Harnessing the Innate Power of CBD in Clinical Practice for Pain and Beyond: recording and transcript

Rick: Good afternoon and welcome to the Tuesday webinar series, “Chiropractic Economics Webinar for Doctors of Chiropractic.” I’m Rick Vach, Editor in Chief of “Chiropractic Economics Magazine.” Today’s webinar, Harnessing the Innate Power of CBD in Clinical Practice Pain and Beyond, is sponsored by TruGen3. And as always, our program is being recorded and will be archived at Chiropractic Economics website, www.chiroeco.com/webinar for one year. Our expert is on board here today to speak with you, and when his presentation is complete we’ll follow with the Q&A.

You can submit questions throughout the presentation by clicking on the appropriate icon on the right side of your screen. Our presenter today is Dr. Chris Meletis. He is an Independent Clinical Educator for TruGen3, and he is helping chiropractors and their patients understand CBD’s fast growing popularity in the pain management realm. Dr. Meletis, thank you for taking the time to participate in our webinar, and for sharing your expertise with CBD, and helping our audience get a better understanding of what many are describing as a miracle drug. Before we get started, Dr. Meletis, can you please give us a brief background on yourself, and your work with TruGen3.

Dr. Meletis: Well certainly. Well, thank you one and all for attending. I am a huge fan of chiropractic. In fact, I have three chiropractors that work on my body. And thank goodness for you folks because you’ve saved the bacon for myself and my family. So first and foremost, thank you for what you do. I have been a naturopathic physician for 26 years here in Oregon, I serve as a Primary Care Provider. I was a dean at the Naturopathic College for seven years. I have written a couple hundred national articles. I’ve gone around the country lecturing for Category 1-A in CME.

And I’ve written this whole series of articles on the endocannabinoid system, one of the items we’ll talk about today. CBD and the applications in clinical practice. We’re all the foots on the ground. We’re all there trying to help our patients liberate themselves from their stuckness and their brokenness, and regain homeostasis. So I also provide a 16-hour lecture series that trains practitioners on the applications of CBD everything from the brain, the gut, onwards and onwards.

In fact, one of the interesting things before we get started, there’s a new word called endocannabinoidom, a big, long word, and we can’t win Scrabble with that because of course it takes too many letters. But how even the endocannabinoid system is altering our microbiome, our friendly bacteria. So lots of fun conversation today. My goal today is to leave everybody regardless of your knowledge base coming into this conversation with pearls that you did not know or were not fully aware of. So I love being an independent educator because the word in Latin docēre means doctor and we are all teachers.

So as we look at the human body, and we look at the applications of CBD, first and foremost we see that we have a lot of pain. In fact, as you can see on the second bullet here, chronic pain affects some 11 to 40% of the population with subgroups being higher. And who says this? The Centers for Disease Control. So we see it, but we know it’s not only affecting quality of life, it’s affecting their ability to participate fully in the life that we have. And so anything that can help with pain is, of course, a remarkable blessing to our patients and, of course, to our family members and to ourselves.

So we were gonna talk about pain, but we’re gonna talk about other topics relative to the endocannabinoid system. We’ve all heard the crisis. We have an opioid issue. So why don’t we move from the poppy, the source of opioids, to hemp? And that’s gonna be the nature of our conversation. But, once again, so we don’t step in different proverbial mud again, we want to make sure we do it in a methodical fashion.

But unlike opioids, CBD is not addictive. It doesn’t have that same effect physiologically in the body, so that’s the good thing. The question is, whenever something takes off in any of our fields, where is fact? Where is fiction? Where is the fad? So we’re gonna focus on the science behind how does this work in clinical practice. And when patients come in claiming that CBD is a panacea, where’s the evidence to this? So we’ll discuss that today. And, of course, I’d love questions at the end of the conversation today.

So I created this slide just for our presentation today as a foundation. And so when we look at the CB1 and CB2 receptors, it was actually Mechoulam and Devane out of Israel in ’92 that discovered the CB1 receptor was having an affinity towards anandamide. Anandamide and 2-AG are two endocannabinoids which you make, I make. Our cat and dog makes it. Any other mammal we love makes. So these endocannabinoid systems are working within the body. So we’re working within the confines of the human body as we were designed, so that’s the first thing.

So whenever we start fiddling around with that with CBD or whatnot, we have to realize we’re working to maintain the homeostasis, and not shifting it too much one way or the other. So we’ll talk a little bit about dosing as we go along. And realizing that these are innate processes that right now, if you have a patient with fibromyalgia, a patient with a disc issue, their CB1 and CB2 receptors are actually helping modulate their pain, but there is such a thing called endocannabinoid deficiency.

Many of us are familiar with the term adrenal burnout or adrenal fatigue. The same things that get us worn out on our adrenal glands or stressed out psychologically can also impact our endocannabinoid system. So when we see that sick and tired patient, most likely their endocannabinoid system has also taken a licking, probably continues to keep on ticking. But we need to nudge the endocannabinoid system. And so just like once again, a great adjustment, just the right amount to get the job done, but not too much.

So this is what we’re talking about. And you’ll see on the right-hand side here the words FAAH, fatty acid hydrolase. That’s an enzyme it breaks down anandamide. We’ll talk more about that. There’s 2-AG. It’s broken down by MAGL. So once again, just like we have serotonin, re-uptake inhibitors, and think of SSRIs. Our body has these built-in systems and this is called our endocannabinoid system. Hopefully, this picture captures it nicely.

So it was actually in ’92 that Mechoulam and Devane in Israel, Israeli doctors, actually discovered anandamide. But prior to that, they were doing research on THC. And remembering that a hemp derived product has less than 0.3% THC… I have a slide on that. So it does have that psychoactive effect. So anandamide was actually affecting the receptor, a CB1 receptor, much like THC, the psychoactive, but not creating a psychoactive effect.

So remember anandamide made in your body every day, and for some people more, some people less. The Sanskrit word for anandamide, ananda, means bliss. Once again sick and tired, worn out, stressed out, anxious, in pain. Often we have to wonder are their anandamide pathways insufficient to meet the commensurate amount of stress and pain that got them to your office. And the answer is invariably, often more than not, yes.

And so once again what we used to think about anandamide in ’92, was it only affected CB1 receptors. Well, if that’s true, then now we know there’s many other receptors being affected by our natural endocannabinoid system. And likewise, when we use hemp-derived CBD, we’re also gonna to affect TrpV1, another pathway called 5-HT1A. And this is controlling anxiety, pain, and pain perception and also the PPAR pathway. So lots of research coming out. In my last slide, you’ll see that we have to stay humble because data is coming fast and furious with the advancement of scientific research and the boom, and the green rush of CBD research.

So we’ve all learned this back in basic sciences, so when we learned our physiology and biology. We have a homeostasis. But when we get ill, we got a fever. I’ve fallen and I can’t get up phenomena. We actually start triggering more endocannabinoid release. So once again, a natural pathway that actually helps support the body in a fundamental way. But if it’s not there to do it commensurately, then we end up with problems.

Think about the patient that goes in for a cortisone injection. If they had enough hydrocortisone to deal with their aches and pains, they probably wouldn’t need that injection. But the worn out executive, busy mom, or individual that’s just taken a licking and keeps on ticking, but they’re really not ticking very well. They get a cortisone injection. Well, why wouldn’t we give an oral dose of endocannabinoid or a topical delivery to actually help sustain another pathway which we know exists in the body? It’s all about nudging the body in the right direction to stay in the Goldilocks zone.

So when we look at the CB1 and CB2 receptors, we look at the distribution. We used to think, and once again, how science has changed, CB1 was just neurological, just a spinal cord and brain. Now we know that’s not the case. We used to think the CB2 was only immunological and peripheral. We also know that’s not the case. And you’ll see, of course, the little chevrons throughout the body here. So CB1 and CB2 receptors are key players in the endocannabinoid system. We all have them and we all have an endocannabinoid system.

So when we use a CBD from hemp, for example, we’re gonna nudge those pathways. And I have a philosophy. Start low, go slow, because, once again, if we can get enough vertebrae or subluxation addressed with minimal impact or force, wonderful. It’s all about getting the job done with respect to the body. CB1 and CB2 receptors are located on the surface of many cell types. And, once again, CB1 are more abundant in the central nervous system. That’s a fact, but they’re throughout the body. And CB2 receptors are found outside the body. In fact, a little interesting tidbit, CB2 receptors actually affect the mu opioid receptor and the microbiome, and the GI tract.

It’s like okay, so it has affected opioid receptor activity. That’s a CB2. It’s a cannabinoid. But once again, our bodies, as we all know philosophically, work in concert, holistic medicine. What a concept. And this picture once again created uniquely for our presentation today. And if you want to read some of my articles for free, go to doctormeletis.com. I have several articles that I’ve had published in the “Townsend Letter” on the endocannabinoid system.

But as you can see here, anandamide perfectly fits within the CB1 receptor. That’s what Mechoulam in ’92, along with Devane, discovered. But that little rectangle, square, actually fits here partially, so it has a CB2 activity, whereas 2-AG and one of the other endocannabinoid all fits perfectly within the CB2 receptor. But there’s crossover, so once again, there’s duplicity in the body. There’s redundant systems to say, “Okay, we’re gonna get this job done. We’re gonna maintain homeostasis and fight entropy.”

So as you can see, anandamide is broken down by FAAH. We had that on earlier slide. That’s an enzyme, so it’s gonna break it down. So once again, just like we have serotonin in a synapse or another substance in the synapse, we’re also gonna break it down. Likewise, 2-AG is broken down by MAGL. These two enzymes… you say, “Well, why are you emphasizing this so much?” Because it’s gonna be related to our conversation today about Tylenol and NSAIDs, and how they alter the endocannabinoid system as well.

So MAGL and FAAH will come into our conversation later on. That’s why I’m going over the biochemistry here. So we know that CBD interaction with the endocannabinoid system is dynamic, and they’re referring to a term called the endocannabinoid tone. And CBD inhibits the FAAH enzyme. Remember, we were just talking about the FAAH enzyme. What does it do? It breaks down anandamide. So it inhibits it. So if you don’t break down the endocannabinoid, like, anandamide so much… so FAAH breaks down anandamide. CBD inhibits FAAH. All of a sudden you have more natural endocannabinoid in your body.

A penny saved is a penny earned as you can see down here. If I can save my naturally created anandamide by using CBD, and clearly, the body homeostasis wise, knows how to use anandamide, we’re gonna sustain the tone, aka endocannabinoid tone. So one of our therapeutic concepts here is by using a CBD, we’re actually conserving anandamide, and we’re conservative the tone. CBD can also increase anandamide levels by preventing FAAH from breaking it down, and inhibiting the FAAH enzyme has been shown to be a useful strategy for treating anxiety disorders.

So when our patients come in hurting we know that an inflamed brain… and once again CBD and anandamide are used for inflammation, as well. Research is clear and I’ve given many lectures on the topic. An inflamed brain is more anxious and more depressed, and more foggy. So that brain fog people complain about or perseverating on this thing, overthinking something. Once again, CBD has a phenomenal role there. It’s also used for post traumatic brain, as well as PTSD as well, in other lectures that I give.

FAAH and MAGL are the key enzymes for the endocannabinoid system. We just talked about it. I’m repeating it just like we do with our patients. And the reason is we all come to our conversation today with different levels of knowledge. So once again, I’m just recapping this because this is gonna be a pearl that we talk about quite a bit further down about conservation, and how medications where you thought used to work a certain way, like NSAIDs, have a whole another mechanism. And we’re even gonna talk about capsaicin ever so briefly, and how… remember how we thought it depleted substance P? Well, it probably does that too, but it does something else kind of cool.

So interesting. Lots of research out here from South Carolina. Tweaking the endocannabinoid system might be a good way to treating inflammatory disease. Well, we use that term inflammatory disease. Well, now we’re thinking, “Well, maybe what about colitis and sinusitis, and rheumatoid arthritis, and all these other -itisis, maybe something else that’s not so specific?” And one of our slides will even talk about endometriosis and pain and the endocannabinoid system.

So most of our research… and I quote here, once again, this professor from South Carolina, of, “Our research demonstrates that endocannabinoids are produced upon activation of immune cells and may help regulate the immune response by activating and acting as anti-inflammatory agent. Thus interventions that manipulate the metabolism or production of endocannabinoid may serve a novel treatment modality against a wide range of inflammatory problems.” That doesn’t mean we don’t use Boswellia or curcumin or something else in addition to help control the cytokines. But we want to support our first volley, our first defense, our endocannabinoid system.

But remembering if our endocannabinoid system is worn down, it doesn’t have good tone, it means other aspects of the body, which also count on the endocannabinoid system, are also gonna be waxing and waning. And we’ll chat about that as well. So once again, Goldilocks zone, whether it be infection or inflammation, and we release more endocannabinoids, if we have that ability. But now we don’t have that ability and we have breakthrough pain. Breakthrough inflammation, of course, brings our patients to us. Then we’re saying, “Well, let me go ahead and conserve it, prevent the endocannabinoid from breaking down as much with some CBD.” Remember how it conserves by altering those enzymes that otherwise break down the endocannabinoids? So that mechanism is very, very important. 

So you’re more familiar with this that even I in clinical practice when it comes to the brain and thalamic nociception levels. But the CB1 receptors are also expressed in cells of the midbrain periaqueductal grey matter and in the substantia gelatinosa of the spinal cord that’s actually receiving primary afferent neuron activity. So it’s okay but there’s a CB1 receptor. Ah, anandamide. Actually, Mechoulam in ’92, he discovered anandamide interacted with the CB1 receptor, our endocannabinoid system, which is worn down like every other aspect of the modern human being, and especially westernized world where we just don’t have a lot of adrenal reserve, a lot of mental reserve, a lot of immune reserve, because we live in a helter skelter world.

So in the medulla oblongata and the spinal cord, structures are involved in the process of pain signals more intense concentration. The CB1 receptors are detected in the superficial dorsal horn and the dorsolateral funiculus in the spinal cord. Isn’t that cool? Once again, remember until ’92 we didn’t even know we had anandamide in the human body, like, oh wow, our body makes. And if you graduated before ’92, it wasn’t even a concept and even after ’92, it wasn’t a concept. It wasn’t made into our clinical research, and now it is. And this is why a lot of people are excited.

And when we look at the synaptic side of things, once again, lots of research has gone into this and you can see this beautiful picture capturing the fact that we need to have a calcium in flux postsynaptically in order to have a release of the cannabinoid receptor situated in a specific small area where that synthetization for the endocannabinoid to be synthesized. Interesting, as you can see in red here, noxious stimuli increase endocannabinoid release, once again, assuming that you haven’t already squeezed out your full endocannabinoid capacity and you’re overwhelmed with chronic pain or allodynia like a fibromyalgia, that chronic nagging centralized pain.

And then once again, you can only do that for so long before, just like a race or a marathon, you hit that wall, and the pain is unquenchable. And we would go into management as opposed to resolution of a patient. So anandamides, whole body wellness factor, is quite impressive. It helps with pain. It helps with appetite. It helps with memory. Once again, we’re not talking about THC here. We’re talking about something naturally in our body. And we’re using CBD to help conserve it and to allow it to actually have a greater function within the body. It’s also used for memory. Other lectures I give, and you can once again go to doctormeletis.com, and read some more articles on all these cool topics with oodles of references in all of my articles.

And so what’s compelling here is we make our anandamides and our 2-AG from arachidonic acid. Most of us in our basic science training learned that arachidonic acid, that’s pro-inflammatory. That’s gonna feed prostaglandin e2 pathways. That’s not good. But now you’ll totally eliminate arachidonic acid to a large degree, well, that’s also you’re building block for your anandamides and your 2-AG. So that’s not good. Once again balance. Not too much of any one thing. We see fad diets. We see all kinds of things in our clinical practice. And the more we practice and live in the clinical environment, the more we see.

But what’s interesting here focusing on the crux here, anandamides yes, it affects CB1 and to a degree CB2. Anandamide also affects a whole another receptor, TrpV1, which we’ll chat about. And it also affects direct brain components, like the 5-HT1A. But if you look here, anandamide can be metabolized through the LOX and COX pathway. Remember, lipoxygenase, cyclooxygenase. There’s drug categories here and if you remember Boswellia, often called 5-LOXIN as a branded item, kind of interesting.

So we’re seeing all these mechanisms that our body didn’t realize that even existed, and now we’re seeing the mechanism. And always keeping it simple is my philosophy as a researcher, as an educator. I always like to see what’s going on within the body. And always remember structure begets function and function begets structure. And so as we look at the antinociception by inhibiting the release of proinflammatory factors by non-neuronal cells located near nociceptive neuron terminals, CB2 activation helps.

It’s called CB2. Remember, 2-AG anandamide impact this, so our endocannabinoid system. The CBD conserves these, so by doing CBD, we’re having an effect on these receptors. But more important, we’re having an indirect nurturing effect. And philosophically you can think of it this way. Is it better to teach a person to fish or give them a fish? The sustainable model is to teach them how to fish. So that’s our goal here is you support with CBD supporting the innate system as existed in the mammalian species for eons, and you’re actually covering the basis of getting the body up to speed in a foundational way. So once again, structure begets function and function begets structure.

Just a glimpse of the research. I actually put it in red down here, 2016 excerpt. And what you’re seeing here is research showing what happens if you use a CB2 agonist, something that stimulates that receptor. And so they gave various treatments throughout all kinds of drugs, other medications because they now use lot of synthetic agonist or stimulants to see what does it do. Decrease arthroscroratic [SP] plaques, macro fascia filtration, leukocyte adhesion, tumor necrosis factor alpha, onwards and onwards. They are saying if this, then that. And once again, lots of research, so if you really wanna go into the weeds, this is a great article to read. And so once again, you can read the whole article for free on “PubMed, or if you can’t gain access to it. I’ll be more than glad to share it with you through TruGen3.

CB2 simulation and endorphins, CB2 immunolabeling has been detected on beta endorphin containing keratinocytes and the stratum granulosum throughout the epidermis of rat hind paws. And they’ve actually showed the mechanism going on here, a beautiful graphic. But they’re saying here these CB2 receptors when activated stimulate release, so endogenous opioid beta endorphins. That’s the takeaway. So CB2 receptors would activate, stimulate, endogenous opioid beta endorphins. So you say, “Well, go get a runner’s high. But doc, my back hurts. Remember I have a disc issue, or remember, I have that knee issue, or I have fibromyalgia. I can’t go exercise. I can’t get that beta endorphin. Could CB2 be one of the mechanisms?” The answer is yes.

Remember, also CB2 and microbiome also play a role in stimulating the neuro opioid receptor activity as well. So kind of cool to know there’s a workaround when it comes to helping our patients with beta endorphins. So when we look at the activation of antinociception by stimulating peripheral release of endogenous opioids, CB2 cannabinoid receptor selective agonists are promising candidates for pain treatment. And it’s been shown to have helped with neuropathic pain. And one of my articles I also talk about a substance called Palmitoylethanolamide. Once again, Palmitoylethanolamide.

A substance abbreviated PEA. It has nothing to do with the vegetable, by the way. And it actually is also a fatty acid amide and it has an endocannabinoid like system you can also give for your neuropathic patients, along with the CBD, if the CBD is not doing the full trip. So just an amazing time in the scientific literature. As you can tell, I kind of geek out in going in the literature say “Wow, isn’t our body magnificently made?” And the answer is yes, they are. Researchers tested the hypothesis that CB2 receptor activation stimulates the release of the endogenous opioid beta endorphins.

And they talked about the mechanism and it allows for the local release of the beta endorphins where CB2 receptors are present, leading to anatomical specificity of opioid effect. Once again, you can get a hydrocortisone injection into your shoulder, or your knee, or your hip or whatnot. But it’ll look a little bit systemic, but it’s localizer. Isn’t it kind of interesting that the body sequesters and allows for a localized effect of where it’s needed? And that substance I mentioned briefly before, the Palmitoylethanolamide, which is written out on one the latter slides, in passing I’ll point it out to you, actually also goes to target at tissues where it’s “needed” per the medical literature.

So CBD our topic for the day. Now we know a little bit more about how it works, but let’s take a highlight of in a standard practice where we deal with musculoskeletal issues how can it help. Well, let’s take a look here. It’s neuroprotective. It decreases reactive oxygen species. It is vasorelaxant. This is good. It helps with blood supply, and helps diminish some of that congestion, and helps with the PPAR gamma pathway. Now, you started thinking, “Well, I wonder if that can help with some blood sugar or some other things.” Your thinking is correct.

Anti-spasmodic tight muscles aren’t our friends, of course, our guardian of course, but their excessive spasmodicity is not. Anti-ischemic, we only need blood supply for healing. And that’s that one I kept on saying 5-HT1A. This is also controlling and helping with the neurotransmitters and having a happier perspective of outcomes from your aches and pains because sometimes, no matter the happiest Tigger in the world it feels like an Eeyore after they’ve suffered enough pain. The TrpV1, which we’ll chat about more, another effect of CBD.

And bone stimulant. Hmm. Might that help with a fracture or maybe even with the osteoporotic patient? I’m not making that claim. Here just doing a little head scratching as we’re chatting as colleagues. And anti-inflammatory. Go figure that. All from CBD and why am I excited about it? You can see why. And the title for this article is “Non-psychotropic Plant Cannabinoids: New Therapeutic Opportunities From An Ancient Herb.” It was a 2009 pharmacological journal that actually was commenting upon this.

So then we get to the cannabinoids and the prostaglandin inhibitors. So when we do that, we actually look at the fact that the enhancement… and you can focus on the red, if you wish. The enhancement is CB1 receptor activity by some NSAIDs, you know, methoxine, some others has been confirmed. So are you saying that a non-steroidal anti-inflammatory drug affects your CB1 receptors? We were all taught a whole different mechanism, and that mechanism still is true.

But once again, to think that we only work in the microcosm of linear human mechanism, of course, not the case. And so to think that if a person has taken a nonsteroidal anti-inflammatory, or you have to wonder they’re taking an herbal anti-inflammatory, might we have an effect on CB1 receptor? I would argue the answer is yes. And, of course, we know one of the challenges of taking the prescription or OTC NSAIDs is gastrointestinal problems and increased risk of dying of a heart attack.

We know that if taking a single dose of ibuprofen way on to this column actually increases your risk of having a heart attack. It could be the first dose. It could be the hundredth dose. We know there’s a cardiovascular warning now about how NSAIDs can cause problems. So is there a time and place for NSAIDs? That’s a personal and a philosophical conversation, but if we can avoid them or minimize them, we’re gonna decrease the deleterious GI problems, in addition to over ulcers and bleeding and bleeding out, but also leaky gut, as well as, of course, cardiovascular sequelae.

Plus, as many of you are familiar, NSAIDs have been shown in some of the literature actually to cause more damage to the chondrocytes and joints, and decrease the healing within the joint. So it’s purely palliative. It’s important to control the inflammation. We would all agree with that. But the question is if it’s also taking away from the health savings account of that joint, is it really the best long-term solution? Of course, we would argue no.

So NSAIDs and the endocannabinoid systems have the capacity once again NSAIDs to inhibit FAAH. Remember how I emphasized FAAH. That’s the one that breaks down anandamide. An alternative hypothesis suggests that COX-2 enzyme can metabolize the endocannabinoids like anandamide and 2-AG, and that epidural administration of NSAIDs prevent anandamide destruction by inhibiting the action of COX-2. Okay, that’s another mechanism, but once again, it’s coming back to what? Our endocannabinoid system, which, of course, CBD can help conserve and support.

The administration of NSAIDs increases the amount of anandamide by impeding the metabolism through inhibition of the COX-2 and/or FAAH, as we chatted about. And the only COX-2 inhibitor that I’m aware of is Celebrex currently on the market.

So our patients get an accident. They get neck injury. They get inflammatory processes going on. And what happens? Well, the COX-2 exerts a negative influence on the endocannabinoid because it catabolizes them. Remember, anabolism like anabolic steroids builds things. Catabolism breaks things down, like too much prednisone, too much stress. And so as anandamide and 2-AG have been shown to have neuroprotective properties in injured brains. 

So this is why CBD is becoming very popular in the football and sports arena as well or the hockey players, or the high school sports person, or the person playing a gentle game of lacrosse and takes a hit to the head. It’s just all these considerations of how, once again, CBD can be used prophylactically, therapeutically, and it’s actually helping rebuild and recuperate some of the endocannabinoid tone that we’ve chatted about. 

In a traumatic brain injury model COX-2 inhibitors treatments protect 2-AG levels, enhance functional recover, and reduced cell death in the inflammation confirming an interaction between endocannabinoid 2-AG and COX-2 enzyme. This also suggest that COX-2 inhibitors treatments may produce an indirect enhancement of the cannabinoid receptor activity by increasing endocannabinoid levels.

But you say, “But doc, we were just talking about COX-2 too maybe isn’t the best thing for people to take. It’s a drug, right,” but what else can increase the endocannabinoid system? Well, CBD seems to increase endocannabinoids. So we can do the drug therapy, if necessary, or if it’s a commensurate level of injury short-term. But while at the same time in my clinical opinion, using CBD, as well. And we look at the neuropathic side of pain, because of course nerve pain sucks, and we all know that. We have patients with that burning neuropathy, or the tingling or [inaudible 00:32:10] seizures or whatnot.

And they looked at five recent preclinical studies that published from 2013 to ’16… And this was actually in the “Annals of Palliative Medicine” 2017 reported. And they looked at the studies, and they looked at chemo drugs, which cause allodynia, that centralized kind of pain, that fibromyalgia and, you know, chemo patients will have. And they looked at it in terms of can it help. And the answer was, yes, it does seem to have great promise in allodynia and systemic pain.

So I’m thinking, “Well, what about the fibromyalgia patients with allodynia?” The answer is it makes good sense. Once again, looking at always the cause. Am I claiming this is a panacea? No. But does it make sense to support the endocannabinoid system in a way, and why are our patients so excited they hear this soft science? But here’s the hard science thing. There is a mechanism here and as clinicians that we employ that mechanism, wow, especially with a start low, dose slow concept, we can actually do it in a very safe and methodical fashion.

So that same study 2017, these studies also provide insight into the biological mechanism behind the therapeutic utility of cannabis compounds and managing chemotherapy induced neuropathic pain and provide a basis for conduct future clinical studies in patients of populations. I used the cannabis word. What does that mean? 

Well, there’s two plants that are known as cannabis. There’s the cannabis hemp, which is low naturally in THC. And then there’s cannabis marijuana, which is high in THC, which we think of recreational high THC. Hemp-derived CBD with little or no THC doesn’t have any psychoactive effect. We’ll go over that when we go over a certificate of analysis showing we don’t have the psychoactive component. But when we hear the word cannabis, it can be used interchangeably.

We don’t like to use it in a hemp industry because it’s confusing that hemp is cannabis. So is marijuana. But we’re not talking about marijuana in the clinical applications here even though, of course, you could use it that way. But then you add that psychoactive effect, and most of our patients couldn’t maintain their job or function with a large amount of THC. 

So beyond CB1 and CB2 receptors we have additional proteins. You heard me talk about the 5-HT1A, the TrpV1, the CB1, CB2. We also have coupling proteins. So is there science here? Yes, there’s a lot of science saying, “Hey, look it here.” So this is actually in a 2017 “PubMed” article talk about G coupling proteins and how they also have an effect via the phytocannabinoids like hemp and CBD. And so they looked at the GPR18 and GPR55 receptors, and they looked at the extensive sequence of homologies of CB1, CB2 and then say that there’s a whole another mechanism her, a different set of ligands rather than just the endocannabinoid CB1 and CB2.

So when we give CBD, we’re affecting coupling proteins. We’re affecting CB1 and CB2. We’re affecting anandamide and 2-AG. We’re affecting TrpV1 and the 5-HT1A. But we’re nudging it at a gentle level and we’re increasing that endocannabinoid tone. A patient will start on maybe let’s say like 20 milligrams once or twice a day. And you’ll see okay, how is that working as it replenishes or I call it re-soaks the sponge? So imagine a dry sponge in your office where you’re using electrostem [SP] or something. It takes a while to really get it fully saturated for good conduction.

Well, it’s the same thing here. It takes a while to saturate and get the body back up with endocannabinoid tones. So going slow and being methodical is very, very important here. So they talk about the GPR18 and GPR55 may also recognize the phytocannabinoids CBD. Aha, so once again, another mechanism. We’re teaching a person how to fish. We’re supporting the body with CBD and allowing it to go rippling through ever so gently the natural pathways, some of which we know and some of which are yet to be discovered. Remember, it wasn’t until ’92 even knew we had an anandamide endocannabinoid substance.

So as promised, I was gonna talk about TrpV1. Well, TrpV1 is compelling because many of us have used capsaicin topically for patients, right, cayenne. And we often learn about substance P. Well, if you take capsaicin, apply it to let’s say shingles or a neuropathy it’ll deplete substance P. Okay, that’s fine.

But now we’re saying it also affects TrpV1 much like CBD does. So a different mechanism probably at some fundamental level, but now imagine doing some capsaicin for a neuropathy or nerve pain, some CB. Might we have a beautiful overlap? And clinically I see that all the time. Once again, figuring out the body. It’s like a puzzle. We have to basically tease it away. And so this TrpV1 stands for type one Vanilloid receptor and it may regulate some cannabinoid effect.

Once again remember, we didn’t even know we had a receptor or even had anandamide until ’92. Now I wonder what else we’re gonna find. But look at the de-polarization and actual potential initiation, and once again, burning state, itching sensations. You can see where this could be very nice. “Oxford University Press” is the source of this picture. So then we can look at the two serpentine receptors classified among orphan receptors, because when they were discovered, they did not exist a specific ligand or binary. They say, “Hey, there’s these receptors over there.”

And well, are they are cannabinoid receptors? These two receptors are still named GPR55 and 119. Another receptor for anandamide is a transient receptor, which we talked about the TrpV1, and the receptor for capsaicin. Overlap and the beauty of this as we practice longer and longer, I think we’re just gonna continue to be baffled by what’s happening within the body. 

To recap, when it comes to another journal article that was in 2011, we see some NSAIDs have additional influence on a cannabinoid system either by inhibiting fatty acid amide hydrolase, that’s the FAAH. Remember, that’s the one that breaks down anandamide, or by inhibiting the possible intracellular transport of the endocannabinoids. So once again, we do not know and I’m gonna say it humbly, we do not know all the mechanisms. We just know it’s well tolerated. You start low. You go slow. You could apply it topically. You do it orally. Sometimes you have to Oreo cookie at both directions. 

But once again, once you get to that saturation level where you replump and improve the endocannabinoid tone, it’s gonna have a myriad of effects throughout the body. Mental, you know, the psychological side of things, the physical, the neurological, and it can even affect the GI health. And though I don’t want to go over on time, I will share an interesting tidbit. 

Many of you know of the disease called respiratory syncytial virus. It affects children most likely or most often. And if we had two children and one child has a CBD receptor mutation, aka a polymorphism, the other one does not have that polymorphism, they have found a direct correlation that if that person with that polymorphism for CBD receptors exists, and they’ve got respiratory syncytial virus, they’re more likely to be hospitalized for that respiratory syncytial virus as a kid, than if you didn’t have that polymorphism.

So it’s going so much further into immunological effect and even the inflammatories side of things. And also there are CBD receptors that have now been linked. If you have a polymorphism, a genetic mutation, to whether or not you actually will have a higher propensity towards irritable bowel syndrome. Go figure. So once again, it breaks down anandamide. It breaks down 2-AG. Once again, important talking points as we talk to our patients that we’re actually helping to conserve the body.

There’s a relationship between the gut pain and endocannabinoids. A rodent study where they use an inhibitor for FAAH, and they looked at the mechanism, and they looked at did it decrease gut pain. And their answer is yes, it did. And IBS subtypes and their symptoms, so to sync alteration of endocannabinoids and endocannabinoids, like fatty acid activity and levels and partially results from the reduction of FAAH. Once again, always going back to those words we learned early on, that FAAH just like we have MAGL.

And so what’s interesting is we can help with IBS. Any of us have a stomach flu? How do we feel mentally? Not good. Do we have body aches? Probably. Do we have some reactive arthritis? Conceivably. Feel like death warmed over? Yeah. So healthy gut, healthy body, gut/brain connection, all of these things. So by also using CBD for those people that need to improve their endocannabinoid tone, we’re actually gonna be able to see some improvement and a healthier gut, healthier us, healthier GI, healthier microbiome. After all, there’s 100 trillion visitors in our GI tract. There’s 5,200 trillion cells that make up the human body as many of them as us, so it’s all about balance, once again, out of the medical literature, as you can see at the bottom.

Then we get the homeostatic role of the endocannabinoid also extends to the control of the intestinal inflammation. So, well, why is that important? Once again, if your GI tract which has 80% of the immune system and 70 to 80% of your serotonin and the happy brain chemical is unhappy, you’re gonna not have as good outcome as a person that has a messed up GI tract as an unhealthy or a healthy GI tract, if there’s such a thing as a healthy GI tract in today’s world.

So CB1 is a sensory ganglion. It controls visceral sensations and transcription of the CNR1 and is modified through epigenetic processes under conditions of chronic stress. That can be physical stress. That can be psychological stress. It might have been before they even showed up to your office, they got worn out. They’re complaining about their elbow, or their shoulder, or their first or second rib, or whatever it might be, or intercostal problems. And they’re like, but it’s what got them to your office, which is always important, that whole history of finding out what’s led the patient to the brokenness and symptoms that they have.

And so the endocannabinoid systems are also involved centrally in the manifestation of stress. Ah ha. So now if we have a worn out endocannabinoid system, might we have greater manifestation of stress physically or psychologically? Yes. The endocannabinoid signaling reduces the activity of the hypothalamic-pituitary-adrenal pathways via actions in specific brain regions, notably the prefrontal cortex. That’s rational thought. Amygdala and hypothalamus.

So how many of our patients can benefit from some Dramamine or some adrenal support? Well, quite a few. Well, if we do some support the endocannabinoid system, might we help with some those innate [inaudible 00:43:18]? Remember, we’re teaching the body to fish, to take care of itself. I love this quote. So just phenomenal out of the peer-reviewed literature. I’m not gonna spend a lot of time on this. I just want you to take a view here of CB1 receptors and how it affects the lower esophageal relaxation. 

So once again, think GERD. Think of digestive problems. Think of suppression of motility secretions. And also over here, help with inflammation, visceral pain. I think about that colicky pain that adults get as well. So it’s like, okay, so it’s having all these effects. And we’re seeing CB2 and CB1. Remember, we thought CB1 was only in the nervous system. No, it’s elsewhere as well. Likewise, we’re seeing the same thing here with motility and regulation of the intestinal lining permeability. 

So if you’re working with a gut patient, and it’s kind of interesting, because once again, it’s not just about the spinal. It’s also about all the [inaudible 00:44:20] that occur from that spine, and once again, that feedback loop. And I’ve written a whole article on the vagal nerve, which is also available on my website, also for free. So when we look at the degradation, this is what’s happening to the best of the knowledge at this point in time, and the peer-reviewed literature about the receptor activity. And really all you want to be focused on is the 2-AG and AEA, which is a fancy word for anandamide, and that it has all these different interactions 

Now you’ll see the MAGL breaking it down and the cellular function. And once again, it’s going for MAPK and some of these other postsynaptic effects. But anandamide 2-AG can also be metabolized by COX-2, which is shown in the postsynaptic neurons. But it can also occur presynaptically. So it’s getting broken down every which way. We start to simulate a COX pathway because of injury in our body. We wanna kind of build up… In my mind as a clinician 26 years, we wanna be supporting that pathway, shoring it up.

And when we go for the GI tract and we look at receptors, we can see that CB1 appears to be the receptor that is most active under physiological conditions. Anandamide is a natural ligand of the TrpV1. And once again endocannabinoids, ECS, endocannabinoid system, also secretions, motility, inflammation, and visceral hypersensitivity. So once again, lots of compelling information here. Healthy gut, healthy brain. Healthy brain, better neurological function all things being equal.

And a tease on a much larger lecture that I give, oral administration or probiotic strains of lactobacillus that reduce visceral sensitivity were found to up-regulate CB2 and mu opioid receptors in the intestinal epithelium of rats blocking CB2 attenuates a reduction of visceral sensory thresholds caused by alteration of gut microbiome. So I’ve got a little yogurt there, but you’ve got to figure a friendly probiotic of your choosing could actually help support this.

So now we’re looking at the endocannabinoidom, and once again the microbiome endocannabinoid system, and how the CB2 interacts with the probiotics naturally within the GI tract or they’ve taken an antibiotic the day before they come to your office. They’ve been on multiple antibiotics for multiple infections because they are one of those travelers that we have in our practice. And they constantly are ill because they’re worn down. Their adrenals are worn out. Well, we’ve learned about CB2 and the hypothalamic pituitary pathway. We’ve learned about the gut health. It’s like wow, we’re really teasing it away here with CBD and the relationship here. 

And as you can see, chronic stress alters these pathways. It could increase short-term 2-AG and AEA, but that’s like asking your body to do a wind sprint. You can only wind sprint so long before you are no longer sprinting. You’re barely walking one foot in front of another. So chronic stress, you get that endocannabinoid fatigue or deficiency that occurs. And so lots of times our patients are coming to us with some of those symptomologies and once again, always looking at the innovation pathways, afferent, and efferent.

And that’s one reason I wrote about the vagal nerve so much because 80% of it’s afferent and only 20% is efferent. And there’s a whole condition called Roemheld syndrome, which also CBD seems to be helpful for in my clinical practice. And when we look at chronic stress and pain, the ECS is involved in the response to pain. Stress evokes changes in the levels of anandamide 2-AG. So once again, that’s assuming they have that reserve. If not, this is where CBD comes into play. And you’ll know whether a person is doing really well with their CBD because they’re gonna start having some symptom relief within a few days usually, and definitely within the month. That’s what I see, assuming you dose judiciously. And, once, again it’s also about getting it delivered to the tissues bioavailability wise. And we’ll chat about that briefly as well. 

So I think I’m on time. So do not worry. Lots of time for questions. And chronic stress causes down-regulation or loss of CB1. That’s a take home as well. Chronic stress. Hey, are any of us as practitioners chronically stressed? Wait. We went from ICD9 to ICD10 coding. We just got an audit from another insurance company. They want more chart notes to justify what we already know we’re doing well. And it’s like, “Oh no, no chronic stress for us either.” And we cause the loss of CB1. And these changes are widespread and occur throughout the brain. 

So once again, this whole aging process, we looked at our hormones. Remember, we talked about hypothalamic pituitary and that feedback loop gets messed up. Is this part of that excess of aging process that might affect growth hormone, testosterone, estrogens? It hasn’t shown up in the literature yet, but I’ve written a whole book on his change of life, and how testosterone levels are very, very broad in terms of what’s causing the problem. It’s not just one thing causing low hormones or worn out adrenals.

And so they talk about increased 2-AG signaling correlates with the termination adaption of activity of the hypothalamic pituitary axis. So the brain adrenals, it contributes to changes in pain perception. How many patients come in with adrenal burnout? A lot or adrenal fatigue, you know, lower cortisol levels. And cortisol/cortisone interchange in terms of conversion. So once again, if you don’t have enough hydrocortisone, you’re gonna have more breakthrough pain, more inflammation. But now we’re seeing there’s this whole another mechanism with the endocannabinoids. And once again, how does CBD come to play?

And a beautiful picture here in my opinion in terms of stress. It’s altering our hypothalamic pituitary axis. It’s altering the cortical steroids, cortisol, cortisone, and as a result, we’re getting sick patients. And all this time until ’92, we didn’t know it existed. And until possibly this conversation, you didn’t even know that along with that adrenal fatigue, we had not been addressing the endocannabinoid system for this chronic pain and patients with the breakthrough inflammation, which doesn’t seem to do the trick. Because I can tell you all the turmeric in the world, all the Boswellia in the world can’t make up for a dysfunctional endogenous system, which is unhappy. 

Just like all the herbs in the world can’t make the adrenal glands work better, unless there’s an innate healing capacity that is president as being nurtured. So when we look at the complexity of it… and I just do this as a brain wow, look at where the receptors are that we currently know. Once again, a beautiful graphic out of this medical journal. It’s like okay, I’m humble and the more I research this stuff, the more humbled I am.

So anxiety, appetite, nausea, pain. Well, we have patients all the time with all of those. Depression, yes. Affect to the prefrontal cortex. So maybe the hypothalamus and hippocampus, yes. And so once again this is where CBD comes to play. You nurture a pathway. You see what that body’s resilience is, the vital force, if you wanna call it that. And then you’ll see how much more does it take to get the job done starting low, going slow.

Acetaminophen, Tylenol, once again they looked at endocannabinoid re-uptake inhibitors and CB1 receptors, and it may be responsible for the analgesia induced by acetaminophen. Okay I thought there was a very vague other understanding of that. Well, this is a 2018 article last January. It talked about well, no actually, maybe acetaminophen is working on another mechanism. And maybe a CB1 receptor, which really makes us wonder, as clinicians, where does CBD come into play in modulating everything? And when we look at acetaminophen being used or NSAIDs being used, if they can impact the endocannabinoids are they disruptors? And are they positive or negative disruptors? 

And I will tell you on another lecture I give I talk about how acetaminophen, it’s also a poison to the mitochondria. Of course, that’s a whole another conversation in a book I just wrote on the mitochondria. But acetaminophen has been shown to cause a problem with mitochondria. And it’s also strongly discouraged for my patients which are pregnant to avoid acetaminophen even though they say it’s okay because it actually could cause mitochondrial issues. And there’s a link to susceptibilities to these non-neuro typical problems such as autism.

So acetaminophen relieves inflammatory pain through CB1, cannabinoid receptors in a rostral ventromedial medulla. And I quote here. “Our results indicate the cannabinoid system contributes not only to acetaminophen analgesia against acute pain but also acute inflammatory pain and suggests that the relevant CB1 receptors reside the rostral ventromedial medulla.” I know I was not taught that at all in basic sciences, clinical training whatsoever.

Wow, a 2008 standard medical journal saying, “Hmm. So why is CBD exciting for us as clinicians? Yes, our patients know about it. They’re bringing it to us, but now we know more about the mechanism and that it’s real.” It’s very, very real and our bodies have been using an endocannabinoid system for eons, and now we’re seeing the mechanism here, whether it be the NSAIDs, mu opiate receptors presynaptic GABA release, that uptake of the neurons. But once again where does 2-AG and AEA, which is anandamide once again, come into play? Well, it comes into play there.

So FAAH breaks down anandamide. They should have here MAGL for the breakdown of 2-AG. But they’re saying here, “Indicating that increasing levels of endogenous endocannabinoid protect against the damaging effects of the drug.” And which drug is this? The NSAIDs because what does the NSAIDs do? They could cause ulcers. So I’m not saying that if you do enough CBD, you’re gonna avoid ulcers when you give a patient an NSAID. But the fact is like, wow, there’s a natural protective mechanism here. And once again, “European Journal of Pharmacology” 2017.

So lots of research going in here. We already know that GW Pharmaceuticals made a drug out of CBD. So once again, it’s kind of very interesting that it’s coming to this play. And NSAIDs that are known to block COX-2 can interact with a cannabinoid system due to a potential important degradation, once again, of the anandamide 2-AG and the COX, which we’ve chatted about. So I’m repeating some of this on purpose because they’re important takeaways that that mechanisms of actions which were taught in graduate school were, once again, things which were not fully delineated and they’re delineated in a more and more and more.

And what we thought was the case and if we had an exam and we were taking our board exams, and like, okay, that was answer. Yeah, but the real answer should have been endocannabinoids, COX-2, you know. So once again, what we know, we stay humble about. So we wanna bolster the endocannabinoid system without question. A beautiful graphic. Once again, all these slides are gonna be available for you folks. And we’re going to be able to look at these, review them again, and I’m hoping to offer more presentations like this at different levels.

But I wanted to speak very broadly to the group as we all come with different knowledge and different foundational research before we get there. So a couple more slides and we’re gonna open up for questions. Well, what about endometriosis and endocannabinoids? In women with endometriosis there are elevated circulating levels of anandamide and 2-AG with the decline and local CB1 expression, which implies a negative feedback loop. This may interfere with the capability of these mediators to manage pain.

Once again, pain takes all kinds of forms. And once again, the authors say, “These preliminary data suggests that the pharmacological manipulation of the action or levels of these mediators may offer alternative option for the management of endometriosis-associated pain,” reproductive sciences. So once again, they’re looking all over to see now that we found our best new friend, the endocannabinoid system. Remember, Han Celia back in the ’30s talk about the fight or flight response, and how he discovered the stress response.

Well, now this was the ’92 discovery 60 years later. I wonder what else they’re going to discover. I hope I can hear the next big thing before I’m done practicing. Joint pain. Once again, lots of research showing that it has tremendous ability with joint pain. Preclinical and human data that do exist indicate that the use of cannabis should be taken serious as a potential treatment for joint pain. That must have been one 2017.

And when we look at modulation of pain, once again, that’s affecting the GABAergic which is GABA. Remember, that’s inhibitor. That’s calming. It’s relaxing the body’s responsiveness. And they talk about the fact that the cannabinoid agonist retain their efficacy while some morphine does not in animal models of neuropathic pain. Remember, how we started with a move from the poppy to the hemp, changing plants? Well, once again, we know that morphine, you get habituated. You need more and more opioids? Well, the cannabinoids, you don’t end up needing that especially when you start low, go slow, and work within that person’s need.

If a person is a little thirsty, you give them a little bit of water. A person is really thirsty, you give them more water. Very common sensical for us as clinicians. But patients in our country are, “Supersize me,” and they go for more. Not necessarily. And so as we finish the slides here CB1, and CB2 receptors very important, but there are other receptors as well, the TrpV1, the 5-HT1A, as well as G coupling proteins and phytocannoids such as THC and CBD are also known to activate CB1 and CB2. But in our clinical practices, we are not wanting THC in the clinical practice. We do recreational as a whole another conversation between us and our boards. 

But the CBD you wanna make sure that we’re just using CBD and we’re not going into the marijuana side of things. So this is why we’re using a company which has either no THC or documented very clearly less than 0.3% THC. Well, that’s where the Farm Bill and the Hemp Rule comes in. That’s considered hemp less than 0.3%. 

So what happens is you can increase the absorption of a substance, not only as you take it in orally but it gets through the GI tract better. It goes systemically better. Well, that would make good sense. And this is called a VESIsorb. It’s a technology that’s used by TruGen to actually help with the dissolution of things which otherwise might be hard to actually get delivered. So once again, something is only as good therapeutically as the ability to absorb. You found this with topicals before, one that smells really and really powerful, but really didn’t help a patient. And you found your favorite topical in your clinical practice.

Well, it’s the same thing, well something like, “I tried CBD it didn’t work.” I have patients all the time come in “Well, I tried magnesium and it didn’t work,” but did you take the right form and the right delivery mechanism? So the concept here of VESIsorb is it causes an association colloid. So if you were to pierce a capsule of a VESIsorb, put it in water, it’s actually going to dissolution. It’s gonna dissolve much better than one that does not have this technology. So as a result, what are we? We’re largely water so it makes sense that we have that dissolution.

And if you look at the COA here, Certificate of Analysis, any CBD product I have in my clinical practice, I want a certificate of analysis. I want to see what are the actors, but I want to make sure there’s no THC here. As you can see, none detected. So there’s no question. Is there a psychoactive? There’s no psychoactives documented. Plus you’re looking for what’s called the hemptourage affect. So there’s an entourage effect, which is usually limited to marijuana. Well, the hemptourage effect is kind of a dials interaction with the beta caryophyllene, the CBG, the D-Limonene and others.

Once again, plants come with a whole array of other actors, like vitamin C is great, but Vitamin C with bioflavonoids is more natural and more effective on…some says it’s on absorption. So the concept here is we know a lot about CBD. We know it’s what we’re talking about today, but some of these other things like the beta caryophyllene the D-Limonene are all things which also have their own therapeutic effect, even Muracine [SP] and other things.

Plus you want to make sure you’re not giving a patient, and we all know this, things that are toxic and/or contaminated. So once again, a CofA for all your supplements is very important, but particularly in CBD land. So once again, not detected. Very important. You want to have a non-detected. So start low. Go slow. Work with a gentle modulatory pathway of endocannabinoid system, or working within something our body has been doing for eons and eons and eons for generations.

I usually start with 15 to 25 milligrams per day. You can start higher if you want and then move to two to three times. Always put the foot in the water and see… It kinda aligns with that show “Jaws,” [inaudible 01:01:47]. I always start low. Hey, if a little bit does a trick over a few days wonderful. We found the magic dose. If not, we go higher. Once again. BID twice a day, TID three times a day as tolerated and as needed. If less get the job done, wonderful. Mission complete. Some patients will need much higher doses. But once again, don’t overshoot because we don’t wanna overshoot the minimal effective dose because we’re nudging the pathways.

Scientific literature has shown up to hundreds of milligrams per dose. In fact, one of the lectures I give on anxiety, the scientific literature shows 600 milligrams per dose for anxiety. Like, was that really needed, but once again they funded the study. They wanted it to have an effect. So they went for a very high dramatic dose I usually find these lower doses do the trick the vast majority of the time. We can always go higher. Nothing wrong with that.

And we wanna support other biochemical pathways, of course, always diet, lifestyle, supplements. And remember that fancy word I told you about, Palmitoylethanolamide? That is this another fatty acid amide which is endocannabinoid like which helps neuropathic pain. So once again, a whole another pathway, but the literature is just so compelling. I always like to use other anti-inflammatory herbs. So I’ll work on either the COX or LOX pathways in lieu of majority of the time the NSAIDs.

So as a result, we are I think done, but I think we just need to stay humble in realizing that we’re continuously learning. There’s recent reviews, so 65 potential molecules target for CBD, and 65 so far is what I would say. So I’m gonna open it up for questions.

Rick: Thank you, Dr. Meletis. This has been extremely informative. We’ve been collecting some questions from the audience that we’re gonna get to. We’ve got time for three questions, but any questions that haven’t been answered we’ll add them to the final transcript. And afterwards, we’ll have a special offer for our webinar participants. Our first question, a doctor, a, “Do we need to worry about drug interactions when prescribing CBDs?”

Dr. Meletis: That’s a great question, and I can actually provide some information on this. GW Pharmaceuticals, the drug company, did some studies on this. When you go for high, high milligram doses, yeah possibly. When you go for the lower dosing, I have never seen a problem. There is something called a cytochrome 450 pathway. It seems like this doctor’s dialed in on drug interactions. So if you do too much grapefruit, you’ll affect cytochrome 450 pathway. If you BBQ too much, you affect another pathway. So the answer is on the lower doses I was talking about, never seen a problem. If a person is super sensitive, tell them to talk to their pharmacist, but never seen a problem with a reasonable dosing regime.

Rick: All right. Another question for you. Is vaping CBD more or less effective than a capsule?

Dr. Meletis: The vaping inside of things, of course, beyond the fact that you’re absorbing through a lung. The lung is a great way to absorb things. But I think using it in a more bioavailable oral dosing really works better and offers more deliverable, and it’s also more economic. I’ve had patients do CBD vaping and it just doesn’t seem to actually have the same effect. Now if it’s working for the patient and from a regulatory perspective, okay, then I would say use what works, but I’m usually an oral dose person myself or topical.

Rick: Okay and our third question. Is CBD okay to recommend to a pregnant patient?

Dr. Meletis: The ultimate question that nobody wants to touch. I would say that would I consider doing that? The answer is yes. Would I do it in exciting fashion in today’s ligatory world? No. With 1 in 38 children coming out with autism if they’re boys, 1 in 145 for girls, do I want any part of even be part of that equation? The answer is no. Now philosophically the body has an endocannabinoid system, could it be helpful? Probably it could be helpful. Do I want to have the liability for it? No, I do not.

Rick: All right, thank you, Dr. Meletis. We also have a special offer for our webinar participants, a free one-week sample of TruEase hemp oil, a $32 value. You can sign up for the free sample on the registration page at www.chiroeco.com/tg3truease, T-R-U-E-A-S-E GEN. That’s chiroeco.com/tg3truease, the registration page. In addition to the free sample, you also receive an offer for three free when you purchase 12, which is a 20% savings.

So at this time, we’d like to thank our sponsor, TruGen3 and Dr. Chris Meletis for today’s webinar. And thank you all for attending. Remember, this webinar including our speaker’s PowerPoint presentation, has been recorded. We will alert you when the webinar is available online. Thanks again for attending and we look forward to seeing you next time. Have a great day.