Opioid abuse and hospitalization rates in patients with schizophrenia.

“Substance abuse worsens the course of schizophrenia, but it is not known whether or not there are differences between specific substances concerning their association with the hospitalizations of patients with schizophrenia.

The primary aims of this study were to examine the possible associations between amphetamine, cannabis, and opioid abuse, and the risk of hospitalizations among patients with schizophrenia.

The risk of hospitalizations was significantly higher for opioids when compared with amphetamine or cannabis.

Harmful use or dependence of opioids among patients with schizophrenia is associated with significantly higher risk of hospitalizations than either harmful use or dependence of amphetamine or cannabis.”

http://www.ncbi.nlm.nih.gov/pubmed/26313367

Cannabinoids and Schizophrenia: Risks and Therapeutic Potential.

“The endocannabinoid system has been implicated in psychosis both related and unrelated to cannabis exposure, and studying this system holds potential to increase understanding of the pathophysiology of schizophrenia.

Anandamide signaling in the central nervous system may be particularly important.

Δ9-Tetrahydrocannabinol in cannabis can cause symptoms of schizophrenia when acutely administered, and cannabidiol (CBD), another compound in cannabis, can counter many of these effects.

CBD may have therapeutic potential for the treatment of psychosis following cannabis use, as well as schizophrenia, possibly with better tolerability than current antipsychotic treatments. CBD may also have anti-inflammatory and neuroprotective properties.

Establishing the role of CBD and other CBD-based compounds in treating psychotic disorders will require further human research.”

http://www.ncbi.nlm.nih.gov/pubmed/26311150

http://www.thctotalhealthcare.com/category/schizophrenia/

Does cannabis affect dopaminergic signaling in the human brain? A systematic review of evidence to date.

“While abnormalities in multiple pathways may lead to schizophrenia, an abnormality in dopamine neurotransmission is considered to be the final common abnormality.

One would thus expect cannabis use to be associated with dopamine signaling alterations.

This is the first systematic review of all studies, both observational as well as experimental, examining the acute as well as chronic effect of cannabis or its main psychoactive ingredient, THC, on the dopamine system in man…

In man, there is as yet little direct evidence to suggest that cannabis use affects acute striatal dopamine release or affects chronic dopamine receptor status in healthy human volunteers. ”

http://www.ncbi.nlm.nih.gov/pubmed/26068702

Endocannabinoids activate transient receptor potential vanilloid 1 receptors to reduce hyperdopaminergia-related hyperactivity: therapeutic implications.

“Knockout (KO) mice invalidated for the dopamine transporter (DAT) constitute a powerful animal model of neurobiological alterations associated with hyperdopaminergia relevant to schizophrenia and attention-deficit/hyperactivity disorder (ADHD).

CONCLUSIONS:

These data indicate a dysregulated striatal endocannabinoid neurotransmission associated with hyperdopaminergic state.

Restoring endocannabinoid homeostasis in active synapses might 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.”

http://www.ncbi.nlm.nih.gov/pubmed/16199010

Dopaminergic function in cannabis users and its relationship to cannabis-induced psychotic symptoms.

“Substance dependence and schizophrenia are both associated with dopaminergic dysfunction.

It has been proposed, although never directly tested, that the link between cannabis use and schizophrenia is mediated by altered dopaminergic function.

These findings indicate that chronic cannabis use is associated with reduced dopamine synthesis capacity and question the hypothesis that cannabis increases the risk of psychotic disorders by inducing the same dopaminergic alterations seen in schizophrenia.”

http://www.ncbi.nlm.nih.gov/pubmed/23820822

“There is robust evidence that stimulants increase striatal dopamine levels and some evidence that alcohol may have such an effect, but little evidence, if any, that cannabis and opiates increase dopamine levels. Moreover, there is good evidence that striatal dopamine receptor availability and dopamine release are diminished in individuals with stimulant or alcohol dependence but not in individuals with opiate, nicotine or cannabis dependence.”  http://www.ncbi.nlm.nih.gov/pubmed/25873042

The relationship between cannabidiol and psychosis: A review.

“Cannabis sativa is the most widely used illicit drug in the world…

THC is considered responsible for the main psychotropic effects of the drug, while CBD seems to antagonize these effects, particularly those that induce psychosis.

The effects of Cannabis seem to depend on several variables related to the type of plant, its strength, usage patterns, and intersubjective variations.

CBD could be used to treat several conditions, including psychosis, when the current treatment is associated with significant side effects.

…further research involving the possible antipsychotic effect and other potential positive effects of Cannabis are needed.”

http://www.ncbi.nlm.nih.gov/pubmed/25954940

http://www.thctotalhealthcare.com/category/schizophrenia/

Cannabidiol effects in the prepulse inhibition disruption induced by amphetamine.

“Drugs that facilitate dopaminergic neurotransmission such as amphetamine induce PPI disruption in human and rodents.

Clinical and neurobiological findings suggest that the endocannabinoid system and cannabinoids may be implicated in the pathophysiology and treatment of schizophrenia.

Cannabidiol (CBD), a non-psychotomimetic constituent of the Cannabis sativa plant, has also been reported to have potential as an antipsychotic.

Our aim was to investigate if CBD pretreatment was able to prevent PPI disruption induced by amphetamine…

Pretreatment with CBD attenuated the amphetamine-disruptive effects…

These results corroborate findings indicating that CBD induces antipsychotic-like effects.

In addition, they pointed to the nucleus accumbens as a possible site of these effects.”

http://www.ncbi.nlm.nih.gov/pubmed/25943166

http://www.thctotalhealthcare.com/category/schizophrenia/

 

Cannabidiol in medicine: a review of its therapeutic potential in CNS disorders.

“Cannabidiol (CBD) is the main non-psychotropic component of the glandular hairs of Cannabis sativa.

It displays a plethora of actions including anticonvulsive, sedative, hypnotic, antipsychotic, antiinflammatory and neuroprotective properties.

However, it is well established that CBD produces its biological effects without exerting significant intrinsic activity upon cannabinoid receptors.

For this reason, CBD lacks the unwanted psychotropic effects characteristic of marijuana derivatives, so representing one of the bioactive constituents of Cannabis sativa with the highest potential for therapeutic use.

The present review reports the pharmacological profile of CBD and summarizes results from preclinical and clinical studies utilizing CBD, alone or in combination with other phytocannabinoids, for the treatment of a number of CNS disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/18844286

The dopamine theory of addiction: 40 years of highs and lows.

“For several decades, addiction has come to be viewed as a disorder of the dopamine neurotransmitter system; however, this view has not led to new treatments. In this Opinion article, we review the origins of the dopamine theory of addiction and discuss the ability of addictive drugs to elicit the release of dopamine in the human striatum.

There is robust evidence that stimulants increase striatal dopamine levels and some evidence that alcohol may have such an effect, but little evidence, if any, that cannabis and opiates increase dopamine levels.

Moreover, there is good evidence that striatal dopamine receptor availability and dopamine release are diminished in individuals with stimulant or alcohol dependence but not in individuals with opiate, nicotine or cannabis dependence. These observations have implications for understanding reward and treatment responses in various addictions.”

http://www.ncbi.nlm.nih.gov/pubmed/25873042

http://www.thctotalhealthcare.com/category/addiction/