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"ADD" / "ADHD"
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Preferred Strains
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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MSNBC News
Dr. Reports Children improve in school Administered orally helps Cannabinoids last throughout the day with focus, calm, & Happy |
David Bearman MD.
Grades go From D's & E's To A's & B's A simplified Breakdown Cannabinoids produce retrograde inhibition & Homeostasis |
testimonial
Mother Treats 6 year old cannabis tincture The oil is working so well they are starting to try it with other issues |
ADD / ADHD, Overview:
Attention deficit disorder or attention deficit hyperactivity disorder (ADD/ADHD) is a neurological disorder characterized by impulsiveness, inattention and hyperactivity. ADD/ADHD is one of a group of neuropsychiatric conditions (that also includes schizophrenia and autism) now linked to a dysfunctional endocannabinoid system.
ADHD are mostly involved in dopaminergic signalling—which is now known to be modulated in part by compounds related to the endocannabinoid system,
ADHD are mostly involved in dopaminergic signalling—which is now known to be modulated in part by compounds related to the endocannabinoid system,
Attention deficit hyperactivity disorder (ADHD) is one of the most common childhood disorders. ADHD is a broad term, and the condition can vary from person to person. There are an estimated 6.4 million diagnosed children in the United States, according to the Centers for Disease Control and Prevention. Attention deficit hyperactivity disorder (ADHD) is a mental disorder of the neurodevelopmental type.[9][10] It is characterized by problems paying attention, excessive activity, or difficulty controlling behavior which is not appropriate for a person's age.[1][2] The symptoms appear before a person is 12 years old, are present for more than six months, and cause problems in at least two settings (such as school, home, or recreational activities).[3][11] In children, problems paying attention may result in poor school performance.[1] Although it causes impairment, particularly in modern society, many children with ADHD have a good attention span for tasks they find interesting.[12]
This condition is sometimes called attention deficit disorder (ADD), but this is an outdated term. The term was once used to refer to someone who had trouble focusing but was not hyperactive. The American Psychiatric Association released the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) in May 2013. The DSM-5 changed the criteria to diagnose someone with ADHD.
Types of ADHD:
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There are three types of ADHD:
1. Inattentive Inattentive ADHD is what’s usually meant when someone uses the term ADD. This means a person shows enough symptoms of inattention (or easy distractibility) but isn’t hyperactive or impulsive. 2. Hyperactive/impulsive This type occurs when a person has symptoms of hyperactivity and impulsivity but not inattention. 3. Combined Combined ADHD is when a person has symptoms of inattention, hyperactivity, and impulsivity. |
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Hyperactivity & Impulsivity
A doctor may diagnose a child as hyperactive or impulsive if the child:
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Inattention
Inattention, or trouble focusing, is one symptom of ADHD. A doctor may diagnose a child as inattentive if the child:
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Environment
See also: Diet and attention deficit hyperactivity disorderIn addition to genetics, some environmental factors might play a role in causing ADHD.[88] Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD or symptoms like it.[89] Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD.[4][90] Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive.[91] Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.[4][92]
Extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk[4][93] as do certain infections during pregnancy, at birth, and in early childhood. These infections include, among others, various viruses (measles, varicella zoster encephalitis, rubella, enterovirus 71).[94] There is an association between long term but not short term use of acetaminophen during pregnancy and ADHD.[95][96] At least 30% of children with a traumatic brain injury later develop ADHD[97] and about 5% of cases are due to brain damage.[98]
Some studies suggest that in a small number of children, artificial food dyes or preservatives may be associated with an increased prevalence of ADHD or ADHD-like symptoms[4][99] but the evidence is weak and may only apply to children with food sensitivities.[99][100][101] The United Kingdom and the European Union have put in place regulatory measures based on these concerns.[102] In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms.[103]
See also: Diet and attention deficit hyperactivity disorderIn addition to genetics, some environmental factors might play a role in causing ADHD.[88] Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD or symptoms like it.[89] Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD.[4][90] Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive.[91] Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.[4][92]
Extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk[4][93] as do certain infections during pregnancy, at birth, and in early childhood. These infections include, among others, various viruses (measles, varicella zoster encephalitis, rubella, enterovirus 71).[94] There is an association between long term but not short term use of acetaminophen during pregnancy and ADHD.[95][96] At least 30% of children with a traumatic brain injury later develop ADHD[97] and about 5% of cases are due to brain damage.[98]
Some studies suggest that in a small number of children, artificial food dyes or preservatives may be associated with an increased prevalence of ADHD or ADHD-like symptoms[4][99] but the evidence is weak and may only apply to children with food sensitivities.[99][100][101] The United Kingdom and the European Union have put in place regulatory measures based on these concerns.[102] In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms.[103]
Genetics
Twin studies suggest that up to 75% of ADHD cases are genetic in origin, and various studies have shown that the many genes implicated in ADHD are mostly involved in dopaminergic signalling—which is now known to be modulated in part by compounds related to the endocannabinoid system, such as anandamide. There has also been at least one study indicating that infection or trauma to the brain can later lead to development of ADHD.
Typically, a number of genes are involved, many of which directly affect dopamine neurotransmission.[77][78] Those involved with dopamine include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH.[78][79][80] Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF.[77][78] A common variant of a gene called LPHN3 is estimated to be responsible for about 9% of cases and when this variant is present, people are particularly responsive to stimulant medication.[81] The 7 repeat variant of dopamine receptor D4 (DRD4–7R) causes increased inhibitory effects induced by dopamine and is associated with ADHD. The DRD4 receptor is a G protein-coupled receptor that inhibits adenylyl cyclase. The DRD4–7R mutation results in a wide range of behavioral phenotypes, including ADHD symptoms reflecting split attention.[82]
Evolution may have played a role in the high rates of ADHD, particularly hyperactive and impulsive traits in males.[83] Some have hypothesized that some women may be more attracted to males who are risk takers, increasing the frequency of genes that predispose to hyperactivity and impulsivity in the gene pool.[84] Others have claimed that these traits may be an adaptation that help males face stressful or dangerous environments with, for example, increased impulsivity and exploratory behavior.[83][84] In certain situations, ADHD traits may have been beneficial to society as a whole even while being harmful to the individual.[83][84][85] The high rates and heterogeneity of ADHD may have increased reproductive fitness and benefited society by adding diversity to the gene pool despite being detrimental to the individual.[85] In certain environments, some ADHD traits may have offered personal advantages to individuals, such as quicker response to predators or superior hunting skills.[86]
People with Down syndrome are more likely to have ADHD.[87]
Twin studies suggest that up to 75% of ADHD cases are genetic in origin, and various studies have shown that the many genes implicated in ADHD are mostly involved in dopaminergic signalling—which is now known to be modulated in part by compounds related to the endocannabinoid system, such as anandamide. There has also been at least one study indicating that infection or trauma to the brain can later lead to development of ADHD.
Typically, a number of genes are involved, many of which directly affect dopamine neurotransmission.[77][78] Those involved with dopamine include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH.[78][79][80] Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF.[77][78] A common variant of a gene called LPHN3 is estimated to be responsible for about 9% of cases and when this variant is present, people are particularly responsive to stimulant medication.[81] The 7 repeat variant of dopamine receptor D4 (DRD4–7R) causes increased inhibitory effects induced by dopamine and is associated with ADHD. The DRD4 receptor is a G protein-coupled receptor that inhibits adenylyl cyclase. The DRD4–7R mutation results in a wide range of behavioral phenotypes, including ADHD symptoms reflecting split attention.[82]
Evolution may have played a role in the high rates of ADHD, particularly hyperactive and impulsive traits in males.[83] Some have hypothesized that some women may be more attracted to males who are risk takers, increasing the frequency of genes that predispose to hyperactivity and impulsivity in the gene pool.[84] Others have claimed that these traits may be an adaptation that help males face stressful or dangerous environments with, for example, increased impulsivity and exploratory behavior.[83][84] In certain situations, ADHD traits may have been beneficial to society as a whole even while being harmful to the individual.[83][84][85] The high rates and heterogeneity of ADHD may have increased reproductive fitness and benefited society by adding diversity to the gene pool despite being detrimental to the individual.[85] In certain environments, some ADHD traits may have offered personal advantages to individuals, such as quicker response to predators or superior hunting skills.[86]
People with Down syndrome are more likely to have ADHD.[87]
Pathophysiology
Current models of ADHD suggest that it is associated with functional impairments in some of the brain's neurotransmitter systems, particularly those involving dopamine and norepinephrine.[109][110] The dopamine and norepinephrine pathways that originate in the ventral tegmental area and locus coeruleus project to diverse regions of the brain and govern a variety of cognitive processes.[109][111] The dopamine pathways and norepinephrine pathways which project to the prefrontal cortex and striatum are directly responsible for modulating executive function (cognitive control of behavior), motivation, reward perception, and motor function;[109][110][111] these pathways are known to play a central role in the pathophysiology of ADHD.[109][111][112][113] Larger models of ADHD with additional pathways have been proposed.[110][112][113]
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Brain structure
In children with ADHD, there is a general reduction of volume in certain brain structures, with a proportionally greater decrease in the volume in the left-sided prefrontal cortex.[110][114] The posterior parietal cortex also shows thinning in ADHD individuals compared to controls.[110] Other brain structures in the prefrontal-striatal-cerebellar and prefrontal-striatal-thalamic circuits have also been found to differ between people with and without ADHD.[110][112][113] |
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Neurotransmitter pathways
ADD/ADHD is one of a group of neuropsychiatric conditions (that also includes schizophrenia and autism) now linked to a dysfunctional endocannabinoid system.
Abnormal dopamine (DA) transmission in the striatum plays a pivotal role in attention‐deficit/hyperactivity disorder (ADHD). As striatal DA signalling modulates the endocannabinoid system (ECS) it was thought that the elevated number of dopamine transporters in people with ADHD was part of the pathophysiology but it may be that the elevated numbers are due to adaptation to exposure to stimulants.[115] Current models involve the mesocorticolimbic dopamine pathway and the locus coeruleus-noradrenergic system.[109][110][111] Also reduced anandamide levels, specifically in striatum, the dopamine nerve terminal region. Furthermore, three distinct indirect endocannabinoid agonists, the selective anandamide reuptake inhibitors AM404 and VDM11 and the fatty acid amidohydrolase inhibitor AA5HT, attenuated spontaneous hyperlocomotion in DAT KO mice. The hypolocomotor effects of AM404, VDM11, and AA5HT were significantly attenuated by co-administration of the transient receptor potential vanilloid 1 (TRPV1) antagonist capsazepine but not the selective cannabinoid type 1 (CB1)receptor antagonist AM251.ADHD psychostimulants possess treatment efficacy because they increase neurotransmitter activity in these systems.[110][111][116] There may additionally be abnormalities in serotoninergic, glutamatergic, or cholinergic pathways.[116][117][118]
Associated disorders
In children, ADHD occurs with other disorders about 2⁄3 of the time.[12] Some commonly associated conditions include:
In children, ADHD occurs with other disorders about 2⁄3 of the time.[12] Some commonly associated conditions include:
- Learning disabilities have been found to occur in about 20–30% of children with ADHD. Learning disabilities can include developmental speech and language disorders and academic skills disorders.[48] ADHD, however, is not considered a learning disability, but it very frequently causes academic difficulties.[48]
- Tourette syndrome has been found to occur more commonly in the ADHD population.[1]
- Oppositional defiant disorder (ODD) and conduct disorder (CD), which occur with ADHD in about 50% and 20% of cases respectively.[49] They are characterized by antisocial behaviors such as stubbornness, aggression, frequent temper tantrums, deceitfulness, lying, and stealing.[50] About half of those with hyperactivity and ODD or CD develop antisocial personality disorder in adulthood.[51] Brain imaging supports that conduct disorder and ADHD are separate conditions.[52]
- Primary disorder of vigilance, which is characterized by poor attention and concentration, as well as difficulties staying awake. These children tend to fidget, yawn and stretch and appear to be hyperactive in order to remain alert and active.[53]
- Sluggish cognitive tempo (SCT) is a cluster of symptoms that potentially comprises another attention disorder. It may occur in 30–50% of ADHD cases, regardless of the subtype.[54]
- Mood disorders (especially bipolar disorder and major depressive disorder). Boys diagnosed with the combined ADHD subtype are more likely to have a mood disorder.[55] Adults with ADHD sometimes also have bipolar disorder, which requires careful assessment to accurately diagnose and treat both conditions.[56]
- Anxiety disorders have been found to occur more commonly in the ADHD population.[55]
- Obsessive-compulsive disorder (OCD) can co-occur with ADHD and shares many of its characteristics.[50]
- Substance use disorders. Adolescents and adults with ADHD are at increased risk of substance abuse.[19] This is most commonly seen with alcohol The reason for this may be an altered reward pathway in the brains of ADHD individuals.[19] This makes the evaluation and treatment of ADHD more difficult, with serious substance misuse problems usually treated first due to their greater risks.[57][58]
- Restless legs syndrome has been found to be more common in those with ADHD and is often due to iron deficiency anaemia.[59][60] However, restless legs can simply be a part of ADHD and requires careful assessment to differentiate between the two disorders.[61]
- Sleep disorders and ADHD commonly co-exist. They can also occur as a side effect of medications used to treat ADHD. In children with ADHD, insomnia is the most common sleep disorder with behavioral therapy the preferred treatment.[62][63] Problems with sleep initiation are common among individuals with ADHD but often they will be deep sleepers and have significant difficulty getting up in the morning.[64] Melatonin is sometimes used in children who have sleep onset insomnia.[65]
- People with ADHD have an increased risk of persistent bed wetting.[66]
- A 2016 systematic review found a well established association between ADHD and obesity, asthma and sleep disorders, and tentative evidence for association with celiac disease and migraine,[67] while another 2016 systematic review did not support a clear link between celiac disease and ADHD, and stated that routine screening for celiac disease in people with ADHD is discouraged.[68]
~ How Cannabis AIds ~
The Endo-cannabinoid systems direct role in Cognitive & Pyschomotor Development
From the reproductive process, through the development Stages and Adulthood.
The Endo-cannabinoid systems direct role in Cognitive & Pyschomotor Development
From the reproductive process, through the development Stages and Adulthood.
Prenatal disruption of the endocannabinoid system may be an underlying cause of ADHD. Correct functioning of the endocannabinoids anandamide and 2-AG, along with the cannabinoid receptors themselves, have been repeatedly demonstrated to play a fundamental role in the normal cognitive and psychomotor development of developing infants, not just in humans but also in various animal models. Endocannabinoids exert a neurotrophic effect on developing mesencephalic dopamine neurons. Since an altered mesocorticolimbic system seems to underlie hyperactivity and attention deficit in clinical and animal studies of attention deficit hyperactivity disorder (ADHD),
The balance between novelty-seeking behaviour and the development of risk-averse behavioural inhibition is fundamental to normal psychomotor development, and it is known that the endocannabinoid system has an integral role to play in the management of this important balance. Excessive novelty-seeking coupled with reduced behavioural inhibition is a key feature of ADHD. Different compounds that inhibit the uptake of anandamide (either directly or by inhibiting the release of the anandamide-degrading enzyme, fatty acid amide hydrolase or FAAH) cause levels of naturally-produced anandamide to increase in the bloodstream, and are increasingly being found to exert a range of important effects throughout all stages of life.
Anandamide is fundamentally important to countless developmental processes necessary for proper cognitive and psychomotor performance. Anandamide (or the mimicker phyto-cannabinoids, cannabis) has a role to play at every stage of the reproductive process, from influencing parental fertility, to overseeing embryonic implantation into the uterus, to guiding the development of the brain and central nervous system in the foetus and we can't forget its dominant role in the Immune system.
Due to this growing awareness of the importance of anandamide and the endo-cannabinoid system, serious consideration is now being given to the hypothesis that prenatal disturbances to the endocannabinoid system underlie the later development of a range of neuropsychiatric disorders including autism, schizophrenia, ADHD and more.
An Italian study investigated the relationship between cannabinoid, anandamide and ADHD by administering the anandamide reuptake inhibitor AM404 to pregnant rats from the Naples High Excitability (NHE) lineage, which is well-known to exhibit hyperactivity and other ADHD-like symptoms. The researchers found that NHE rats administered with AM404 exhibited reduced hyperactivity and increased attention spans compared to NHE rats given placebo.
These data suggest that reduced anandamide levels in pregnant NHE rats may underlie ADHD-symptoms, and that elevating anandamide levels are likely to have therapeutic potential in human ADHD.
A studies are showing when (mice) bred to lack CB1-receptors either in the glutaminergic or the GABAergic neurons (brain cells that produce glutamine and gamma-Aminobutyric acid respectively) found that glutaminergic CB1-deficient mice exhibited reduced novelty-seeking while those lacking in GABAergic neurons exhibited reduced behavioural inhibitions. Thus, activation of the CB1-receptors can exert the opposite functions on novelty-seeking and behavioral inhibition, depending on the type of neuron in question. This demonstrates that the correct functioning of the ECS in relation to impulsive behaviours is a finely-tuned and complex system, and disorders such as ADHD can result if the balance is disrupted.
Cannabis (THC) is an anandamide agonist, that is it stimulates the anandamide (CB1) receptor sites. Anandamide—sometimes called the “bliss chemical”—Regulates ie. slows down the rate of neurotransmission if needed ( As cannabis up & Down-regulates), and that stimulating anandamide receptors also stimulates Renshaw cells, which turn off some cells that provide sensory input. The overall effect would be to increase the ability to regulate behavior and reduce the overstimulation that causes ADHD brains to become distracted.
The balance between novelty-seeking behaviour and the development of risk-averse behavioural inhibition is fundamental to normal psychomotor development, and it is known that the endocannabinoid system has an integral role to play in the management of this important balance. Excessive novelty-seeking coupled with reduced behavioural inhibition is a key feature of ADHD. Different compounds that inhibit the uptake of anandamide (either directly or by inhibiting the release of the anandamide-degrading enzyme, fatty acid amide hydrolase or FAAH) cause levels of naturally-produced anandamide to increase in the bloodstream, and are increasingly being found to exert a range of important effects throughout all stages of life.
Anandamide is fundamentally important to countless developmental processes necessary for proper cognitive and psychomotor performance. Anandamide (or the mimicker phyto-cannabinoids, cannabis) has a role to play at every stage of the reproductive process, from influencing parental fertility, to overseeing embryonic implantation into the uterus, to guiding the development of the brain and central nervous system in the foetus and we can't forget its dominant role in the Immune system.
Due to this growing awareness of the importance of anandamide and the endo-cannabinoid system, serious consideration is now being given to the hypothesis that prenatal disturbances to the endocannabinoid system underlie the later development of a range of neuropsychiatric disorders including autism, schizophrenia, ADHD and more.
An Italian study investigated the relationship between cannabinoid, anandamide and ADHD by administering the anandamide reuptake inhibitor AM404 to pregnant rats from the Naples High Excitability (NHE) lineage, which is well-known to exhibit hyperactivity and other ADHD-like symptoms. The researchers found that NHE rats administered with AM404 exhibited reduced hyperactivity and increased attention spans compared to NHE rats given placebo.
These data suggest that reduced anandamide levels in pregnant NHE rats may underlie ADHD-symptoms, and that elevating anandamide levels are likely to have therapeutic potential in human ADHD.
A studies are showing when (mice) bred to lack CB1-receptors either in the glutaminergic or the GABAergic neurons (brain cells that produce glutamine and gamma-Aminobutyric acid respectively) found that glutaminergic CB1-deficient mice exhibited reduced novelty-seeking while those lacking in GABAergic neurons exhibited reduced behavioural inhibitions. Thus, activation of the CB1-receptors can exert the opposite functions on novelty-seeking and behavioral inhibition, depending on the type of neuron in question. This demonstrates that the correct functioning of the ECS in relation to impulsive behaviours is a finely-tuned and complex system, and disorders such as ADHD can result if the balance is disrupted.
Cannabis (THC) is an anandamide agonist, that is it stimulates the anandamide (CB1) receptor sites. Anandamide—sometimes called the “bliss chemical”—Regulates ie. slows down the rate of neurotransmission if needed ( As cannabis up & Down-regulates), and that stimulating anandamide receptors also stimulates Renshaw cells, which turn off some cells that provide sensory input. The overall effect would be to increase the ability to regulate behavior and reduce the overstimulation that causes ADHD brains to become distracted.
Dopamine: Hypolocomotor/Hyperactivity
Cannabis Aiding In Neuroregulation of Hyperactivity
Cannabis Aiding In Neuroregulation of Hyperactivity
There are reduced anandamide (Cannabinoids) levels, specifically in striatum, the dopamine nerve terminal region in ADHD patients. By supplementing Cannabinoids with eg. Cannabis, three distinct indirect endocannabinoid agonists are activated, the selective anandamide reuptake inhibitors AM404 and VDM11 and the fatty acid amidohydrolase inhibitor AA5HT,reducing dopamine and attenuating spontaneous hyperlocomotion. The hypolocomotor effects of cannabinoid induced AM404, VDM11, and AA5HT were significantly attenuated by co-administration of the transient receptor potential vanilloid 1 (TRPV,) (Vanailloid TRPV receptor, is another receptor also directly regulated/induced/activated by cannabinoids/cannabis) antagonist capsazepine but not the selective cannabinoid type 1 (CB1)receptor antagonist AM251. Through this function cannabinoids/cannabis facilitates regulation of neurotransmittion calming persons in a hypo state. Restoring endocannabinoid homeostasis in active synapses constitute an alternative therapeutic strategy for disorders associated with hyperdopaminergia. In this process, TRPV1 receptors seem to play a key role and represent a novel promising pharmacological target for cannabinoid therapy.
Serotonin
Imaging studies revealed that cannabis alters PFC regional cerebral blood flow by arterial dialation and increase metabolic activity, increases blood flow, & Oxygen. As well The degree that cannabis generates homeostasis, facilitating positive state of mind increasing concentration, through the metabolic function increase blood flow & calm biological systems, was correlated with subjective effects, and the pattern was consistent with CB1R localization (Volkow et al., 1991; Matthew et al., 2002). Third, CB1R agonism alters 5-HT1A and 5HT2A receptor-mediated behavioral responses (Hill et al., 2006) and inhibits 5-HT reuptake 5-HT is believed to be responsible for mood control and implicated in antidepressant-like actions. Research evidences have pointed out the action of CBD in the serotonin (5-HT) system and related neurons. Administration of CB1R agonists such as phytocannabinoids into the ventromedial prefrontal cortex of the brain has resulted in enhanced 5-HT neuronal activity and CB1R-dependent antidepressant-like effects in the experimental animals. This study clearly shows the dose-dependent antidepressant benefit of CBD, which can be particularly useful for the treatment of mood disorders
Norepinephrine
Cannabinoids also affect autonomic tone.
In the sympathetic nervous system, cannabinoids will dampen sympathetically mediated pain and modulate the hypothalamic- pituitary-adrenal axis and the hypothalamic locus coerulius-norepinephrine axis.
CB1 receptor stimulation can inhibit noroepinephrine release which in turn helps reduce hyperactivity (gidders)
In the sympathetic nervous system, cannabinoids will dampen sympathetically mediated pain and modulate the hypothalamic- pituitary-adrenal axis and the hypothalamic locus coerulius-norepinephrine axis.
CB1 receptor stimulation can inhibit noroepinephrine release which in turn helps reduce hyperactivity (gidders)
Neurological
It has been recently demonstrated that CBD promotes cerebral neurogenesis , and even more specifically related CBD promotes CNS & hippocampal neurogenesis by activating CB1 receptors [39](As dose THC by also activating the CB 1 receptor. Such an assumption was supported by the observation that the CBD neurogenic effect was lost in mice with the CB1 receptor knocked-out, suggesting that the pro-neurogenic action of this phytocannabinoid was clearly dependent on the interaction at the CB1 receptor, which shows a wide expression over the entire DG, including the neuronal precursor cells. Trials are also showing that on top of the healing properties of CBD. CBD-mediated activation of PPARγ is associated with a significant neurogenic activity in the granule cell layer of the hippocampal DG. Moreover, CBD mediated activation of PPARγ has been reported to promote neurogenesis and agonists at these receptors regulate neuronal stem cell proliferation and differentiation as well [37]. In addition PPARγ activation promotes neurite outgrowth in mature neurons, significantly contributing to a proper neuronal connectivity in neuronal networks [38]. Moreover, with CBD regulating the immune system, through the suppressing of pro-inflammatory proteins and the suppression of the fat protein Beta-Amyloid which in itself promotes cellular inflammation and neurological miss-fire in the brain & nervous system,
Neuro Expression & gene Transcription:
Cannabis Facilitating gene & Neurogenesis & Plasticity
Cannabis Facilitating gene & Neurogenesis & Plasticity
Endogenous cannabinoid (eg. THC, CBD) ligand interaction with cannabinoid type 1 receptor is highly expressed in the cortex, substantia nigra pars reticulata, globus pallidus, cerebellum, hippocampus, and brainstem, thereby modulating a wide range of neural functions, making the activation of the type 1 receptors directly aid in the areas in question for AD, PD, Autism, bipolar, MS, Tourette's, etc. such as motor activity, learning, and memory. CB1R, located presynaptically on GABA and glutamate neurons, decreases their release by inhibition of presynaptic Ca2+ influx through voltage-gated Ca2+ channels (VGCCs). CB1R activation is coupled with inhibition of adenylyl cyclase, downregulation of the cAMP/PKA pathway, and activation of the MAP kinase/ERK pathway, thereby regulating expression of genes through gene modulation transcription, recoding the potentially missing coded genetic script. eCBs are the best characterized retrograde messenger for carrying out neurological actions of endocannabinoids. Cannabinoids activate the enzyme phospholipase Cb (PLCb), which triggers short and long term plasticity aiding in the repair of damaged neurons, common within a neuropsychiatric disorder (Hashimotodani et al., 2007). eCBs interaction with CB1R is capable of inducing presynapsis forms (eCB-LTD) at both excitatory and inhibitory synapses.
Clinical Studies
Study - 2006 Mar - Endocannabinoids activate transient receptor potential vanilloid 1 receptors to reduce hyperdopaminergia- related hyperactivity: therapeutic implications.
Study - 31 October 2011- Loss of striatal cannabinoid CB1 receptor function in attention‐deficit / hyperactivity disorder mice with point‐mutation of the dopamine transporter
Study - 2003, - Prenatal elevation of endocannabinois corrects the unbalance between dopamine systems and reduces activity in the Naples High Excitability rats
Study - 31 October 2011- Loss of striatal cannabinoid CB1 receptor function in attention‐deficit / hyperactivity disorder mice with point‐mutation of the dopamine transporter
Study - 2003, - Prenatal elevation of endocannabinois corrects the unbalance between dopamine systems and reduces activity in the Naples High Excitability rats
