is a fundamental review of some research methods used in science.
A longitudinal study is a study looking at a group of participants over a period. Longitudinal studies are good at identifying changes in a system over time. However, they are not good at establishing causation.
Experimental research another conventional method used in science establishes cause and effect. Unfortunately, many restrictions on cannabis prohibit most experimental studies on humans.
A meta-analysis is a form of research synthesis that takes a group of studies and uses statistics to increase the power of an outcome. One-way researchers use a meta-analysis is to increase the likely hood that a variable is affecting a change. A meta-analysis is only as good as the studies used in the analysis. Note, if studies examined in a meta-analysis are from longitudinal research, the reader should not disregard information when experimental research is missing. However, the reader should realize these shortfalls and take into consideration that there may be more than the examined variable affecting the outcome.
Tetrahydrocannabinol (THC) is the psychoactive component of cannabis. Significant one-time doses of THC can produce a temporary mild psychotic episode in healthy naive cannabis users. Very little is known about THC increasing the prevalence of psychotic disorders in the cannabis population. This article reviews recent finding involving cannabis and psychosis.
A widely cited meta-analysis found that regular cannabis users may have a two-fold increase in psychosis. Another analysis examining the early onset of psychosis found adolescent cannabis use increased the risk of psychosis late in life. However, the method of analysis from both studies consisted of longitudinal and population-based all of which does not establish causation. Moreover, the studies used did not set a starting point for comparisons. Without a baseline, researchers cannot ascertain if an individual with psychosis is attracted to cannabis use or does cannabis use increase the risk of psychosis.
People do not need cannabis to develop psychosis. However, cannabis may add to the development of psychosis in at-risk individuals. A journal article from the Current Opinion in Psychiatry revealed that adolescent and adults already at risk of psychosis increase their risk when using cannabis.
That does not mean cannabis does not benefit individuals diagnosed with psychosis or schizophrenia. In another meta-analysis, researchers observed that people diagnosed with schizophrenia who use cannabis function better cognitively than individuals with schizophrenia that do not use cannabis. The at-risk population should consult proper medical professionals about the hazards cannabis may contribute to their mental health and seek information on the proper use of cannabis.
The cannabinoid Cannabidiol (CBD) is known to counter the psychoactive effect of cannabis. Additionally, scientist found CBD to have the same effect and a superior safety profile compared to the standard ant-psychotic medication. Therefore, CBD may reduce psychotic episodes and may soon be a safe alternative to aggressive antipsychotic medication after more studies.
In closing, cannabis use may increase the risk of psychosis and schizophrenia by two-fold in the cannabis population. Meaning the risk of a psychotic disorder may increase from 3.50% to 7% or from 1% to 2% in schizophrenia. Nevertheless, researchers will need more experimental studies to prove further how cannabis affects psychosis.
Although cannabis increases the risk of psychosis in the at-risk population, when correctly used, cannabis improved cognition in people with schizophrenia. At-risk individuals should seek professional medical advice before starting cannabis.
CBD is shown to counter the psychoactive effect of THC. Recently CDB presented an improved safety profile compared to the standard ant-psychotic medication suggesting CBD may be a safer alternative. More studies will be needed using CBD as an alternative to conventional medication.
Lastly, cannabis is not as dangerous as many perceive, and it is not as safe as others argue; the truth will be found somewhere in the middle.
Bhattacharyya, S., Morrison, P. D., Fusar-Poli, P., Martin-Santos, R., Borgwardt, S., Winton-Brown, T., . . . McGuire, P. K. (2009). Opposite effects of Δ-9-tetrahydrocannabinol and cannabidiol on human brain function and psychopathology. Neuropsychopharmacology, 35, 764. Retrieved from http://dx.doi.org/10.1038/npp.2009.184
Di Forti, M., Morrison, P. D., Butt, A., & Murray, R. M. (2007). Cannabis use and psychiatric and cogitive disorders: The chicken or the egg? Current Opinion in Psychiatry, 20(3) Retrieved from https://journals.lww.com/co-psychiatry/Fulltext/2007/05000/Cannabis_use_and_psychiatric_and_cogitive.10.aspx
D’Souza, D. C., Perry, E., MacDougall, L., Ammerman, Y., Cooper, T., Wu, Y., . . . Krystal, J. H. (2004). The psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in healthy individuals: Implications for psychosis.Neuropsychopharmacology, 29, 1558. Retrieved from http://dx.doi.org/10.1038/sj.npp.1300496
Large, M., Sharma, S., Compton, M. T., Slade, T., & Nielssen, O. (2011). Cannabis use and earlier onset of psychosis: A systematic meta-analysis. Archives of General Psychiatry, 68(6), 555-561. Retrieved from http://dx.doi.org/10.1001/archgenpsychiatry.2011.5
Leweke, F. M., Piomelli, D., Pahlisch, F., Muhl, D., Gerth, C. W., Hoyer, C., . . . Koethe, D. (2012). Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia. Translational Psychiatry, 2, e94. Retrieved from http://dx.doi.org/10.1038/tp.2012.15
Moore, T. H. M., Zammit, S., Lingford-Hughes, A., Barnes, T. R. E., Jones, P. B., Burke, M., & Lewis, G.Cannabis use and risk of psychotic or affective mental health outcomes: A systematic review. The Lancet, 370(9584), 319-328. doi:10.1016/S0140-6736(07)61162-3
Perala , J., Suvisaari, J., Saarni, S. I., & al, e. (2007). Lifetime prevalence of psychotic and bipolar i disorders in a general population. Archives of General Psychiatry, 64(1), 19-28. Retrieved from http://dx.doi.org/10.1001/archpsyc.64.1.19
Yucel, M., Bora, E., Lubman, D. I., Solowij, N., Brewer, W. J., Cotton, S. M., . . . Pantelis, C. (2012). The impact of cannabis use on cognitive functioning in patients with schizophrenia: A meta-analysis of existing findings and new data in a first-episode sample. Schizophrenia Bulletin, 38(2), 316-330. Retrieved from http://dx.doi.org/10.1093/schbul/sbq079
Growers in Massachusetts must grow cannabis from seed. Germination is the process by which an organism is produced from seed. The Seedling stage is the most vulnerable part of a plant’s life. Therefore, increasing both germination and growth rate is a priority for all gardeners. Studies exposing a variety of seeds to an induced low-frequency magnetic field (25 mT to 200 mT) for a short period time (10-25 min) are shown to significantly improve germination and growth rate as well as the dry weight of many plants including hops. Hops are a close relative to cannabis. The cost of producing a low-frequency magnetic field is inexpensive. Therefore, it would be of benefit for cannabis growers to experiment with an induced low-frequency magnetic field to increase crop production.
De Souza, A., Sueiro, L., García, D., & Porras, E. (2010). Extremely low frequency non-uniform magnetic fields improve tomato seed germination and early seedling growth. Seed Science and Technology, 38(1), 61-72.
De Souza, A., García, D., Sueiro, L., & Gilart, F. (2014). Improvement of the seed germination, growth and yield of onion plants by extremely low frequency non-uniform magnetic fields
Iqbal, M., ul Haq, Z., Malik, A., Ayoub, C. M., Jamil, Y., & Nisar, J. (2016). Pre-sowing seed magnetic field stimulation: A good option to enhance bitter gourd germination, seedling growth, and yield characteristics
Maffei, M. E. (2014). Magnetic field effects on plant growth, development, and evolution. Frontiers in Plant Science, 5, 445.
This approximate four-week-old ninja fruit is starting to mature to adulthood. Primordium cells the are the smallest group of cell able to trigger organ growth. During this development phase, both pistillate (female) and staminate (male) of C. Sativa species are indistinguishable with the exception of general trends in shape.
Clarke, R. C. (1981). Marijuana botany an advanced study: The propagation and breeding of distinctive cannabis. Oakland, CA: Ronin Publishing.
Kidner, C. A. (2001). Plant organ primordia. Els () John Wiley & Sons, Ltd.
For over thousands of years, people have used cannabis for industrial, recreational and medicinal uses. In Egypt, hemp was grown along the banks of the Nile and used to produce fibers for building materials. Additionally, some of the earliest recorded medical uses of cannabis come from ancient China. In China, cannabis resin was used along with wine as an anesthetic during major surgery. Similarly, the earliest reports of recreational use come from China.
The ancient Indian writings of the Vedas tells a story about the god Shiva finding refuge under a cannabis plant after having a devastating argument. As Shiva calmed down, he ate the leaves of the plant. Soon cannabis became his favorite food, and he was known as the lord of Bhang. In India Bhang is a drink served at ceremonies and celebrations containing cannabis.
By the end of the 19th century, the Indian Hemp and Drug Commission investigated the use of cannabis in India. The commission concluded that cannabis is essential to the culture and religion of India. Moreover, the commission reasoned that along with religious and cultural uses, cannabis also has medical benefits. The commission found that the plant helped to relieve symptoms of dysentery, sunstroke, clears phlegm, stimulates digestion, and sharpens the mind.
A doctor named William Brooke O’Shaughnessy first introduced cannabis to western medicine in 1839. Shortly after O’Shaughnessy started working for the British East Indian Company in Calcutta, he began to investigate the indigenous plants of the region. The therapeutic effects of cannabis became known to O’Shaughnessy soon after interviewing native people. Through experiments, the doctor soon found cannabis relieves pain, calms nerves; has anti-inflammatory, anti-spastic, and anti-convulsive properties. In 1856 O’Shaughnessy was knighted by Queen Victoria for his work on Cannabis.
Sadly, in America Cannabis was/is used as a political weapon for control and fear. In the early 20th century Harry Anslinger, the head of the Federal Bureau of Narcotics (today’s DEA), used fear-based race propaganda to frighten American’s into the prohibition of cannabis. Harry Anslinger is quoted to say:
“Reefer makes darkies think they’re as good as white men.”
“There are 100,000 total marijuana smokers in the US, and most are Negroes, Hispanics, Filipinos, and entertainers. Their Satanic music, jazz, and swing result from marijuana usage. This marijuana causes white women to seek sexual relations with Negroes, entertainers and any others.”
“The primary reason to outlaw marijuana is its effect on the degenerate races.”
In 1937 after years of misleading stories in local newspapers reporting about “killer weed,” along with Anslinger’s fear-based race propaganda, Congress passed the Marijuana Tax Act. The Marijuana Tax Act not only banned the use of cannabis for recreation but also banned cannabis for medical research. The Act crippled the ability of scientists to study cannabis for the following 70+ years worldwide. Only recently are people rediscovering the therapeutic and enrichment properties of cannabis.
Abel, E. L. (1980). Marihuana: The first twelve thousand years. New York: Springer.
Brecher, E. M. (1973). Licit and illicit drugs: The consumers union report on narcotics, stimulants, depressants, inhalants, hallucinogens, and marijuana
O’Shaughnessy, W. B. (1839). On the preparations of the indian hemp, or gunjah: Cannabis indica their effects on the animal system in health, and their utility in the treatment of tetanus and other convulsive diseases”. Journal of the Asiatic Society of Bengal, 8(839)
The science of marijuana, 2nd edn. (2008). British Journal of Clinical Pharmacology, 67(2), 268-268.
Many people hear urban legends about the damage that cannabis can do to memory. Most if not all of the myths lack evidence-based research. Additionally, if the tale was from a study, it was cited incorrectly, or the storyteller had a personal bias. This post explores the recent studies involving memory impairment and cannabis.
Thus far evidence points to cannabis temporarily impairing both short-term memory and the ability to make long-term memories from short-term. The experience of memory impairment happens when an acute dose is taking at once or during prolonged exposure. Nevertheless, cannabis does not reduce the ability to recall information once a memory is in long-term storage.
Reductions in attention and short-term working memory function are debatable cognitive impairments associated with cannabis. Both are said to have similar handicaps as short-term memory. Still, they are controversial because of the method of analysis. When running a meta-analysis with a large group of studies, one team of researchers found no causation of cannabis affecting attention or working memory. However, a second team rerunning the analysis with fewer studies found temporary cognitive impairments. Nevertheless, researchers found that the absence of cannabis for approximately 30 days (one month), eliminated any previous cognitive limitations. At a follow-up test of cognition, past cannabis users tested the same as non-cannabis users. Meaning when a person decides to suspend cannabis there may be no lasting cognitive impairments.
One of many cannabinoids is tetrahydrocannabinol (THC); THC is the psychoactive component of cannabis; it is the primary causal agent in temporary memory impairment when using Cannabis. Another cannabinoid Cannabidiol (CBD) whose medical value is still in the infancy of research is antagonistic to many of THC’s impairing effects. CBD reduces the psychoactive effect and cognitive impairments of THC. Thus, taking CBD with THC may counteract any acute and long-term cognitive impairments when using cannabis.
In closing, data shows THC a cannabinoid in cannabis effect short-term memory and diminishes the ability to store short-term memory in long-term storage. However, long-term memory recall is not affected by cannabis use. Cannabis may or may not affect attention and short-term working memory. Suspending use for one month stopped any cognitive impairments associated with cannabis. Lastly, CBD may hinder any acute and long-term cognitive impairments when using cannabis.
Broyd, S. J., van Hell, H. H., Beale, C., Yücel, M., & Solowij, N. (2016). Acute and chronic effects of cannabinoids on human Cognition—A systematic review. Biological Psychiatry, 79(7), 557-567.
GRANT, I., GONZALEZ, R., CAREY, C. L., NATARAJAN, L., & WOLFSON, T. (2003). Non-acute (residual) neurocognitive effects of cannabis use: A meta-analytic study. Journal of the International Neuropsychological Society, 9(5), 679-689.
Morgan, C. J. A., Schafer, G., Freeman, T. P., & Curran, H. V. (2010). Impact of cannabidiol on the acute memory and psychotomimetic effects of smoked cannabis: Naturalistic study. The British Journal of Psychiatry, 197(4), 285-290.
Nadia Solowij, R. B. (2008). The chronic effects of cannabis on memory in humans: A review. Current Drug Abuse Reviews, 1(1)
Schreiner, A. M., & Dunn, M. E. (2012). Residual effects of cannabis use on neurocognitive performance after prolonged abstinence: A meta-analysis. Experimental and Clinical Psychopharmacology, 20(5), 420-429.
Volkow ND, Swanson JM, Evins AE, DeLisi LE, Meier MH, Gonzalez R, Bloomfield MAP, Curran HV, Baler R. (2016). Effects of cannabis use on human behavior, including cognition, motivation, and psychosis: A review. JAMA Psychiatry, 73(3), 292-297.