Early bird ends tomorrow. Register today and save $50!

Laboratory, Endocrine, & Neurotransmitter Symposium

October 4 - 6, 2019

Portland, OR

Earn up to 14.5 CME credits!

Approved for 4.25 Pharm CEs from the OBNM!

Gain additional clinical insight and treatment considerations to evaluate some of the most prevalent and challenging conditions that patients present with, including depression, anxiety, altered mental focus and stamina, sexual dysfunction, sleep disturbances, addictions and dependencies, weight management, and chronic disease. Register now to get the early bird price of $329 (reg. $379).

 

Wellness Wednesday

Webinar Series

Topic: Comprehensive Neurotransmitter Primer

By: Laura Neville, ND

September 4, 2019

Join Labrix clinical staff and special guests on the first Wednesday of every month at 9:30 AM and 12:00 PM PST. This free, live webinar series will cover a variety of neuroendocrine topics that will enhance your knowledge, with clinically applicable testing and treatment considerations. 1 CE credit available upon attendee request.

 

AARM

San Diego, CA:

September 12-15, 2019

Make sure to visit our booth at AARM in San Diego. Chat with our booth representatives to learn what's new.

 

IFM (AFMCP)

Seattle, WA:

September 16-20, 2019

Labrix will be in Seattle for the IFM Conference later this month. Come chat with our booth representative and learn more about testing with Doctor's Data and Labrix.

Cannabidiol and Neurotransmitters

 

By Fiona Campbell, ND | September 3, 2019

Cannabidiol (CBD) is a phytocannabinoid that has become widely available in the wake of legalization of cannabis by multiple states. Even in states where cannabis itself has not been legalized, CBD products such as topical creams and lotions, tinctures, and capsules are largely accessible as a result of CBD extraction from legally-grown hemp. These products contain nearly undetectable amounts of tetrahydrocannabinol (THC), which is the main psychoactive component in cannabis. A 2017 study by a cannabis investment group found that CBD is now widely used (both self-prescribed and recommended by practitioners) to replace pharmaceuticals in conditions such as anxiety, insomnia, and depression.1

Phytocannabinoids are plant-derived compounds that interact with the endocannabinoid system in humans and other animals. There are over 100 known phytocannabinoids, with CBD being the most abundant in the cannabis plant. The endocannabinoid system in humans has two primary receptors: CB1 and CB2. The endogenous cannabinoid, anandamide, and its phytocannabinoid equivalent, THC, mostly interact with the CB1 receptor, while the endogenous cannabinoid 2-arachidonoylglycerol and its phytocannabinoid equivalent, CBD, interact with both CB1 and CB2 receptors, among others.

Research on CBD and its effects in the body, including neurotransmitter modulation, is still mainly preliminary and thus not fully understood. CBD has been shown in multiple studies to improve anxiety and depression, relieve pain, and was recently approved by the FDA as the drug Epidiolex for the treatment of certain seizure disorders. Some of these effects are mediated by CBD’s complex interaction with CB1 receptors as a non-competitive antagonist. The CB1 receptor facilitates inhibition and ongoing release of both excitatory and inhibitory neurotransmitters including norepinephrine, dopamine, 5-HTP, GABA, and glutamate.2

Neuroimaging studies on CBD and the brain have shown that its influence changes activity in brain regions involved in emotional processing, including the amygdala. CBD interacts with the 5-HT1A receptor (aka serotonin 1A) as an agonist in these key brain areas, which is likely a cause of its anxiolytic and anti-depressant effects.3 The anxiety medication buspirone works similarly as a 5-HT1A receptor agonist. Another mechanism for CBD’s antidepressant effects may be its ability to rapidly increase brain-derived neurotrophic factor (shown in mice models), similar to drugs like ketamine, but without a psychoactive component.4

CBD also has direct action at specific GABAA receptor subtypes, perhaps further accounting for its anxiolytic quality. Because this GABAA receptor subtype differs from the one targeted by benzodiazepines, CBD may be helpful for individuals with anxiety who do not want to use or do not respond to benzodiazepines.5 Additionally, an in vitro study showed that CBD reduces the inflammation-mediated metabolism of tryptophan, and therefore may be especially useful in mood disorders related to chronic inflammatory diseases.6

Are you curious about your patient’s neurotransmitter levels? Whether you have clinically recommended CBD or your patients are self-supplementing, the NeuroBasic Profile (serotonin, GABA, dopamine, norepinephrine, epinephrine, glutamate, histamine, glycine, and PEA) can illuminate neurotransmitter levels reflective of potential CBD influence.

For more information, click here.

 

References

1.      Hilderbrand RL. Hemp & Cannabidiol: What is a Medicine?. Mo Med. 2018;115(4):306-309.

2.      Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin. Br J Pharmacol. 2008;153(2):199-215.

3.      Campos AC, Moreira FA, Gomes FV, Del bel EA, Guimarães FS. Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders. Philos Trans R Soc Lond, B, Biol Sci. 2012;367(1607):3364-78.

4.      Sales AJ, Fogaça MV, Sartim AG, et al. Cannabidiol Induces Rapid and Sustained Antidepressant-Like Effects Through Increased BDNF Signaling and Synaptogenesis in the Prefrontal Cortex. Mol Neurobiol. 2019;56(2):1070-1081.

5.      Bakas T, Van Nieuwenhuijzen PS, Devenish SO, Mcgregor IS, Arnold JC, Chebib M. The direct actions of cannabidiol and 2-arachidonoyl glycerol at GABA receptors. Pharmacol Res. 2017;119:358-370.

6.      Jenny M, Schröcksnadel S, Überall F, Fuchs D. The Potential Role of Cannabinoids in Modulating Serotonergic Signaling by Their Influence on Tryptophan Metabolism. Pharmaceuticals (Basel). 2010;3(8):2647-2660.

Disclaimer: All information given about health conditions, treatment, products, and dosages are for educational purposes only and do not constitute medical advice.