Nanobles Corp. / Global Cannabinoid Research Center (GCRC)

In the 2012 study on “Biphasic Effects of Cannabinoids in Anxiety Responses,” researchers explored how cannabinoids exert different effects at varying doses, finding that CB1 and GABA_B receptors control the balance between GABAergic (inhibitory) and glutamatergic (excitatory) neurotransmission. The study illuminates a critical point for understanding CBGa: I have found in my research that it displays biphasic action—different physiological responses at different doses—not because CBGa itself directly causes these varied effects but because it triggers the Endocannabinoid System’s (ECS) response, creating a concert of the impact that shift from relaxation to energy and activity at higher levels. I've also found it to have Biphasic activity with the same dose over some time; I study on myself using up to 2,500mg at once - an overwhelming amount of CBGa for anyone that doesn't know how to counter it with other cannabinoids and dietary substances. In these studies, after a period of high-level energy that was difficult to maintain thought in super high doses but less so in doses of 1250mg, very productive thought patterns (cognitive responses) developed at doses of 1000-1250mg after 4 hours, and very productive thought patterns developed 5-6 hours after doses of up to 2,500mg. At the same time, productive cognition was increased at all doses ranging from 250 to 500mg, and in doses from 500 to 1000mg, the energy bursts lasted up to 2 hours before relaxation started. In the 2012 study, a CB1 receptor agonist, CP-55,940 (a THC-like substance), was used at low doses to produce an anxiolytic (anti-anxiety) effect, while higher doses triggered anxiogenic (anxiety-inducing) responses. These effects appear mediated by distinct neural pathways, with CB1 receptor activation on glutamatergic neurons generating calming effects. In contrast, activation on GABAergic neurons elicited heightened anxiety and exploration tendencies at higher doses. Significantly, GABA_B receptor modulation influenced these reactions by attenuating the anxiety response at high doses, revealing the intricate and collaborative role between ECS and GABA pathways in dose-dependent effects. Understanding this biphasic action is pivotal in unlocking CBGa’s therapeutic potential. Low doses may engage the ECS to foster relaxation, while higher doses activate it to increase alertness, mimicking the ECS's natural rhythm in modulating activity and restfulness. This “energy effect,” as I call it, is thus ECS-driven; in its action, it's balancing GABA and glutamate to shift from calm to alertness as needed. This knowledge is intriguing and crucial for the future of cannabinoid research and therapeutic applications. I've found for years that CBGa is a modulator that leverages the ECS to fine-tune physiological states through natural, dose-responsive mechanisms. -Mike Robinson, Founder Global Cannabinoid Research Center #CannabisMyMedicine #HempMyMedicine ResearcherOG.com

"Reducing CB1 receptor activity under hypothermic stress can blunt the body's response to cold exposure, making it more challenging to maintain a stable core temperature. THIS? I just learned today - So, I hope people read as much as possible and learn how to survive in an environment of harm, including overworked doctors who are rushed and unable to manage caseloads. If I don't treat myself, the outcome will be fatal; slowly, over 4 months, I've become more sedentary due to the increased pain, decreased energy, and overall disruption of homeostasis - just as I entered complete remission in a Cancer battle. Now I know I need to concentrate on CB1 action. Does that mean I should hammer THC and CBN all day? No, it means I need Anandamide to be doing that - so my balance and intake of cannabinoids and other supplements to allow that must happen - a dietary change will occur to go back to the basics of eating Salmon for dinner - right now, I don't have the building blocks in my diet to create endocannabinoids. While supplements help, food is the number one way to make the body do what it should. Harsh Impact on Immune and Pain Response: Hypothermia temporarily weakens immune function, and this immune suppression also affects the ECS, as many immune cells express CB2 receptors. CB2 receptor activation generally helps reduce inflammation and promote balance within the immune system. Over the summer, it took double the amount of THC to stop the pain, and now I'm facing a super high THC tolerance with ingested - and CBN. I'm using over 2,000 mg a day of the two, intense, huh? The immune suppression caused by hypothermia, combined with altered ECS signaling, can increase susceptibility to infections during recovery and may mask or alter the body’s pain signals, affecting overall pain perception. So, as a Cancer patient, I'm fighting infection after infection, fever after fever, and viruses that walk through my door are almost like an automatic that I'll get - keeping my ECS very active with up and down-regulation is imperative to my survival - it's that crucial." Read the article here: https://lnkd.in/gskYdxph

"When you find out you have Cancer - you fight. When you discover within yourself that you're addicted to a substance, at first, you hide it. It's such a big difference, so when it comes down to it? Fighting Cancer is not a choice - you do it, or you die. Now, how you do so is I chose Cannabis oils, plant extracts, and nature in this battle and the last one a decade ago. But, quitting any addiction or substance that has your life turned upside down? That's a very personal choice, and it's hard to make - the more people telling you what to do, the harder it becomes. Cannabis is definitely a friend and extracts of the plant can be of serious value as they ping the base of the MU-1 Opioid Receptor; at every receptor site, there are CB1 cannabinoid receptors. That makes it the most opportune plant to help any addiction, as pinging that area causes the reward center to light up and that slows withdrawal and stops urges. In my battle, I defended the use of Oxy for Cancer until the same doctor who helped me say goodbye to opioid addiction on 1/26/2019 told me I did not need Oxycodone and that she wouldn't give it to me - but at first, she gave me 12 10mg Norco a day to stop taking the 90mg of Oxycodone. When I was slow to refill it due to not needing that many, she reduced it to 8, then to 6, then to 4. So, by the time I quit, it was only 40 mg of Norco - which is now determined to be more challenging to stop using than the 90mg of Oxy! So, keep in mind that some doctors were trying to help us when they got us hooked - because she was with the Norco. When you're addicted, it's up to you to find a new path. Anytime you're fighting a shark - it's up to you to get yourself free from it. That includes Cancer." -Mike Robinson, Founder Nanobles Corp. / Global Cannabinoid Research Center (GCRC)

"I was always a stoner who loved weed far before legalization. THC has always been something that soothed my soul and allowed me relaxation. I never thought I'd have problems with it until I decided to quit using Opioids after a 24-year pharmaceutical addiction. I got head rushes that would cause nausea and had other issues that led me to the bathroom far more than I wanted, as withdrawal isn't pretty. As a researcher, I had CBGa on hand when trying to quit Opioids in the final exit - and in a form that could be dabbed or ingested. I was never interested in it until I used it both ways and found relief. I found in research much later that the lack of endocannabinoid balance was causing issues as I had used heavy doses of THC oils in a cancer battle that lasted years. I never quit the strong pharmaceutical pain medications I started getting in 1995 until I began using CBGa. THC is still a massive part of my protocol, but I keep myself balanced and operate a good amount of the day on a solid dose of the acidic mother major, which keeps me productive. Even today, so many years later, CBGa kept me behind the desk as if I hadn't felt that great, but she never let me down that way. When people are tired, have high tolerances, or complain about a lack of energy? I always have the same words "CBGa Baby"!! -Mike Robinson, founder Nanobles Corp. / Global Cannabinoid Research Center (GCRC)

"Is this ECS the answer? Hypoxic-ischemic encephalopathy (HIE) is a severe condition caused by insufficient blood and oxygen to the brain, often affecting newborns after a difficult birth. It is fatal or permanent brain damage in severe cases. The 2023 study "The Long-Term Neuroprotective Effect of the Endocannabinoid 2-AG and Modulation of the SGZ’s Neurogenic Response after Neonatal Hypoxia-Ischemia" investigates the potential neuroprotective and neurogenic effects of endocannabinoid 2-AG in neonatal rats subjected to hypoxic-ischemic (HI) brain injury, a condition leading to hypoxic-ischemic encephalopathy (HIE). The researchers aimed to explore whether administering 2-AG - abundant during the perinatal period - could reduce brain injury and enhance neurogenesis in the hippocampus, specifically in the subgranular zone (SGZ) of the dentate gyrus (DG), following HI. Key Findings: Neuroprotection at Postnatal Day 14: 2-AG treatment reduced brain injury, with lower hemispheric and hippocampal damage than untreated HI animals. This was observed through improved hemispheric ratios and larger hippocampal areas, suggesting a significant neuroprotective effect in the short term. The DG in the hippocampus, a critical region for neurogenesis, showed higher cellularity and proliferation in 2-AG-treated rats. Ki67-positive (a marker for proliferating cells) and DCX-positive (a marker for neuroblasts) cells increased, indicating enhanced cell proliferation and neuroblast formation after treatment. Long-Term Protection at Postnatal Day 90: The study extended to P90 to assess whether 2-AG's neuroprotective effects were long-lasting. The results showed that 2-AG-treated animals had lower neuropathological scores, indicating sustained neuroprotection. However, hippocampal recovery was incomplete, while brain damage was reduced in 2-AG-treated rats. DG cellularity was still lower on the ipsilateral (damaged) side, suggesting that while 2-AG stimulates early neurogenesis, the survival of new neurons may be compromised long-term. Mechanisms of Action: The neuroprotective and neurogenic effects of 2-AG are likely mediated through its interaction with CB1 and CB2 cannabinoid receptors, which are involved in cell proliferation, differentiation, and survival. 2-AG activation of these receptors helps mitigate the inflammatory, excitotoxic, and oxidative stress processes triggered by HI. Clinical Implications: The results support 2-AG's therapeutic potential as an intervention for neonatal HI. Its neuroprotective effects were notable even under normothermic conditions, suggesting relevance for clinical settings, particularly in regions where therapeutic hypothermia is not routine. Further studies should investigate the long-term neurogenic effects of 2-AG and optimize conditions to support the survival and integration of newly generated neurons in the hippocampus." -Mike Robinson, Founder Nanobles Corp. / Global Cannabinoid Research Center (GCRC)

"Depression is painful, but most people don't align their emotions with that pain. People talk about stress being a killer but leave out the depression, and what goes up must come down. When our mood gets that low, there's one thing that can make us get high - Cannabis. It's the answer to so many of the issues we face daily. When we're not concentrating on the negative, our ECS changes how it uses endocannabinoids. When we laugh instead of stress, our ECS flourishes. Both anxiety and depression cause fluctuations in what endocannabinoids you may have; with most people already displaying a low tone (amount of them + receptor availability), it's straightforward to bounce back and forth from depressed to anxious and stressed - and in all of it feel way more pain than you usually would because the retrograde signaling of the ECS is hindered - you're chewing up endocannabinoids used to stop pain while stressing or glooming out about life. I know personally how hard it is not to do those two things, but we must find ways to smile - to reverse what's going on with us inside, with or without the use of Cannabis. We can balance our ECS; we have control. Take charge of your body by learning all you can about how your ECS works and how unique you are compared to everyone else!" -Mike Robinson, Founder Nanobles Corp. / Global Cannabinoid Research Center (GCRC)

"We have this system within us that controls our entire body - it's been marginalized and ignored, and its features curbed while our mainstream medical industry has financially thrived on our illnesses. We know now that cannabis has been medicine for at least 10,000 years - documented. Our nation unjustly prohibited a plant that could have likely saved 10,000,000 lives since 1937. The vast majority know what a cannabinoid is, but these endocannabinoids are a bit different. And what about this ECS—a system that controls other systems in our body that keep us alive? It sure seems like we all need to know a lot more - especially our doctors, who we leaned upon through illness and pain. The same ones that gave us drugs that didn't work out too great. So, let's keep this post very simple. Endocannabinoids are internally made substances that are 'cannabis-like' to make it easy - and they work in this system that directs and controls them. It's much like an air traffic controller deciding which plane goes where - but it's even more intense. The Endocannabinoid system also decides when new runways the cannabinoids and endocannabinoids land on must be built at its airport - based on the number of these substances in the system. These runways are called 'Cannabinoid Receptors'—the two that we know the most about are CB1 and CB2. While many favor THC due to its ability to medicate us in a way we can feel, others like cannabinoids like CBD, CBDa, or CBGa, which don't have that high to them. The exciting part is that they all cause the ECS to work. While some cannabinoids land on the CB1 and CB2 receptors directly, other cannabinoids help the body produce endocannabinoids to activate these receptors or to make them more available to the system. Fascinating, isn't it?" -Mike Robinson, Founder Nanobles Corp. / Global Cannabinoid Research Center (GCRC)

"Some people look at Autism like it's some type of disease that should be treated and cured, when I look at my daughter I only see a human being that knows how to love on a level most never will." -Mike Robinson, Genevieve's Daddy and founder Nanobles Corp. / Global Cannabinoid Research Center (GCRC) #AutismAcceptance

"I can attest that the research on this is true, in many regards, both in that Cannabis and its extracts help us quit the medications - and that we stay on them due to that fear of withdrawal. Most of us who have been addicted to any substance have continued taking it, sometimes for extended periods, after it lacked efficacy but still stopped what would happen without it. We'd face a world that we might not be able to handle. With seizure drugs, quitting them has a twofold effect because of the fear of what will happen - the consequences of not taking the drug can be deadly, much like the consequences of continuing that very same substance for extended periods. It's a catch-22; many people who have to use pharma for long periods, for whatever reason, have arthritis and other bone health issues, including dental, down the line. It's pretty hard to offset what the substances do to our system - but we can with diet, our lifestyle, and what we use. The plant's value is immense. Regardless of what we face in life, there are variations of cannabinoids that work well, do the job, and help us either offset the damage or allow sparing doses to avoid continued synthetic substances." -Mike Robinson, Founder Nanobles Corp. / Global Cannabinoid Research Center (GCRC) #AddictionFree #CannabisMyMedicine

Smoking cannabis helps OCD, according to a 2023 study titled "Treatment-resistant OCD: Pharmacotherapies in Adults," published in the journal Comprehensive Psychiatry. The study explored the "clinical features of obsessive-compulsive disorder (OCD) that are associated with poorer response to serotonin reuptake inhibitors (SSRIs)" and discussed alternative treatments, including cannabinoids from cannabis and hemp, for cases of treatment-resistant OCD. Obsessive-compulsive disorder is typically a chronic condition characterized by repeated unwanted thoughts (obsessions) and ritualized behaviors (compulsions) that sufferers engage in to reduce anxiety. The Mayo Clinic describes OCD as a cycle where patients, despite efforts to stop or ignore their obsessions, are driven to compulsive behaviors to ease their anxiety, resulting in significant distress and interference with daily life. While research on cannabinoids for OCD remains limited, some studies have shown promising results. For example, dronabinol, a synthetic version of THC, led to a "significant decrease in OCD symptoms" in some patients. However, another clinical trial involving nabilone, another synthetic THC, showed only minimal symptom improvement. A different trial with 14 OCD patients who smoked cannabis found no significant difference between those using cannabinoids and those receiving a placebo. Despite mixed results in clinical trials, an online survey of OCD patients self-reported an "acute positive effect" of smoking cannabis on their symptoms. For those with both OCD and Tourette syndrome, the results are similarly mixed, with some showing improvement and others showing little change. As with most studies on cannabis, the authors emphasized the need for more comprehensive research, including pre-clinical studies and long-term human trials involving larger groups of participants. Larger studies can provide more reliable data, but they also present challenges in terms of cost and management." -Mike Robinson, Founder Nanobles Corp. / Global Cannabinoid Research Center (GCRC) Research Link: https://lnkd.in/eJNQh22h