The safety and efficacy of 3% Cannabis seeds extract cream for reduction of human cheek skin sebum and erythema content.

Posted on July 6, 2015 by David

“Escalated sebum fabrication is seen with an unattractive look and adds to the growth of acne. We aimed to investigate the efficacy and safety of 3%Cannabis seeds extract cream on human cheek skin sebum and erythema content.

For this purpose, base plus 3% Cannabis seeds extract and base (control) were prepared for single blinded and comparative study. Healthy males were instructed to apply the base plus 3% Cannabis seeds extract and base twice a day to their cheeks for 12 weeks.

Adverse events were observed to determine skin irritation. Measurements for sebum and erythema content were recorded at baseline, 2nd, 4th, 6th, 8th, 10th and 12th week in a control room with Sebumeter and Mexameter.

Base plus 3% Cannabis seeds extract was found to be safe in volunteers.

Measurements demonstrated that skin sebum and erythema content of base plus 3%Cannabis seeds extract treated side showed significant decrease (p<0.05) compared with base treated side.

Base plus 3% Cannabis seeds extract showed safety.

It was well tolerated for the reduction of skin sebum and erythema content.

Its improved efficacy could be suggested for treatment of acne vulgaris, seborrhea, papules and pustules to get attractive facial appearance.”

http://www.ncbi.nlm.nih.gov/pubmed/26142529

Modulatory effects by CB1 receptors on rat spinal locomotor networks after sustained application of agonists or antagonists.

Posted on July 2, 2015 by David

“Sustained administration of cannabinoid agonists acting on neuronal CB1 receptors (CB1Rs) are proposed for treating spasticity and chronic pain…

Our data suggest that CB1Rs may control the circuit gateway regulating the inflow of sensory afferent inputs into the locomotor circuits, indicating a potential site of action for restricting peripheral signals disruptive for locomotor activity.”

http://www.ncbi.nlm.nih.gov/pubmed/26126926

Roles for the endocannabinoid system in ethanol-motivated behavior.

Posted on July 1, 2015 by David

“Alcohol use disorder represents a significant human health problem that leads to substantial loss of human life and financial cost to society. Currently available treatment options do not adequately address this human health problem, and thus, additional therapies are desperately needed.

The endocannabinoid system has been shown, using animal models, to modulate ethanol-motivated behavior, and it has also been demonstrated that chronic ethanol exposure can have potentially long-lasting effects on the endocannabinoid system.

For example, chronic exposure to ethanol, in either cell culture or preclinical rodent models, causes an increase in endocannabinoid levels that results in down-regulation of the cannabinoid receptor 1 (CB1) and uncoupling of this receptor from downstream G protein signaling pathways.

Using positron emission tomography (PET), similar down-regulation of CB1 has been noted in multiple regions of the brain in human alcoholic patients.

In rodents, treatment with the CB1 inverse agonist SR141716A (Rimonabant), or genetic deletion of CB1 leads to a reduction in voluntary ethanol drinking, ethanol-stimulated dopamine release in the nucleus accumbens, operant self-administration of ethanol, sensitization to the locomotor effects of ethanol, and reinstatement/relapse of ethanol-motivated behavior.

Although the clinical utility of Rimonabant or other antagonists/inverse agonists for CB1 is limited due to negative neuropsychiatric side effects, negative allosteric modulators of CB1 and inhibitors of endocannabinoid catabolism represent therapeutic targets worthy of additional examination.”

http://www.ncbi.nlm.nih.gov/pubmed/26123153

Δ-9 Tetrahydrocannabinol inhibits growth and metastasis of lung cancer.

Posted on June 29, 2015 by David

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“Lung cancer is the major cause of cancer-related mortality worldwide.

Many of these over-express epidermal growth factor receptor (EGFR), and are usually highly aggressive and resistant to chemotherapy.

Recent studies have shown that Δ-9 Tetrahydrocannabinol (THC), the major component of Cannabis sativa, possess anti-tumor properties against various types of cancers.

However, not much is known about its effect on lung cancer. In this study, we sought to characterize the effect of THC on EGF-induced growth and metastasis of human non small lung cancer cell (NSCLC) lines A549 and SW-1573.

We demonstrate that these cell lines and primary tumor samples derived from lung cancer patients express cannabinoids receptors CB₁ and CB₂, the known targets for THC action.

We further show that THC inhibits EGF-induced growth in these cell lines.

In addition THC attenuated EGF-stimulated chemotaxis and chemoinvasion.

Next we characterized the effect of THC on in vivo lung cancer growth and metastasis in a murine model. A549 cells were implanted in SCID mice (n=6 per group) through subcutaneous and intravenous injections to generate subcutaneous and lung metastatic cancer, respectively. THC (5mg/kg body wt.) was administered once daily through intraperitoneal injections for 21 days. The mice were analyzed for tumor growth and lung metastasis.

A significant reduction (~50%) in tumor weight and volume were observed in THC treated animals compared to the vehicle treated animals.

THC treated animals also showed a significant (~60%) reduction in macroscopic lesions on the lung surface in comparison to vehicle treated control.

Immunohistochemical analysis of the tumor samples from THC treated animals revealed anti-proliferative and anti-angiogenic effects of THC with significant reduction in staining for Ki67, a proliferative marker and CD31, an endothelial marker indicative of vascularization. Investigation into the signaling events associated with reduced EGF-induced functional effects revealed that THC also inhibits EGF-induced Akt phosphorylation. Akt is a central signaling molecule of EGFR-mediated signaling pathways and it regulates a diverse array of cellular functions, including proliferation, angiogenesis, invasion and apoptosis.

Cumulatively, these studies indicate that THC has anti-tumorigenic and anti-metastatic effects against lung cancer. Novel therapies against EGFR overexpressing, aggressive and chemotherapy resistant lung cancers may include targeting the cannabinoids receptors.”

http://cancerres.aacrjournals.org/content/67/9_Supplement/4749.short

http://www.thctotalhealthcare.com/category/lung-cancer/

Ultralow doses of cannabinoid drugs protect the mouse brain from inflammation-induced cognitive damage.

Posted on June 28, 2015 by David

“In our previous studies, we found that a single ultralow dose of tetrahydrocannabinol (THC)… protects the brain from different insults that cause cognitive deficits.

Because various insults may trigger a neuroinflammatory response that leads to secondary damage to the brain, the current study tested whether this extremely low dose of THC could protect the brain from inflammation-induced cognitive deficits…

Our results suggest that an ultralow dose of THC that lacks any psychotrophic activity protects the brain from neuroinflammation-induced cognitive damage and might be used as an effective drug for the treatment of neuroinflammatory conditions, including neurodegenerative diseases.”

http://www.ncbi.nlm.nih.gov/pubmed/25042014

Drug-drug interaction between clobazam and cannabidiol in children with refractory epilepsy.

Posted on June 27, 2015 by David

“Under an expanded access investigational new drug (IND) trial, cannabidiol (CBD) is being studied as a possible adjuvant treatment of refractory epilepsy in children.

Of the 25 subjects in the trial, 13 were being treated with clobazam (CLB). Because CLB and CBD are both metabolized in the cytochrome P450 (CYP) pathway, we predicted a drug-drug interaction, which we evaluate in this article…

Monitoring of CLB and nCLB levels is necessary for clinical care of patients concomitantly on CLB and CBD.

Nonetheless, CBD is a safe and effective treatment of refractory epilepsy in patients receiving CLB treatment.”

http://www.ncbi.nlm.nih.gov/pubmed/26114620

http://www.thctotalhealthcare.com/category/epilepsy-2/

Activation of cannabinoid receptors prevents antigen-induced asthma-like reaction in guinea pigs.

Posted on June 24, 2015 by David

“In this study we evaluated the effects of the CB1/CB2 cannabinoid receptor agonist on antigen-induced asthma-like reaction in sensitized guinea pigs…

These findings suggest that targeting cannabinoid receptors could be a novel preventative therapeutic strategy in asthmatic patients.”

http://www.ncbi.nlm.nih.gov/pubmed/18266975

Evaluation of Serum Cytokines Levels and the Role of Cannabidiol Treatment in Animal Model of Asthma.

Posted on June 24, 2015 by David

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“Asthma represents a public health problem and traditionally is classified as an atopic disease, where the allergen can induce clinical airway inflammation, bronchial hyperresponsiveness, and reversible obstruction of airways.

Studies have demonstrated the presence of T-helper 2 lymphocytes in the lung of patients with asthma. These cells are involved in cytokine production that regulates immunoglobulin synthesis.

Recognizing that T cell interaction with antigens/allergens is key to the development of inflammatory diseases, the aim of this study is to evaluate the anti-inflammatory potential of cannabidiol (CBD) in this setting.

CBD treatment was able to decrease the serum levels of all analyzed cytokines except for IL-10 levels.

CBD seems to be a potential new drug to modulate inflammatory response in asthma.” http://www.ncbi.nlm.nih.gov/pubmed/26101464

“In conclusion, we here demonstrate that the administration of CBD in an animal model of asthma could blunt the serum cytokine response to OVA in sensitized animals. These effects suggest a potential for a new asthma treatment since CBD controls the exaggerated inflammatory response observed in this model.” https://www.hindawi.com/journals/mi/2015/538670/

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

Medical Marijuana for Treatment of Chronic Pain and Other Medical and Psychiatric Problems: A Clinical Review.

Posted on June 24, 2015 by David

“Use of marijuana for chronic pain, neuropathic pain, and spasticity due to multiple sclerosis is supported by high-quality evidence.

Several of these trials had positive results, suggesting that marijuana or cannabinoids may be efficacious for these indications.

CONCLUSIONS AND RELEVANCE:

Medical marijuana is used to treat a host of indications, a few of which have evidence to support treatment with marijuana and many that do not. Physicians should educate patients about medical marijuana to ensure that it is used appropriately and that patients will benefit from its use.”

http://www.ncbi.nlm.nih.gov/pubmed/26103031

Cannabinoids for Medical Use: A Systematic Review and Meta-analysis.

Posted on June 24, 2015 by David

“Cannabis and cannabinoid drugs are widely used to treat disease or alleviate symptoms, but their efficacy for specific indications is not clear.

To conduct a systematic review of the benefits and adverse events (AEs) of cannabinoids.

There was moderate-quality evidence to support the use of cannabinoids for the treatment of chronic pain and spasticity. There was low-quality evidence suggesting that cannabinoids were associated with improvements in nausea and vomiting due to chemotherapy, weight gain in HIV infection, sleep disorders, and Tourette syndrome.

Cannabinoids were associated with an increased risk of short-term AEs. Common AEs included dizziness, dry mouth, nausea, fatigue, somnolence, euphoria, vomiting, disorientation, drowsiness, confusion, loss of balance, and hallucination.”

http://www.ncbi.nlm.nih.gov/pubmed/26103030

http://jama.jamanetwork.com/article.aspx?articleid=2338251