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Changing Medicine Together!
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~ PTSD ~
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Page Legend
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Preferred Strains
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OG Kush
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Critical Kush
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THC 14.36/19.38%
CBD 1.05/1.77% CBN 0.51/2.66% THC/CBD Ratio 60/40% Sativa Dominant |
THC 17.0/20.0%
CBD 0.10/13.21% CBN 0.30/0.70% 90/10% Indica Dominant |
THC 16.00/20.00%
CBD 0.10/0.30% CBN 0.0/0.30% THC/CBD RATIO 55/45% Sativa Dominant |
THC 21.5/25.0%
CBD 0.01/0.32% CBN 0.01/0.05% THC/CBD Ratio 90/10% Indica Dominant |
THC 18.0/23.0%
CBD 0.03/0.2% CBN 0.0/0.03% THC/CBD Ratio Sativa Dominant |
THC 4.0/7.0%
CBD 8.0/16.0% CBN0.0/0.02% THC/CBD Ratio 2:5 75/25% Sativa Dominant |
THC 16.00/25.00%
CBD 0.10/1.10% CBN 0.05/0.52% 60/40% Sativa Dominant |
Preferred Methods to Medicate
Raw Kief/Greens
Ideally one should be eating Raw Kief/Greens for the A molecule THCA, CBDA etc, Over and above the preferred method of medicating, each cannabinoid & Terpenes plays a roll in healing.
Medicating
Ideally one should be eating Raw Kief/Greens for the A molecule THCA, CBDA etc, Over and above the preferred method of medicating, each cannabinoid & Terpenes plays a roll in healing.
Medicating
- Drops/Oil Dropped under tongue for faster absorption (Soft membrane tissue).
- Sprays, if for internal best applied through nasal sprays for soft tissue. (If Issue is eye's or ear's, apply to correlation)
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Fox 21 News
Operation: Grow-4-Vets 22 Suicides a day in U.S. Military Add opioid deaths, Cannabis could make a big difference in our solders lives. |
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PTSD, Overview:
PPosttraumatic stress disorder (PTSD)[note 1] is a mental disorder that can develop after a person is exposed to a traumatic event, such as sexual assault, warfare, traffic collisions, or other threats on a person's life.[1] Symptoms may include disturbing thoughts, feelings, or dreams related to the events, mental or physical distress to trauma-related cues, attempts to avoid trauma-related cues, alterations in how a person thinks and feels, and an increase in the fight-or-flight response.[1][3] These symptoms last for more than a month after the event.[1] Young children are less likely to show distress but instead may express their memories through play.[1] A person with PTSD is at a higher risk for suicide and intentional self-harm.[2][6]
"Despair". For other uses of despair, see Despair (disambiguation). For the mood disorder, see Major depressive disorder. "Hopelessness" redirect see Hopelessness (album).
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Most people who have experienced a traumatic event will not develop PTSD.[2] People who experience interpersonal trauma (for example rape or child abuse) are more likely to develop PTSD, as compared to people who experience non-assault based trauma such as accidents and natural disasters.[7] About half of people develop PTSD following rape.[2] Children are less likely than adults to develop PTSD after trauma, especially if they are under ten years of age.[8] Diagnosis is based on the presence of specific symptoms following a traumatic event.[2] A number of different types of therapy may be useful.[9] This may occur one-on-one or in a group.[3] Antidepressants of the selective serotonin reuptake inhibitor type are the first-line medications for PTSD and result in benefit in about half of people.[4] (Note:"Antidepressants of the selective serotonin reuptake inhibitor type are the first-line medications for PTSD"), as cannabis has a direct regulatory function & more over the system/process governing serotine.
How Cannabis Aids:
Endocannabiniods, CB 1 Receptors, 80/90% located in the Brain & Nervous System, CB 2 largely in Immune System and all major organs. |
Depression
Cannabis Treating Depression Dr. Rachna Patel Discussing cannabis and clinical studies. FDA-Approved investigation: cannabis & PTSD.
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Serotonin is a Neurotransmitter, that regulates the mood.
known for many years, that depletion of the neurotransmitter serotonin in the brain leads to depression.
The anti-depressant and intoxicating effects of cannabis are due to its chemical similarity to natural substances in the brain known as "endo-cannabinoids," which are released under conditions of high stress or pain, They interact with the brain through structures called cannabinoid CB1 receptors. these receptors have a direct effect on the cells producing serotonin, (cannabinoids increase activity in the neurons that produce serotonin) which is a neurotransmitter that regulates the mood. CBD is postulated to act as an agonist to the 5HT1areceptor. Activation of the 5HT1a receptor is understood to modulate the release of serotonin in the brain. This hypothesis was confirmed in a study in which mice were pretreated with a 5HT1a antagonist, the antidepressant effects of CBD were absent. Further evidence of the role of 5HT1a is given by the observed similarities of CBD and isapirone (a 5HT1a partial agonist) in public speaking model.
Anandamide: The Bliss molecule, a fatty acid neurotransmitter
Anandamide is also known as N-arachidonoylethanolamine or AEA, and is an endogenous analogue of tetrahydrocannabinol, or THC. AEA is a fatty acid neurotransmitter responsible for joy, happiness, derived from the non-oxidative metabolism of eicosatetraenoic acid (arachidonic acid) an essential ω-6 polyunsaturated fatty acid. The name is taken from the Sanskrit & Pāli word ananda, which means "joy, bliss, delight", and amide.[1][2] It is synthesized from N-arachidonoyl phosphatidylethanolamine by multiple pathways.[3] It is degraded primarily by the fatty acid amide hydrolase (FAAH) enzyme, which converts anandamide into ethanolamine and arachidonic acid. As such, inhibitors of FAAH lead to elevated anandamide levels and are being pursued for therapeutic use.[4][5] Anandamide has an effect on both the CB1 and CB2 receptors
Patients who suffered from PTSD had over a 50% reduction in their anandamide levels
Anandamide is an important neurotransmitter, that’s also considered to be the “body’s own THC.” In fact, as it’s a source of joy and happiness, it’s often called the body’s “bliss molecule.” Cannabis can help correct this clinical deficiency. Interestingly, other activities including exercise or eating dark chocolate, stimulate production of anandamide.
Neurogenesis: Re-growing brain cells
In the mammalian brain, the CB1 receptor is one of the most abundant G protein–coupled receptors, accounting for most, if not all, of the centrally mediated effects of cannabinoids (5). both embryonic and adult hippocampal NS/PCs express CB1 receptors. The hippocampal dentate gyrus in the adult mammalian brain contains neural stem/progenitor cells (NS/PCs)
known for many years, that depletion of the neurotransmitter serotonin in the brain leads to depression.
The anti-depressant and intoxicating effects of cannabis are due to its chemical similarity to natural substances in the brain known as "endo-cannabinoids," which are released under conditions of high stress or pain, They interact with the brain through structures called cannabinoid CB1 receptors. these receptors have a direct effect on the cells producing serotonin, (cannabinoids increase activity in the neurons that produce serotonin) which is a neurotransmitter that regulates the mood. CBD is postulated to act as an agonist to the 5HT1areceptor. Activation of the 5HT1a receptor is understood to modulate the release of serotonin in the brain. This hypothesis was confirmed in a study in which mice were pretreated with a 5HT1a antagonist, the antidepressant effects of CBD were absent. Further evidence of the role of 5HT1a is given by the observed similarities of CBD and isapirone (a 5HT1a partial agonist) in public speaking model.
Anandamide: The Bliss molecule, a fatty acid neurotransmitter
Anandamide is also known as N-arachidonoylethanolamine or AEA, and is an endogenous analogue of tetrahydrocannabinol, or THC. AEA is a fatty acid neurotransmitter responsible for joy, happiness, derived from the non-oxidative metabolism of eicosatetraenoic acid (arachidonic acid) an essential ω-6 polyunsaturated fatty acid. The name is taken from the Sanskrit & Pāli word ananda, which means "joy, bliss, delight", and amide.[1][2] It is synthesized from N-arachidonoyl phosphatidylethanolamine by multiple pathways.[3] It is degraded primarily by the fatty acid amide hydrolase (FAAH) enzyme, which converts anandamide into ethanolamine and arachidonic acid. As such, inhibitors of FAAH lead to elevated anandamide levels and are being pursued for therapeutic use.[4][5] Anandamide has an effect on both the CB1 and CB2 receptors
Patients who suffered from PTSD had over a 50% reduction in their anandamide levels
Anandamide is an important neurotransmitter, that’s also considered to be the “body’s own THC.” In fact, as it’s a source of joy and happiness, it’s often called the body’s “bliss molecule.” Cannabis can help correct this clinical deficiency. Interestingly, other activities including exercise or eating dark chocolate, stimulate production of anandamide.
Neurogenesis: Re-growing brain cells
In the mammalian brain, the CB1 receptor is one of the most abundant G protein–coupled receptors, accounting for most, if not all, of the centrally mediated effects of cannabinoids (5). both embryonic and adult hippocampal NS/PCs express CB1 receptors. The hippocampal dentate gyrus in the adult mammalian brain contains neural stem/progenitor cells (NS/PCs)
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Figure 1
Expression of CB1 receptors in NS/PCs. (A) Coimmunofluorescent staining of CB1 and nestin in cultured hippocampal NS/PCs derived from E17 embryos. Hoechst staining was conducted to reveal the total cultured cells. The arrow indicates the glial-like cells, ... 
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capable of generating new neurons, i.e., neurogenesis. Most drugs of abuse examined to date decrease adult hippocampal neurogenesis, but the effects of cannabis (marijuana or cannabinoids) on hippocampal neurogenesis DOES promote neurogenesis. This study aimed at investigating the potential regulatory capacity of the potent synthetic cannabinoid HU210 on hippocampal neurogenesis and its possible correlation with behavioral changeis below in clinical studies. The hippocampal NS/PCs are immunoreactive for CB1 cannabinoid receptors, indicating that cannabinoids act on CB1 receptors to regulate neurogenesis. This hypothesis is supported by further findings that HU210 promotes proliferation, but not differentiation, of cultured embryonic hippocampal NS/PCs likely via a sequential activation of CB1 receptors, Gi/o proteins, and ERK signaling. Chronic, but not acute, HU210 treatment promoted neurogenesis in the hippocampal dentate gyrus of adult rats and exerted anxiolytic- and antidepressant-like effects. X-irradiation of the hippocampus blocked both the neurogenic and behavioral effects of chronic HU210 treatment, suggesting that chronic HU210 treatment produces anxiolytic- and antidepressant-like effects likely via promotion of hippocampal neurogenesis.
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Aversive Memory Extinction:
Remove traumatic memories Another way cannabis helps with PTSD is through a mechanism called “aversive memory extinction.” PTSD patients frequently complain of recurrent memories of traumatic events. THC actually helps patients “forget” these memories ( Specifically the (-) memories to a point where they are far less painful. Acquisition and storage of aversive memories is one of the basic principles of central nervous systems throughout the animal kingdom1. In the absence of reinforcement, the resulting behavioural response will gradually diminish to be finally extinct. Despite the importance of extinction2, its cellular mechanisms are largely unknown. The cannabinoid receptor 1 (CB1)3 and endocannabinoids4 are present in memory-related brain areas5, 6 and modulate memory7, 8. Here we show that the endogenous cannabinoid system has a central function in extinction of aversive memories. CB1-deficient mice showed strongly impaired short-term and long-term extinction in auditory fear-conditioning tests, with unaffected memory acquisition and consolidation. Treatment of wild-type mice with the CB1 antagonist SR141716A mimicked the phenotype of CB1-deficient mice, revealing that CB1 is required at the moment of memory extinction. Consistently, tone presentation during extinction trials resulted in elevated levels of endocannabinoids in the basolateral amygdala complex, a region known to control extinction of aversive memories9. In the basolateral amygdala, endocannabinoids and CB1 were crucially involved in long-term depression of GABA (-aminobutyric acid)-mediated inhibitory currents. We propose that endocannabinoids facilitate extinction of aversive memories through their selective inhibitory effects on local inhibitory networks in the amygdala. Clinical Studies:
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Cr. Kristi Webb
Understanding Mental Health PTSD, Anxiety, Depression etc. Veterans, PTSD, & Cannabis
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Study - 2005 ~ Nov 1; 115(11): 3104–3116. Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects
2005 - Study ~ New Antidepressant Drug Increases 'Brain's Own Cannabis'
2006 - Study ~ Decreased depression in marijuana users
2009 - Study ~ Impairments in Endocannabinoid Signaling and Depressive Illness.
Study - 2013 ~ Apr;226(4):781-92 Cannabidiol enhances consolidation of explicit fear extinction in humans.
Patents
US6630507 Cannabiniods as antioxidants & neuroprotectants
For More Clinical Studies Check out,
2005 - Study ~ New Antidepressant Drug Increases 'Brain's Own Cannabis'
2006 - Study ~ Decreased depression in marijuana users
2009 - Study ~ Impairments in Endocannabinoid Signaling and Depressive Illness.
Study - 2013 ~ Apr;226(4):781-92 Cannabidiol enhances consolidation of explicit fear extinction in humans.
Patents
US6630507 Cannabiniods as antioxidants & neuroprotectants
For More Clinical Studies Check out,
- List of Cannabis Studies
- List of Endocannabiniods & Cannabis Studies
- List of THC & Cannabis Studies
- List of CBD & Cannabis Studies
