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Ingestion Methods, Laws, and Strains

PLEASE USE ALL THC PRODUCTS WITH EXTREME CARE: AND AS WITH ALL MEDICATIONS, PLEASE KEEP AWAY FROM PETS AND CHILDREN!

Update on Medical Marijuana as of December 2016 - 

 

 

Where to Buy Clones:

We are getting lots of calls from patients and stores asking where an authorized patient can buy clones. The legislature did not take that into in the 2015 law, so at this time there is no legal way for patients to purchase seeds, plants or clones. 
This is expected to be remedied in the 2017 legislative session and will likely look similar to how cooperatives purchase from licensed growers. We will update you throughout session via this publication.


What are Compliant Products?

The medical marijuana law allows for products that may be beneficial for medical use. These products must pass stringent testing set by the Washington State Department of Health and may be sold sales tax-free. These products fall into one of three categories outlined on the next page and must meet all listed requirements. 
The Department of Health's goal is to: 
• Create voluntary standards for safer and healthier products. 

• Allow consumers the choice of compliant or regular products. 

• Create ratios for high CBD/low THC products that are sales tax free for any adult. 
Products that may be sold or donated to patients at a medically endorsed marijuana store must pass certain standards related to: 

• THC and CBD concentrations/ratios 

• Testing for pesticides, mold, fungus, solvents, etc. 

• Labeling requirements (Note: pesticides used are not required to be listed on the label) 

• Safe handling and employee training requirements. 
For more information, read the specific laws and rules for marijuana product compliance: 

• RCW 69.50.375 

• Chapter 246-70 WAC 

• Chapter 314-55-102 WAC 
See the following page for specifications on the three compliant products. 

  

General Use Products

What they are: 
• Any marijuana product approved by the Liquor and Cannabis Board (LCB), including edibles. 
Packaged Serving Requirements: 
• May be packaged in servings or applications that contain up to 10 mg of active THC. 

• A unit contains no more than 10 servings or applications and must not exceed 100 total mg of active THC. 
Who can sell: 

• Any licensed marijuana store. 
Who can purchase: 
• Any adult age 21 or older. 

• Qualifying patients between the ages of 18 and 20 who are entered into the medical 
marijuana authorization database and hold a valid recognition card. Sales tax-free.

 

High CBD Products 
What they are:

• Any marijuana product approved by the WSLCB, including edibles - except marijuana intended for smoking.

 

Packaged Serving Requirements:

• Concentrates containing not more than 2% THC concentration and at least 25 times more CBD concentration by weight. 

• Marijuana-infused edible products containing not more than 2 mg of active THC and at least 5 times more CBD per serving by weight for solids or volume for liquids. 

• Marijuana-infused topical products containing at least 5 times more CBD concentration than THC concentration. 
Who can sell: 

• Any licensed marijuana store. 
Who can purchase: 
• Qualifying patients between the ages of 18 and 20 who are entered into the medical marijuana authorization database and hold a valid recognition card. Sales tax-free.

High THC Products

What they are: 
• Marijuana products containing more than 10 mg but not more than 50 mg of active THC per serving or application. 

• Only these types of marijuana products qualify for High THC classification: capsules, tinctures, transdermal patches, and suppositories. 
Packaged Serving Requirements: 

• May be packaged in servings or applications containing up to 50 mg of active THC. 

• A unit contains no more than 10 servings or applications and must not exceed 
500 mg total of active THC. 
Who can sell: 

• Only a licensed and medically endorsed marijuana store. 
Who can purchase: 
• Qualifying patients age 18 and older and designated providers who are entered into the medical marijuana authorization database and hold a valid recognition card. Sales tax-free. 
Medically Endorsed Stores Monthly Update - December 2016


WARNING! As with all medications, PLEASE keep away from pets and children!


Ingesting cannabis:


Ingesting cannabis has many benefits over smoking it, the most important of which is the bypass of dangerous chemicals entering the respiratory system. Carcinogens and tars are largely left behind in the preparation for eating and are not released into the lungs. Also, ingesting it leads to a markedly different experience from smoking. Eating cannabis-infused preparations usually leads to a longer, stronger, and much more physical high than smoking alone. Although eating is a perfectly viable way of absorbing cannabis into the bloodstream, higher amounts of the drug must be used in a cooking preparation in order to make the product effective.

Smoking delivers more THC to your neuron’s synapse quicker, via direct contact to your lungs alveoli therefore blocking dopamine quicker. Ingesting it causes the THC to be put into the bloodstream via digestion, therefore delivering smaller doses in a longer span of time. That’s why smoking it lasts 1-2 hours but eating it can last up to 8.

 

Vaporization is an alternative to burning (smoking) that avoids the production of irritating toxic and carcinogenic by-products by heating the material so its active compounds boil off into a vapor. No combustion occurs, so no smoke or taste of smoke is present. Vapor ideally contains virtually zero particulate matter or tar, and significantly lower concentrations of noxious gases such as carbon monoxide. Vaporizers contain various forms of extraction chambers including straight bore, venturi, or sequential venturi, and are made of materials such as metal or glass. The extracted vapor may be collected in a jar or inflatable bag, or inhaled directly through a hose or pipe. With little to no smoke produced and cooler temperatures, less material is required to achieve a given level of effect. Hence, the irritating and harmful effects of smoking are reduced as is secondhand smoke.

 

In conclusion, ingesting cannabis is a different and healthier alternative for those who use it for medicinal purposes. Once again, the versatility of the cannabis plant will always show its true colors.


Possible Side Effects of Cannabis
There are some effects of cannabis that are not beneficial and can be diminished through awareness.
Cannabis may cause dizziness while standing due to lowered blood pressure.
Initial increase in heart rate / blood pressure may be problematic for those with heart conditions or severe anxiety.
Cannabis may cause a decrease in coordination and cognition.
Potential short term memory loss while medicated.
There are no significant withdrawal effects when cannabis medicine is decreased or stopped. However symptom relief will also be reduced or stopped.
Effects vary from person to person.


Safe Use of Cannabis

Do not drive or operate heavy machinery if impaired by cannabis. Indicas can be especially sedating.
Cannabis mixed with alcohol may cause vomiting and nausea.
Those receiving digitalis or other cardiac medications should only use cannabis under careful medical supervision.
Heavy smoking with no harm reduction techniques may lead to respiratory irritation.
If you share joints or other inhaling devices please hold them so lips do not touch the vessel of delivery.
Beware of mold and fungi.
It is illegal in the United States to possess cultivate or distribute medicinal cannabis under federal law.
Choose organic cannabis whenever possible, especially for those with compromised immune systems.


Knowing Your Medication

 

Sativa plants have less chlorophyll than the Indica counterpart. It has a higher THC content to Cannabidiol (CBD) ratio and offers a much more energetic type of mood. Sativa is used most commonly to elevate a depressed mood. Generally speaking, the Sativa plant is the taller and lankier variety, reaching heights of over 5-6 meters. It is characterized by narrow serrated leaves and loose spear-like flower clusters that can be extremely resinous.

Primarily the effects of Sativas are on the mind and emotions. In this regard, they tend to be more stimulating, uplifting, energizing, and creativity enhancing. These benefits can be particularly helpful for the psychological component of many illnesses. Sativas are generally better for daytime use.

 


Benefits of the Endocannabinoid System

Memory


Mice treated with tetrahydrocannabinol (THC) show suppression of long-term potentiation in the hippocampus, a process that is essential for the formation and storage of long-term memory.[35] These results concur with anecdotal evidence suggesting that smoking Cannabis impairs short-term memory.[36]Consistent with this finding, mice without the CB1 receptor show enhanced memory and long-term potentiation indicating that the endocannabinoid system may play a pivotal role in the extinction of old memories. One study found that the high-dose treatment of rats with the synthetic cannabinoid HU-210 over several weeks resulted in stimulation of neural growth in the rats' hippocampus region, a part of the limbic system playing a part in the formation of declarativeand spatial memories, but did not investigate the effects on short-term or long-term memory.[37] Taken together, these findings suggest that the effects of endocannabinoids on the various brain networks involved in learning and memory may vary.

 

Role in hippocampal neurogenesis

 


In the adult brain, the endocannabinoid system facilitates the neurogenesis of hippocampal granule cells.[37][38] In the subgranular zone of the dentate gyrus, multipotent neural progenitors (NP) give rise to daughter cells that, over the course of several weeks, mature into granule cells whose axons project to and synapse onto dendrites on the CA3 region.[39] NPs in the hippocampus have been shown to possess fatty acid amide hydrolase (FAAH) and express CB1 and utilize 2-AG.[38] Intriguingly, CB1 activation by endogenous or exogenous cannabinoids promote NP proliferation and differentiation; this activation is absent in CB1 knockouts and abolished in the presence of antagonist.[37][38]
Induction of synaptic depression.


The inhibitory effects of cannabinoid receptor stimulation on neurotransmitter release have caused this system to be connected to various forms of depressant plasticity. A recent study conducted with the bed nucleus of the stria terminalis found that the endurance of the depressant effects was mediated by two different signaling pathways based on the type of receptor activated. 2-AG was found to act on presynaptic CB1 receptors to mediate retrograde short-term depression (STD) following activation of L-type calcium currents, while anandamide was synthesized after mGluR5 activation and triggered autocrine signalling onto postsynapic TRPV1 receptors that induced long-term depression (LTD). Similar post-synaptic receptor dependencies were found in the striatum, but here both effects relied on presynaptic CB1 receptors.[18] These findings provide the brain a direct mechanism to selectively inhibit neuronal excitability over variable time scales. By selectively internalizing different receptors, the brain may limit the production of specific endocannabinoids to favor a time scale in accordance with its needs.

 

Appetite

 


Evidence for the role of the endocannabinoid system in food-seeking behavior comes from a variety of cannabinoid studies. Emerging data suggests that THC acts via CB1 receptors in the hypothalamic nuclei to directly increase appetite.[40] It is thought that hypothalamic neurons tonically produce endocannabinoids that work to tightly regulate hunger. The amount of endocannabinoids produced is inversely correlated with the amount of leptin in the blood.[41] For example, mice without leptin not only become massively obese but express abnormally high levels of hypothalamic endocannabinoids as a compensatory mechanism.[10] Similarly, when these mice were treated with an endocannabinoid inverse agonists, such as rimonabant, food intake was reduced.[10] When the CB1 receptor is knocked out in mice, these animals tend to be leaner and less hungry than wild-type mice. A related study examined the effect of THC on the hedonic (pleasure) value of food and found enhanced dopamine release in the nucleus accumbens and increased pleasure-related behavior after administration of a sucrose solution.[42] A related study found that endocannabinoids affect taste perception in taste cells[43] In taste cells, endocannabinoids were shown to selectively enhance the strength of neural signaling for sweet tastes, whereas leptin decreased the strength of this same response. While there is need for more research, these results suggest that cannabinoid activity in the hypothalamus and nucleus accumbens is related to appetitive, food-seeking behavior.[40]

 

Energy balance and metabolism

 

The endocannabinoid system has been shown to have a homeostatic role by controlling several metabolic functions, such as energy storage and nutrient transport. It acts on peripheral tissues such as adipocytes, hepatocytes, the gastrointestinal tract, the skeletal muscles and the endocrine pancreas. It has also been implied in modulating insulin sensitivity. Through all of this, the endocannabinoid system may play a role in clinical conditions, such as obesity, diabetes, and atherosclerosis, which may also give it a cardiovascular role.[44]

 

Stress response

 


While the secretion of glucocorticoids in response to stressful stimuli is an adaptive response necessary for an organism to respond appropriately to a stressor, persistent secretion may be harmful. The endocannabinoid system has been implicated in the habituation of the hypothalamic-pituitary-adrenal axis(HPA axis) to repeated exposure to restraint stress. Studies have demonstrated differential synthesis of anandamide and 2-AG during tonic stress. A decrease of anandamide was found along the axis that contributed to basal hypersecretion of corticosterone; in contrast, an increase of 2-AG was found in the amygdala after repeated stress, which was negatively correlated to magnitude of the corticosterone response. All effects were abolished by the CB1antagonist AM251, supporting the conclusion that these effects were cannabinoid-receptor dependent.[45] These findings show that anandamide and 2-AG divergently regulate the HPA axis response to stress: while habituation of the stress-induced HPA axis via 2-AG prevents excessive secretion of glucocorticoids to non-threatening stimuli, the increase of basal corticosterone secretion resulting from decreased anandamide allows for a facilitated response of the HPA axis to novel stimuli.

Exploration, social behavior, and anxiety


Prolonged, systemic exposure to cannabinoids has often been associated with anti-social effects. To investigate this theory, a cannabinoid receptor-knockout mouse study examined the effect that these receptors play on exploratory behavior. Researchers selectively targeted glutamatergic and GABAergic cortical interneurons and studied results in open field, novel object, and sociability tests. Eliminating glutamatergic cannabinoid receptors led to decreased object exploration, social interactions, and increased aggressive behavior. In contrast, GABAergic cannabinoid receptor-knockout mice showed increased exploration of objects, socialization, and open field movement.[46] These contrasting effects reveal the importance of the endocannabinoid system in regulating anxiety-dependent behavior. Results suggest that glutamatergic cannabinoid receptors are not only responsible for mediating aggression, but produce an anxiolytic-like function by inhibiting excessive arousal: excessive excitation produces anxiety that limited the mice from exploring both animate and inanimate objects. In contrast, GABAergic neurons appear to control an anxiogenic-like function by limiting inhibitory transmitter release. Taken together, these two sets of neurons appear to help regulate the organism's overall sense of arousal during novel situations.


Immune function


Evidence suggests that endocannabinoids may function as both neuromodulators and immunomodulators in the immune system. Here, they seem to serve an autoprotective role to ameliorate muscle spasms, inflammation, and other symptoms of multiple sclerosis and skeletal muscle spasms.[5] Functionally, the activation of cannabinoid receptors has been demonstrated to play a role in the activation of GTPases in macrophages, neutrophils, and BM cells. These receptors have also been implicated in the proper migration of B cells into the marginal zone (MZ) and the regulation of healthy IgM levels.[47] Interestingly, some disorders seem to trigger an upregulation of cannabinoid receptors selectively in cells or tissues related to symptom relief and inhibition of disease progression, such as in that rodent neuropathic pain model, where receptors are increased in the spinal cord microglia, dorsal root ganglion, and thalamic neurons.[16]

 

Multiple sclerosis

 


Historical records from ancient China and Greece suggest that preparations of Cannabis indica were commonly prescribed to ameliorate multiple sclerosis-like symptoms such as tremors and muscle pain. Modern research has confirmed these effects in a study on diseased mice, wherein both endogenous and exogenous agonists showed ameliorating effects on tremor and spasticity. It remains to be seen whether pharmaceutical preparations such as dronabinolhave the same effects in humans.[48][49] Due to increasing use of medical Cannabis and rising incidence of multiple sclerosis patients who self-medicate with the drug, there has been much interest in exploiting the endocannabinoid system in the cerebellum to provide a legal and effective relief.[36] In mouse models of multiple sclerosis, there is a profound reduction and reorganization of CB1 receptors in the cerebellum.[50] Serial sections of cerebellar tissue subjected to immunohistochemistry revealed that this aberrant expression occurred during the relapse phase but returned to normal during the remitting phase of the disease.[50] Other studies suggest that CB1 agonists promote the survival of oligodendrocytes in vitro in the absence of growth and trophic factors; in addition, these agonist have been shown to promote mRNA expression of myelin lipid protein. (Kittler et al., 2000; Mollna-Holgado et al., 2002). Taken together, these studies point to the exciting possibility that cannabinoid treatment may not only be able to attenuate the symptoms of multiple sclerosis but also improve oligodendrocyte function (reviewed in Pertwee, 2001; Mollna-Holgado et al., 2002). 2-AG stimulates proliferation of a microglial cell line by a CB2 receptor dependent mechanism, and the number of microglial cells is increased in multiple sclerosis.[51]

 

Female reproduction

 



The developing embryo expresses cannabinoid receptors early in development that are responsive to anandamide secreted in the uterus. This signaling is important in regulating the timing of embryonic implantation and uterine receptivity. In mice, it has been shown that anandamide modulates the probability of implantation to the uterine wall. For example, in humans, the likelihood of miscarriage increases if uterine anandamide levels are too high or low.[52] These results suggest that intake of exogenous cannabinoids (e.g. marijuana) can decrease the likelihood for pregnancy for women with high anandamide levels, and alternatively, it can increase the likelihood for pregnancy in women whose anandamide levels were too low.[53][54]

 

Autonomic nervous system

 


Peripheral expression of cannabinoid receptors led researchers to investigate the role of cannabinoids in the autonomic nervous system. Research found that the CB1 receptor is expressed presynaptically by motor neurons that innervate visceral organs. Cannabinoid-mediated inhibition of electric potentials results in a reduction in noradrenaline release from sympathetic nervous system nerves. Other studies have found similar effects in endocannabinoid regulation of intestinal motility, including the innervation of smooth muscles associated with the digestive, urinary, and reproductive systems.[17]

 

Analgesia

 


At the spinal cord, cannabinoids suppress noxious-stimulus-evoked responses of neurons in the dorsal horn, possibly by modulating descending noradrenaline input from the brainstem.[17] As many of these fibers are primarily GABAergic, cannabinoid stimulation in the spinal column results in disinhibition that should increase noradrenaline release and attenuation of noxious-stimuli-processing in the periphery and dorsal root ganglion.
The endocannabinoid most researched in pain is palmitoylethanolamide. Palmitoylethanolamide is a fatty amine related to anandamide, but saturated and although initially it was thought that palmitoylethanolamide would bind to the CB1 and the CB2 receptor, later it was found that the most important receptors are the PPAR-alpha receptor, the TRPV receptor and the GRP55 receptor.[spelling?] Palmitoylethanolamide has been evaluated for its analgesic actions in a great variety of pain indications[55] and found to be safe and effective. Basically these data are proof of concept for endocannabinoids and related fatty amines to be therapeutically useful analgesics; palmitoylethanolamide is available under the brand names Normast and PeaPure as nutraceuticals.
Endocannabinoids are involved in placebo induced analgesia responses.[56]

 

Thermoregulation

 


Anandamide and N-arachidonoyl dopamine (NADA) have been shown to act on temperature-sensing TRPV1 channels, which are involved in thermoregulation.[57] TRPV1 is activated by the exogenous ligand capsaicin, the active component of chili peppers, which is structurally similar to endocannabinoids. NADA activates the TRPV1 channel with an EC50 of approximately of 50 nM.[clarify] The high potency makes it the putative endogenous TRPV1 agonist.[58] Anandamide has also been found to activate TRPV1 on sensory neuron terminals, and subsequently cause vasodilation.[17] TRPV1 may also be activated by methanandamide and arachidonyl-2'-chloroethylamide (ACEA).[5]

 

Sleep

 


Increased endocannabinoid signaling within the central nervous system promotes sleep-inducing effects. Intercerebroventricular administration of anandamide in rats has been shown to decrease wakefulness and increase slow-wave sleep and REM sleep.[59] Administration of anandamide into the basal forebrain of rats has also been shown to increase levels of adenosine, which plays a role in promoting sleep and suppressing arousal.[60] REM sleep deprivation in rats has been demonstrated to increase CB1 receptor expression in the central nervous system.[61] Furthermore, anandamide levels possess a circadian rhythmin the rat, with levels being higher in the light phase of the day, which is when rats are usually asleep or less active, since they are nocturnal.[62]