Dr. Newton’s unique background, featuring specialized AI certifications in both healthcare and business, allows him to bridge the gap between complex technology and real-world professional application...
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This presentation introduces the endocannabinoid system, or ECS, a critical but often under-taught regulatory system in human physiology. The speaker is an interventional pain physician and medical director with a focus on cannabis therapeutics and healthcare innovation. This material is presented for educational purposes only, with no financial compensation, and it is important to recognize that cannabis remains federally classified as a Schedule I substance, with variability in state laws and many therapies not FDA approved.
The primary goal of this discussion is to clearly define what the endocannabinoid system is, understand where it is located in the body, explain how it functions physiologically, and explore why it is clinically relevant across a wide range of diseases. Additionally, we will examine current research and future directions that may further expand our understanding of this system.
This topic is particularly important today because of the rapid expansion of medical, pharmaceutical, and psychiatric research related to cannabinoids, as well as evolving legal frameworks. Despite this, the ECS remains underrepresented in traditional medical education, creating a gap in understanding that is increasingly relevant in clinical practice.
Recent high-quality studies between 2024 and 2026 highlight the growing clinical relevance of cannabinoid-based therapies. Evidence from systematic reviews and randomized controlled trials suggests modest but statistically significant benefits in conditions such as chronic neuropathic pain, metabolic disorders, and neurodegenerative diseases. At the same time, these studies emphasize important limitations, including side effects, variability in patient response, and the need for careful dosing and patient selection. Emerging therapies targeting cannabinoid receptors, including next-generation ligands and allosteric modulators, are expanding the therapeutic landscape while also introducing new challenges in safety and clinical integration.
Understanding the ECS begins with its discovery, which was driven by cannabis research. The identification of THC in 1964 led to the discovery of the CB1 receptor in 1988, followed by the identification of endogenous cannabinoids such as anandamide in 1992 and 2-arachidonoylglycerol in 1995. This sequence demonstrates that studying plant cannabinoids ultimately revealed a naturally occurring system within the human body designed to regulate physiological processes.
At its core, the endocannabinoid system consists of three main components: endogenous ligands known as endocannabinoids, receptors including CB1 and CB2, and enzymes responsible for synthesis and degradation. The primary endocannabinoids, anandamide and 2-AG, are produced on demand from membrane lipids and are rapidly broken down by enzymes such as FAAH and MAGL. This on-demand production distinguishes them from classical neurotransmitters and allows for dynamic regulation of physiological processes.
Anandamide, often referred to as the “bliss molecule,” plays a key role in mood, reward, and emotional regulation, while 2-AG is more abundant and is heavily involved in immune function and inflammatory processes. Both bind to CB1 and CB2 receptors, influencing a wide range of biological effects.
CB1 receptors are predominantly located in the central nervous system, where they regulate cognition, memory, pain perception, appetite, and motor function. In contrast, CB2 receptors are primarily found in peripheral tissues and immune cells, where they modulate inflammation and immune responses. The widespread distribution of these receptors throughout the body underscores the ECS’s role as a global regulatory system.
Functionally, the ECS operates as a homeostatic system, helping maintain balance across multiple physiological domains. It modulates neurotransmitter release, immune signaling, inflammation, metabolism, and stress responses. At the cellular level, activation of cannabinoid receptors influences intracellular signaling pathways such as cAMP, calcium channels, and protein kinase cascades, ultimately affecting gene expression and cellular behavior.
Phytocannabinoids, such as THC and CBD, interact with this system by mimicking or modulating endogenous signaling. THC acts as a partial agonist at CB1 receptors, producing psychoactive effects, while CBD has more complex, indirect actions across multiple receptor systems, including serotonin, TRPV1, and adenosine pathways. Despite structural differences, both endogenous and plant-derived cannabinoids are able to influence the same receptor systems, illustrating the adaptability of ECS signaling.
Clinically, the ECS plays a significant role in pain modulation, mood regulation, appetite control, and neuroprotection. Dysregulation of this system has been associated with a variety of conditions, including chronic pain syndromes, anxiety, depression, neurodegenerative diseases, and metabolic disorders. The concept of clinical endocannabinoid deficiency has been proposed to explain conditions such as migraine, fibromyalgia, and irritable bowel syndrome, where reduced endocannabinoid tone may contribute to symptom development.
The ECS is also deeply involved in immune regulation, influencing inflammatory responses and cytokine signaling. This has important implications for conditions involving immune dysfunction, as well as for emerging therapies targeting inflammation and neuroinflammation.
In addition to neurological and immune functions, the ECS interacts with multiple physiological systems, including the gastrointestinal tract, cardiovascular system, and endocrine pathways. It plays a role in maintaining energy balance, regulating appetite, and responding to stress. This broad integration highlights its importance as a central regulator of overall health and homeostasis.
Emerging research continues to expand our understanding of the ECS, particularly in areas such as neuroinflammation, chronic pain management, metabolic disease, and substance use disorders. Ongoing clinical trials are investigating cannabinoid-based interventions for conditions including aging-related decline, endometriosis, HIV-related inflammation, and cannabis use disorder itself. These studies suggest that the ECS may serve as both a therapeutic target and a biomarker for disease.
In summary, the discovery of THC led to the identification of a complex and widely distributed physiological system that plays a critical role in maintaining balance within the body. The endocannabinoid system consists of endogenous ligands, receptors, and enzymes that work together to regulate numerous biological processes. CB1 receptors are concentrated in the nervous system, while CB2 receptors are more prominent in immune tissues, and both contribute to the system’s broad functional impact. Clinically, the ECS is increasingly recognized as a key factor in a wide range of diseases, either through direct dysfunction or as a modulator of symptoms. Continued research will further clarify its role and improve our ability to target this system therapeutically for better patient outcomes.
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This presentation begins by introducing the topic of Cannabis Use Disorders, establishing both clinical credibility and context. The speaker is a board-certified anesthesiologist with expertise in pain management, medical cannabis, and healthcare AI, currently serving as Medical Director for a large U.S. dispensary system. It is important to clarify upfront that cannabis remains federally classified as a Schedule I substance, state laws vary, and many cannabis-based treatments are not FDA approved. The content is educational in nature, with no financial conflicts influencing the material.
The module is structured in two major parts. The first focuses on Cannabis Use Disorder, including diagnostic criteria, epidemiology, risk factors, and evidence-based interventions. The second addresses Cannabinoid Hyperemesis Syndrome, including clinical presentation, diagnostic criteria, pathophysiology, and management. The broader goal is to understand how increasing accessibility and normalization of cannabis impacts both individual health and public health systems. Learners are expected to analyze the public health implications of CUD, evaluate research and policy, and identify clinical strategies for managing both CUD and CHS.
The discussion begins with a clinical case of a 16-year-old with daily cannabis use via vaping and edibles. The patient demonstrates hallmark features of CUD including irritability, academic decline, family conflict, tolerance, withdrawal, and craving. Treatment using motivational enhancement therapy combined with cognitive behavioral therapy and contingency management resulted in improved abstinence compared to therapy alone. This highlights the importance of combining behavioral interventions with reinforcement strategies, particularly in adolescents where reward-based systems are highly effective.
A second case examines a 22-year-old with frequent daily cannabis use, poor sleep, mood disturbance, and relationship strain. A text-based peer counseling intervention resulted in significantly higher abstinence rates and reduced cravings. This demonstrates how technology-based, peer-influenced interventions can be highly scalable and effective in young adult populations. These cases illustrate that treatment success improves when interventions are tailored to developmental stage and social context.
The effectiveness of these interventions can be understood through behavioral and social mechanisms. Contingency management works by providing immediate rewards that counterbalance the delayed benefits of abstinence, strengthening behavior change. Text-based interventions leverage peer norms, increase accessibility, and provide support during high-risk moments. Together, these approaches demonstrate that aligning treatment strategies with cognitive and social development improves outcomes.
Both cases map clearly onto DSM-5 diagnostic domains, including impaired control, social impairment, risky use, and pharmacologic features such as tolerance and withdrawal. Cannabis Use Disorder is diagnosed when at least two criteria are present within a 12-month period, with severity classified as mild, moderate, or severe depending on the number of criteria met. These domains provide a structured clinical framework for identifying and categorizing the disorder.
Epidemiologically, approximately 1.5% of U.S. adults meet criteria for CUD, while over 35% of high school seniors report cannabis use within the past year, and globally about 192 million individuals use cannabis annually. Cannabis is now the third most commonly used psychoactive substance worldwide. The risk of progression to CUD varies significantly, with about 1 in 10 regular users developing the disorder, increasing to 1 in 6 for those who begin in adolescence, and as high as 25 to 50 percent among daily users. Early onset and frequency of use are the strongest predictors of progression.
Cannabis Use Disorder has significant public safety implications. These include increased risk of impaired driving and motor vehicle accidents, rising emergency department visits, reduced academic performance, and workplace safety concerns due to impaired judgment and reaction time. Beyond safety, functional impacts include lower educational attainment, decreased productivity, relationship strain, and social isolation, illustrating that CUD affects not only health but also broader social and economic outcomes.
There are strong associations between cannabis use and psychiatric conditions, including depression, anxiety, psychosis—especially with high-potency products—self-harm behaviors, and violence in certain populations. The relationship is bidirectional, meaning cannabis may worsen psychiatric symptoms, while individuals may also use cannabis to self-medicate. Shared genetic and environmental factors further complicate this relationship.
From a policy perspective, legalization has increased accessibility, normalized use, reduced perceived risk, and diversified product types. However, this has also introduced public health challenges such as increased emergency visits, rising cases of CHS, youth exposure, and gaps in potency regulation. One of the most significant risk factors is the dramatic increase in THC potency, which has risen approximately 400% since the 1980s, with modern products often containing 15 to 30 percent THC compared to about 3 percent historically. This increase is associated with higher rates of adverse effects including psychosis and CUD.
Neurodevelopmental vulnerability is a critical factor, as the prefrontal cortex continues to develop until around age 25. Cannabis exposure during this period is associated with memory deficits, attention problems, impaired executive function, and potential long-term structural brain changes. Additionally, modern routes of administration such as concentrates, high-THC vapes, and edibles increase risk due to higher potency, rapid delivery, delayed onset, and longer duration of effects.
Psychosocial factors also play a major role. In adolescents and young adults, peer influence, identity formation, and risk-taking behaviors drive use. In older adults, cannabis use is often related to self-medication for pain, sleep disturbances, or chronic conditions. Medical comorbidities, including chronic pain and insomnia, further increase exposure risk, while polypharmacy raises concerns for drug interactions. Social determinants such as economic stress, community norms, marketing exposure, and access to healthcare create unequal risk distribution across populations.
Cannabis withdrawal typically begins within 24 to 72 hours, peaks at about one week, and resolves within one to two weeks, although some symptoms may persist longer. Common symptoms include irritability, anxiety, sleep disturbances, decreased appetite, restlessness, depression, and cravings. Effective screening requires open-ended, nonjudgmental questioning, assessment of use patterns, and inclusion of specific questions such as hot shower use to identify potential CHS.
Treatment for CUD is primarily psychosocial. Motivational interviewing enhances readiness for change, cognitive behavioral therapy builds coping strategies, and contingency management provides reinforcement. Family and school-based interventions are particularly important for adolescents, while digital interventions such as text-based counseling and online feedback tools offer scalable solutions for young adults. Pharmacologic treatments such as N-acetylcysteine and gabapentin may help with withdrawal but have limited evidence for long-term effectiveness, reinforcing that medications are adjuncts rather than primary treatments.
Treatment strategies should be tailored to life stage. Adolescents benefit from family involvement and school-based support, young adults respond well to digital and peer-based interventions, and older adults require attention to comorbidities, medication interactions, and age-specific motivations. Relapse prevention focuses on identifying triggers, improving sleep, managing mood, and developing non-using social networks. Progress should be measured through objective metrics such as urine screens and functional outcomes including academic performance, relationships, and quality of life.
The presentation then transitions to Cannabinoid Hyperemesis Syndrome, a paradoxical condition associated with chronic cannabis use. A case of a young adult female demonstrates classic features including cyclic vomiting, severe abdominal pain, multiple emergency visits, and relief only with hot showers. Diagnosis is confirmed using Rome IV criteria, and symptoms resolve completely with cannabis cessation. Another case involving a middle-aged male highlights the effectiveness of haloperidol for symptom management, with caution regarding side effects, and reinforces avoidance of opioids.
CHS is characterized by three phases: a prodromal phase with nausea and continued cannabis use, a hyperemetic phase with severe vomiting and compulsive hot bathing, and a recovery phase following cessation. Diagnostic criteria include prolonged cannabis use, cyclic vomiting, symptom onset after extended exposure, relief with abstinence, and hot bathing behavior. Differential diagnosis includes conditions such as cyclic vomiting syndrome, gastroenteritis, bulimia, and gastroparesis.
The pathophysiology of CHS involves several proposed mechanisms. Chronic CB1 receptor activation may disrupt gastrointestinal motility, while receptor downregulation alters signaling. THC’s lipophilic nature leads to storage in fat and re-release during stress, causing symptom recurrence. Genetic variations in metabolic enzymes may influence susceptibility. The role of TRPV1 receptors explains why hot water and capsaicin provide symptom relief by modulating substance P signaling.
CHS represents a growing public health issue, particularly among youth and young adults with high rates of cannabis use. Emergency department visits for CHS have increased significantly, contributing to healthcare burden and costs due to repeated imaging, hospitalizations, and misdiagnosis. Early recognition is critical to reducing both patient suffering and healthcare utilization.
The definitive treatment for CHS is cannabis cessation, with resolution rates approaching 97 percent. Acute management focuses on hydration, electrolyte correction, symptom control, and patient education. Patients must understand that while temporary treatments provide relief, cessation is the only true cure.
The presentation concludes by emphasizing broader considerations including ethical prescribing, patient safety, public health policy, and the long-term effects of cannabis exposure. The key takeaway is that while cannabis has therapeutic potential, its increasing potency, accessibility, and normalization require careful clinical, educational, and policy responses to mitigate associated risks.
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Detailed Speaker Notes Outline: Exploration of the Endocannabinoid System (ECS)
Detailed Speaker Notes Outline: Exploration of the Endocannabinoid System (ECS)
1 — Title / Conference Introduction
1 — Title / Conference Introduction
Welcome the audience. Acknowledge the Cannabase Conference at Morehouse College, April 10–12.
Brief self-introduction: interventional pain physician, State Medical Director at Trulieve Florida, consultant on opioid alternatives.
Frame the talk: "Today we're going to explore a physiological system most of us were never taught in medical school — and ask why."
2 — Disclosures
2 — Disclosures
Interventional pain physician with research interests in medical cannabis for chronic pain and mental health.
No remuneration for this presentation.
Important legal framing: Cannabis remains Schedule I federally. State laws vary widely.
Many cannabinoid-based medicines discussed today are not FDA approved — distinguish between Epidiolex, Sativex, dronabinol, and unregulated products.
Encourage the audience to apply a critical evidence-based lens throughout.
3 — Goals
3 — Goals
Walk through each goal deliberately:
What constitutes the ECS? — We'll cover its components and historical milestones.
Where is it anatomically? — CB1 and CB2 distribution throughout the body.
How does it function? — Receptor signaling, synthesis, degradation.
Why is it clinically important? — Disease states linked to ECS deficiency or dysfunction.
What research is underway? — Current trials and future directions.
4 — Agenda
4 — Agenda
Briefly preview the four major sections.
Emphasize the "recent publications" section — this is not historical review alone. The ECS science is actively evolving as recently as 2026.
Set expectation: some content will be molecular/pharmacological, but all roads lead back to clinical application.
5 — Why Is This Important Today?
5 — Why Is This Important Today?
Three drivers of urgency:
Recent medical, pharmaceutical, and psychiatric research — landmark Cochrane reviews, Phase 2 trials, neurodegenerative disease data published in 2025–2026.
Georgia-specific policy updates — acknowledge state-level movement on medical cannabis access and what it means for practitioners in this room.
Gap in traditional medical education — the ECS was discovered in 1988 and refined through the 1990s, yet most medical and nursing curricula still do not cover it as a core physiological system. This is a fundamental gap we must address.
6 — Study 1: Cochrane Review on Cannabis for Neuropathic Pain (2026)
6 — Study 1: Cochrane Review on Cannabis for Neuropathic Pain (2026)
Highest level of evidence: systematic review and meta-analysis of 21 RCTs, over 2,100 participants.
Examined THC-dominant, balanced THC/CBD, and CBD-dominant formulations.
A concurrent 2025 review (25 RCTs, n=2,303) found oral synthetic/high-THC products reduced pain scores by ~0.78 points on a 10-point scale — modest but statistically significant.
Nabilone showed the strongest signal at −1.59 points; dronabinol showed no effect.
Key clinical takeaway: benefits are real but modest. Adverse effects — dizziness, sedation, nausea — are notable. Patient selection and monitoring are essential.
This is your evidence base when patients ask: "Does it work for pain?"
7 — Study 2: Monlunabant for Obesity (Phase 2a RCT, 2025)
7 — Study 2: Monlunabant for Obesity (Phase 2a RCT, 2025)
First major trial of a next-generation CB1 inverse agonist — distinct from rimonabant, which was withdrawn from Europe in 2008 due to psychiatric adverse events.
16-week trial, 243 patients across 25 Canadian centers.
Weight loss ranged from 5.9–7.4% across dose groups — clinically meaningful.
However, narrow therapeutic window: 42% of patients on the 50mg dose withdrew due to adverse events — nausea, anxiety, irritability, sleep disorders.
Clinical relevance: The CB1 receptor's role in metabolic regulation is now a legitimate pharmaceutical target again. This represents a new chapter — with caution built in from the Rimonabant era.
8 — Study 3: ECS in Neurodegenerative Disease (Review, 2026)
8 — Study 3: ECS in Neurodegenerative Disease (Review, 2026)
Comprehensive review of ECS-targeted strategies for Alzheimer's, Parkinson's, Huntington's, and multiple sclerosis.
Introduces the concept of the "endocannabinoidome" — hundreds of mediators beyond classical AEA and 2-AG. This is a paradigm expansion.
Key challenges: receptor specificity, blood-brain barrier penetration, defining therapeutic windows.
Why this matters: current therapies for these diseases are symptomatic only. The ECS offers a pathway toward disease modification through neuroinflammation targeting.
9 — Study 4: Next-Generation Cannabinoid Ligands (Review, 2025)
9 — Study 4: Next-Generation Cannabinoid Ligands (Review, 2025)
Evolution from classical agonists to allosteric modulators, biased agonists, and covalent ligands.
Cryo-EM, optogenetics, and chemogenetics are accelerating drug discovery in this space.
Allosteric modulators are particularly exciting — they refine receptor control with potentially fewer side effects than direct agonists.
For clinicians: this is about understanding the pipeline. The next decade of cannabinoid pharmacology will not look like the last.
10 — Study 5: ECS Pharmacological Targets in CNS Disorders (Review, 2025)
10 — Study 5: ECS Pharmacological Targets in CNS Disorders (Review, 2025)
Synthesizes a decade of research (2015–2025) on CB1 and CB2 contributions to depression, anxiety, pain, MS, and Parkinson's.
CB2 receptor is the target for neuroinflammation — relevant to pain physicians and psychiatrists alike.
CB1 allosteric modulation is emerging for psychiatric conditions — potentially without psychoactive effects.
The challenge of safe dosing protocols is real — not yet solved, but actively being studied.
11 — History of Discovery (Timeline)
11 — History of Discovery (Timeline)
Walk through key milestones:
2700 BCE — Cannabis referenced in Hindu scripture (Atharva Veda).
450 BCE — Cannabis seeds burned at Scythian funerals (psychoactive ritual use).
1899 — First isolation of cannabinol from cannabis resin (Wood).
1940 — Cannabidiol discovered (Adams).
1964 — Δ9-THC isolated and structure elucidated by Raphael Mechoulam — this is the pivotal moment.
1988 — CB1 receptor identified in the brain (Devane et al.).
1990 — CB1 receptor cloned (Matsuda et al.).
1992 — Anandamide (AEA) isolated and pharmacology described (Mechoulam/Pertwee).
1993 — CB2 receptor cloned (Munro et al.).
1995 — 2-AG discovered (Mechoulam; Sugiura).
1999 — AEA shown to activate TRPV1 receptors (Zygmunt et al.) — expanding the ECS beyond just CB1/CB2.
2006 — Rimonabant approved in Europe for obesity, withdrawn 2008 due to psychiatric adverse events — a cautionary tale.
2018 — FDA approval of Epidiolex for childhood epilepsy — first plant-derived CBD product with regulatory approval.
12–13 — THC, CB1R, AEA, CB2R, 2-AG
12–13 — THC, CB1R, AEA, CB2R, 2-AG
Clarify the plant cannabinoids (THC, CBD) versus endocannabinoids (AEA, 2-AG).
The structural contrast matters: THC is a rigid bicyclic molecule; AEA is a flexible lipid chain. Yet they bind to the same receptor. This will be addressed later.
Timeline build: 1964 → 1988 → 1992 → 1993 → 1995 → 1999. Each discovery unlocked the next.
The discovery of AEA activating TRPV1 in 1999 was transformative — it revealed the ECS interacts with the vanilloid pain system. Directly relevant to interventional pain practice.
14 — Ligand Structures: Plant, Endo, and Non-Endo N-acylethanolamines
14 — Ligand Structures: Plant, Endo, and Non-Endo N-acylethanolamines
Show the chemical classes:
Phytocannabinoids: Δ9-THC, CBD
Endocannabinoids: AEA, 2-AG
Non-endocannabinoid N-acylethanolamines: PEA, OEA, Synaptamide
PEA (palmitoylethanolamide) and OEA (oleoylethanolamide) are increasingly studied for anti-inflammatory and analgesic effects — not directly cannabinoid, but part of the broader endocannabinoidome.
Clinically, PEA supplements are already available over-the-counter and patients may ask about them.
15–16 — Synthesis and Metabolism Pathways
15–16 — Synthesis and Metabolism Pathways
AEA is synthesized from NAPE via NAPE-PLD enzyme.
AEA is degraded by FAAH (fatty acid amide hydrolase).
2-AG is synthesized from diacylglycerol (DAG) via DAGL enzyme.
2-AG is degraded by MAGL (monoacylglycerol lipase), ABHD6, ABHD12.
Clinical pearl: FAAH inhibitors (e.g., URB597) and MAGL inhibitors (e.g., JZL184) are being studied to increase endocannabinoid tone by slowing degradation — a strategy relevant to pain and ASD research.
2-AG can also be oxidized by COX-2 into prostaglandin-glycerol esters — a convergence point between the ECS and the prostaglandin inflammatory pathway.
17 — Naming AEA and 2-AG
17 — Naming AEA and 2-AG
"Anandamide" derives from the Sanskrit word "ananda" meaning bliss, joy, contentment. Named by Mechoulam's team.
This is not accidental — early research showed its role in mood elevation and reward.
"2-AG" describes its chemistry: the arachidonoyl group attached at the second carbon of the glycerol backbone.
These naming conventions are worth sharing with patients — the "bliss molecule" framing resonates clinically when discussing mood disorders.
18–20 — CB1 and CB2 Receptor Structure and Signaling
18–20 — CB1 and CB2 Receptor Structure and Signaling
Both CB1 and CB2 are G-protein coupled receptors (GPCRs) with 7 transmembrane domains.
CB1 is coupled to Gαi — inhibits adenylyl cyclase, reducing cAMP, and modulates K+ and Ca2+ channels.
CB2 signals similarly but with different tissue expression and downstream effects.
CB1 activates:
Gαi → inhibits cAMP → reduces protein kinase A → modulates neurotransmission
β-Arrestin pathway → receptor internalization
MAPK pathway (ERK, p38, JNK) → gene expression, cell proliferation
Also interacts with TRPV and TRPA channels via Ca2+
Cryo-EM structure of CB2-Gi complex — highlight that we now have atomic-level resolution of how these receptors function. This is driving next-generation drug design.
21–22 — ECS Synaptic Signaling (CBD/AEA/2-AG at the Synapse)
21–22 — ECS Synaptic Signaling (CBD/AEA/2-AG at the Synapse)
Endocannabinoids are retrograde messengers — synthesized post-synaptically, they travel backward across the synapse to inhibit pre-synaptic neurotransmitter release.
This is the opposite of classical neurotransmission — a key distinguishing feature.
CBD's mechanism:
Weakly modulates CB1 (negative allosteric modulator)
Inhibits FAAH → raises AEA levels
Activates TRPV1 → desensitizes pain signaling
Agonizes 5HT1A → anxiolytic and antidepressant potential
Clinically: CBD's mechanism is not simply "binding CB1 less than THC." It is a pleiotropic molecule working across multiple receptor systems.
23–24 — ECS Signaling: GPCR/cAMP/PKA Pathway
23–24 — ECS Signaling: GPCR/cAMP/PKA Pathway
CB1/CB2 activation → Gαi subunit dissociates → inhibits adenylyl cyclase (AC)
Reduced AC activity → less ATP converted to cAMP
Less cAMP → less protein kinase A (PKA) activation
Less PKA → reduced cellular response (neurotransmitter release, ion channel activity)
Simultaneously, β/γ subunit activates MAPK → gene expression, proliferation, apoptosis
Clinical relevance: this is why cannabinoids can modulate pain, mood, inflammation, and cellular proliferation through one receptor system.
25 — Components of the ECS (Summary)
25 — Components of the ECS (Summary)
Core components — three-part system:
1. Endocannabinoids
AEA (anandamide)
2-AG (2-arachidonoylglycerol)
Minor eCBs: NADA, virodhamine (O-AEA)
2. Receptors
CB1 — predominantly CNS
CB2 — predominantly immune system
3. Enzymes
Synthesis: NAPE-PLD (for AEA), DAGL (for 2-AG)
Degradation: FAAH (degrades AEA), MAGL (degrades 2-AG)
Emphasize: the ECS is not a static lock-and-key system. It is a dynamic, on-demand regulatory network. Endocannabinoids are synthesized as needed, not stored pre-synaptically.
26–27 — Synthesis Pathways (Gandhi / Rahaman)
26–27 — Synthesis Pathways (Gandhi / Rahaman)
Walk through both pathways side by side:
2-AG pathway: Phospholipids → DAG (via PLC) → 2-AG (via DAGL) → CB1R/CB2R
AEA pathway: Phospholipids → NArPE (via NAT) → AEA (via NAPE-PLD) → CB1R
Degradation:
AEA → FAAH → arachidonic acid + ethanolamine
2-AG → MAGL, ABHD6, ABHD12 → arachidonic acid + glycerol
Cross-pathway interaction with COX-2 is critical for pain physicians: 2-AG can be shunted toward prostaglandin synthesis under inflammatory conditions. NSAIDs may actually affect eCB tone indirectly.
28 — CB1/CB2 Anatomical Distribution
28 — CB1/CB2 Anatomical Distribution
Reference the body map and address each system:
Brain (CB1): Nociception, neurotransmission, mood, cognition, appetite, motor control, drug addiction
Cardiovascular (CB1): Heart rate, hypotension, cardiac dysfunction
Cardiovascular (CB2): Cardiac protection
Liver (CB1): Steatosis, fibrogenesis, insulin resistance
Liver (CB2): Anti-steatosis, anti-fibrogenesis
Spleen/Immune (CB1 & CB2): Immunomodulation — this is why cannabis affects inflammation
GI Tract (CB1): GI motility, energy balance
Skeletal Muscle (CB1): Energy expenditure, insulin resistance
Bones (CB1 & CB2): Bone mineral density
GI (CB2): Nausea, emesis, diarrhea
Cancer: Both CB1 and CB2 expressed on tumor cells
Clinical pearl for pain physicians: CB1 receptors are co-localized with opioid receptors in the dorsal horn, spinal cord, and periaqueductal gray. This is the mechanistic basis for opioid-sparing potential.
29 — What Is the ECS? (Definitions)
29 — What Is the ECS? (Definitions)
Professional definition: The ECS is a complex regulatory network comprising cannabinoid receptors, endogenous ligands, and metabolic enzymes. It modulates neurotransmission, immune function, inflammation, and metabolic homeostasis to maintain physiological balance (Di Marzo & Piscitelli, 2015).
Patient-facing language: "The endocannabinoid system helps your body maintain a steady state — for your mind and body. When it's not working properly, symptoms like pain, poor sleep, anxiety, and mood instability can follow."
Tailor to condition:
Chronic pain patients: "This system regulates how your body processes pain signals."
Mental health patients: "This system influences anxiety, mood, and stress responses."
Cancer patients: "This system interacts with inflammation pathways relevant to both cancer and treatment side effects."
30 — ECS Homeostasis vs. Allostasis (Stella, 2023)
30 — ECS Homeostasis vs. Allostasis (Stella, 2023)
The inverted U-curve is one of the most important conceptual frameworks in cannabinoid medicine.
Homeostasis = the optimal range of ECS activity
Too little ECS activity (left of curve):
Depression, PTSD, anxiety, epilepsy
Too much ECS activity (right of curve):
Addiction, impulsivity, psychosis, adiposity
Clinical implication: therapeutic goal is to restore homeostasis, not simply to maximize ECS activity. This explains why both activating and inhibiting the ECS can be therapeutic depending on the condition and the patient's baseline state.
This is also why THC can be anxiolytic in low doses but anxiogenic at high doses.
31 — How Do Phytocannabinoids Act Like Endocannabinoids?
31 — How Do Phytocannabinoids Act Like Endocannabinoids?
Transition — pose the question rhetorically before answering.
"If these plant molecules were discovered 5,000 years before we even knew we had cannabinoid receptors — why do they work at all?"
The answer: evolutionary coincidence made possible by structural mimicry at the receptor binding site.
32 — Cannabis Plant Biosynthesis
32 — Cannabis Plant Biosynthesis
Cannabis produces 400+ compounds; over 100 are phytocannabinoids.
The starting point: CBGA (cannabigerolic acid) — the "mother cannabinoid."
Enzymatic divergence from CBGA:
CBGA → THCA → THC (via decarboxylation)
CBGA → CBDA → CBD (via decarboxylation)
CBGA → CBCA → CBC
Also present: terpenes (myrcene, caryophyllene — β-caryophyllene is itself a CB2 agonist), sterols, flavonoids
The entourage effect: the combination of cannabinoids, terpenes, and flavonoids may produce synergistic effects beyond any single compound. This is the scientific rationale behind whole-plant vs. isolate medicine debates.
33 — ECS+: THC's Receptor Interactions
33 — ECS+: THC's Receptor Interactions
THC is a partial agonist at CB1 and CB2.
But THC also acts at:
GLRA3 (glycine receptor α3) — pain modulation
GPR55 — a "third cannabinoid receptor"
5-HT3A — antiemetic mechanism; explains why THC reduces chemotherapy-induced nausea
The "ECS+" concept: THC and CBD don't just work through CB1/CB2. They engage a broader receptor network — GPCRs, ion channels, nuclear receptors.
34 — How Do Structurally Different Molecules Bind the Same Receptor?
34 — How Do Structurally Different Molecules Bind the Same Receptor?
THC is a rigid bicyclic terpenoid; AEA is a flexible polyunsaturated fatty acid amide.
Yet both bind CB1 with similar affinity in the nanomolar range.
The CB1 orthosteric binding site is a hydrophobic pocket that can accommodate both rigid and flexible ligands through different binding conformations.
Cryo-EM studies have now confirmed this — the receptor adopts different conformational states depending on the ligand.
Clinical implication: this flexibility in binding pharmacology is why biased agonists are possible — molecules that activate only select downstream pathways (e.g., analgesia without psychoactivity).
35 — ECS+: CBD's Receptor Interactions
35 — ECS+: CBD's Receptor Interactions
CBD is more pharmacologically complex than THC:
Negative allosteric modulator at CB1 — reduces THC's psychoactive effects
Partial agonist at CB2 — anti-inflammatory
Agonist at GPR55 — pro-motility, anti-cancer signals
Agonist at 5HT1A — anxiolytic, antidepressant
Agonist at TRPV1 — pain and inflammation
Modulator at GABAA — anticonvulsant (basis for Epidiolex)
Inhibitor of ENT-1 (adenosine transporter) → raises adenosine → anti-inflammatory via A2a receptors
CBD does not simply "counteract THC" — it has an entirely independent pharmacological profile.
36 — CBD's Full Target Map (Schouten & Dalle)
36 — CBD's Full Target Map (Schouten & Dalle)
Comprehensive visual showing CBD's interactions across:
Classical cannabinoid receptors (CB1, CB2)
Ion channels (TRPV1, TRPV2, TRP1A, TRPM8, GABAA)
Transcription factors (PPARγ)
GPCRs (GPR55, 5HT1A, opioid receptor, dopamine receptor, adenosine A2a)
Disease relevance:
Neurological: chronic pain, epilepsy, Alzheimer's, Huntington's, Parkinson's
Mental health: psychosis, anxiety, fear, depression, substance use disorder
Behavior: sleep, motor control, cognition, memory
This is why CBD research is so broad — it's not a single-target drug. It's a systems pharmacology agent.
37 — Comparison Table: Endo- vs. Phytocannabinoids
37 — Comparison Table: Endo- vs. Phytocannabinoids
Walk through key parameters:
AEA
2-AG
Δ9-THC
CBD
Half-life
1–2 hrs
5–10 min
20–30 hrs
18–32 hrs
CB1 affinity (Ki)
61 nM
472 nM
41 nM
Low
Metabolizing enzyme
FAAH
MAGL, FAAH
CYP2C9, CYP2C19, CYP3A4
CYP2C19, CYP3A4
Clinical takeaways:
AEA and 2-AG are rapidly degraded — they are on-demand, local messengers.
THC has a much longer half-life — explains persistent psychoactive effects and drug test detection windows.
CBD's metabolism via CYP3A4 is clinically important — drug-drug interactions with statins, anticoagulants, antiepileptics.
38 — Binding Affinity: Phytocannabinoids
38 — Binding Affinity: Phytocannabinoids
THC: Partial agonist at CB1 and CB2 (Ki ~5–80 nM CB1; ~1.7–75 nM CB2). Bioactivities: analgesic, antiemetic, orexigenic, muscle relaxant (MS spasticity).
CBD: Antagonist/inverse agonist, negative allosteric modulator at CB1; partial agonist at CB2 (Ki >10,000 nM CB1 — very low direct affinity). Bioactivities: anti-inflammatory, anti-nociceptive, antioxidant, neuroprotective, immunosuppressive, anxiolytic.
Δ9-THCP: ~1.2 nM CB1 — extremely high affinity. Analgesic. Minor cannabinoids like THCP may explain why some strains have disproportionate effects.
Important: low Ki = higher affinity. CBD's low CB1 affinity does not mean it is pharmacologically inactive — its mechanism is indirect and allosteric.
39 — Binding Affinity: Endocannabinoids / Synthetic Agonists
39 — Binding Affinity: Endocannabinoids / Synthetic Agonists
ACEA, ACPA, Methanandamide, O-1812 — synthetic analogs developed for research.
These help us understand structure-activity relationships — which parts of the molecule drive receptor binding vs. selectivity.
Bioactivities span: antidepressant, anti-nociceptive, antiemetic, anti-proliferative, neuroprotective — reinforcing the ECS as a multi-function system.
40 — Clinical Relevance: AEA and 2-AG
40 — Clinical Relevance: AEA and 2-AG
AEA clinical relevance:
Pain: Modulates central and peripheral pain signals — rationale for cannabis in chronic pain
Mood: CB1 modulation in limbic system → anxiety and depression
Metabolism: Appetite and energy balance — obesity target
Neuroprotection: Parkinson's, Alzheimer's potential
Memory/Cognition: CB1 in hippocampus — bidirectional effects depending on dose
2-AG clinical relevance:
Immune modulation: Strongest anti-inflammatory endocannabinoid
Neuroprotection: TBI and stroke research
Pain modulation: Analgesic via ECS
Cardiovascular: Blood pressure and heart rate regulation
Transition: "Now let's look at where these receptors and molecules are actually operating in the pain pathway."
41 — Pain Pathway and Multiple Receptor Types
41 — Pain Pathway and Multiple Receptor Types
Reference the two diagrams:
Left diagram (dorsal horn targets):
The dorsal horn is the convergence point for multiple analgesic targets: opioid receptors, serotonin receptors, GABA receptors, NMDA receptors — and cannabinoid receptors.
This is the mechanistic basis for combination analgesia and opioid-sparing strategies.
Right diagram (painexplained.com):
Four levels of pain processing:
Peripheral nociceptor — cannabinoids, NSAIDs, capsaicin
Along the nociceptive nerve — local anesthetics, anticonvulsants
Central (brain) — cannabinoids, opioids, tramadol, acetaminophen
Descending inhibitory pathway — cannabinoids, opioids, SNRIs, tricyclics
Dorsal horn — cannabinoids, gabapentinoids, NMDA antagonists, opioids, anticonvulsants
Cannabinoids act at all five levels — this is unique among analgesic drug classes. No other drug class has this breadth of action along the pain neuroaxis.
42 — Endocannabinoids in Immune Regulation
42 — Endocannabinoids in Immune Regulation
The ECS is deeply integrated into immune function — primarily via CB2 on immune cells.
Walk through immune cell types and eCB effects:
T lymphocytes: AEA reduces mitogen-induced proliferation and Th1/Th17 responses → immunosuppression
B lymphocytes: 2-AG enhances B cell migration toward 2-AG (chemotaxis) — immune trafficking
Neutrophils: AEA increases respiratory burst (ROS); 2-AG reduces migration
Monocytes/Macrophages: AEA reduces IL-6, IL-8, TNF-α; 2-AG promotes NO production and increases phagocytic cells
Microglia: AEA raises IL-10, reduces IL-12/23, reduces LPS-induced NO
Dendritic cells: mixed effects on cytokine production
Clinical relevance: ECS modulation in neuroinflammatory diseases (MS, Parkinson's, TBI) may work through microglial CB2 activation as much as through neuronal CB1.
43 — Diseases Associated with ECS Deficiency or Dysfunction
43 — Diseases Associated with ECS Deficiency or Dysfunction
Transition — set up the clinical deficiency framework.
"Now that we understand what the ECS does, what happens when it fails?"
Introduce Clinical Endocannabinoid Deficiency (CED) theory — Ethan Russo, 2004/2016.
44 — Clinical Endocannabinoid Deficiency: Migraine, Fibromyalgia, IBS
44 — Clinical Endocannabinoid Deficiency: Migraine, Fibromyalgia, IBS
Russo's theory: just as dopamine deficiency causes Parkinson's and serotonin dysregulation underlies depression, ECS deficiency may underlie treatment-resistant syndromes.
The Venn diagram shows high comorbidity among migraine, fibromyalgia, and IBS — all three are low-pathology, high-symptom burden conditions with no clear structural cause.
All three are characterized by central sensitization and poor response to conventional analgesics.
Shared features: heightened pain sensitivity, autonomic dysregulation, poor sleep, mood disturbance — all functions regulated by the ECS.
Research finding: lower AEA levels have been found in CSF of migraine patients.
Clinical implication: if CED is real, then raising endocannabinoid tone (via cannabis, FAAH inhibition, lifestyle modification) is the therapeutic strategy.
45–46 — ECS and Autism Spectrum Disorder
45–46 — ECS and Autism Spectrum Disorder
45 (Karhson et al., 2018):
Plasma AEA concentrations significantly lower in children with ASD vs. controls.
The logistic regression curve shows AEA level is a predictor of ASD diagnosis probability.
Effect size is meaningful — not just statistically significant.
46 (Aran et al., 2019):
Replicated and extended findings: AEA, OEA, and PEA all significantly reduced in ASD children (n=93 per group), all p<0.0001, large effect sizes (Cohen's d ~0.65–0.94).
80% of ASD children in this sample were on psychotropic medications — the ECS deficiency is not explained by medication status.
Clinical implication: ECS deficiency may be mechanistically relevant to ASD, not merely correlational.
47 — ECS and Autism: Microglial Mechanism (Su et al., 2021)
47 — ECS and Autism: Microglial Mechanism (Su et al., 2021)
Proposes a microglial mechanism: activated microglia in ASD produce 2-AG and AEA via MAGL and FAAH.
Inhibiting MAGL (e.g., JZL184) or FAAH (e.g., URB597, PF3845) raises eCB tone in the synaptic environment.
This reduces excitatory/inhibitory imbalance — a core neurobiological feature of ASD.
GABAR and NMDA modulation via the ECS helps restore the E/I ratio.
Research and clinical implication: pharmacological augmentation of ECS tone — not just with cannabis, but with FAAH/MAGL inhibitors — is an active research target for ASD.
48 — Quality of Life and a Surveillant ECS
48 — Quality of Life and a Surveillant ECS
The ECS is a surveillant system — constantly monitoring and adjusting physiological balance.
Inputs that modulate the ECS include:
Phytocannabinoids (THC, CBD)
Synthetic molecules (agonists, inverse agonists)
Endogenous peptides (PVNFKLLSH derivatives)
Allosteric mediators — Lipoxins, Resolvins (these are SPMs — specialized pro-resolving mediators — relevant to post-procedure inflammation)
The diagram shows all these inputs converging on CB1/CB2 and TRPV1 — downstream effects on K+ channels, Ca2+ flux, and intracellular signaling (ERK, MAPK, PI3K, PPAR-γ, cAMP-PKA, β-arrestin).
Quality of life message: supporting ECS function is not just about disease treatment — it's about health maintenance and homeostasis.
49 — Physical Activity and the ECS
49 — Physical Activity and the ECS
This introduces the "runner's high" science.
Exercise increases circulating AEA and 2-AG — this is well-documented.
The ECS mediates the euphoric and analgesic effects of aerobic exercise.
Clinically relevant patient counseling: exercise is a non-pharmacological ECS modulator. Patients with CED-type conditions (fibromyalgia, IBS, migraine) may benefit from structured aerobic exercise as ECS tone therapy.
Also introduces ω3 and ω6 eCBs — dietary fatty acids are precursors to endocannabinoids. Omega-3 supplementation may modulate ECS tone.
50 — Future of ECS Research (Active ClinicalTrials.gov Studies)
50 — Future of ECS Research (Active ClinicalTrials.gov Studies)
Walk through active areas:
Anti-aging: "Aging and Marijuana: Benefits, Effects, and Risks" — ECS tone may decline with age; implications for neurodegeneration and longevity.
Pain:
Endocannabinoids, Stress, Craving and Pain Effects Study — relevant to pain-addiction intersection.
CBD for Endometriosis Pain — a high-unmet-need population.
Neuroinflammation: CBD/THC effects on microbiome and neuroinflammation in HIV — ECS as immunomodulatory target in chronic viral illness.
Cannabis Use Disorder: Mapping eCB and opioid levels in adolescents — critical for understanding risk and developing interventions.
Eating Disorders: Exercise response — connects to ECS and reward circuitry.
Closing point: clinicaltrials.gov is your resource. The science is not settled — it is accelerating.
51 — PubMed Research Volume
51 — PubMed Research Volume
PubMed search for "endocannabinoids" returns 6,874+ free full-text results as of 2024.
The bar graph shows exponential growth in publications from 1982 to 2024.
Message: this is no longer fringe science. This is mainstream biomedical research with a rapidly expanding evidence base.
Challenge to the audience: if 6,874 papers exist and none of us were taught this system in medical school, there is a curriculum crisis in medical education that directly impacts patient care.
52 — Cannabinoid Receptor Signaling States
52 — Cannabinoid Receptor Signaling States
The four quadrant diagram summarizes receptor pharmacology:
A. No Ligand / Inactive: GPCR in basal state. G-protein binding site closed. No response.
B. Full Agonist (e.g., FUB — synthetic cannabinoid): Complete G-protein activation. Full downstream response. Risk of overstimulation — synthetic cannabinoids (K2/Spice) act as full agonists, explaining their dangerous toxicity vs. THC's partial agonism.
C. Partial Agonist (THC): Partially opens G-protein binding site. Partial response. This is the therapeutic safety window — partial agonism = ceiling effect on psychoactivity.
D. Antagonist (Taranabant/Rimonabant): Blocks agonist binding. No receptor activation. Rimonabant's psychiatric adverse events showed that eliminating CB1 tone is as dangerous as overwhelming it.
Clinical lesson: pharmacological nuance matters. Full agonist ≠ partial agonist ≠ antagonist ≠ inverse agonist. The therapeutic utility depends on the type and degree of receptor modulation.
53 — Summary
53 — Summary
Close with the five key takeaways:
THC discovery led to ECS discovery — a molecule from a plant revealed an entire human physiological system.
ECS = three components: endocannabinoids (AEA, 2-AG, minor eCBs), receptors (CB1, CB2), and enzymes (NAPE-PLD, DAGL, FAAH, MAGL).
CB1 is concentrated in the nervous system; CB2 in the immune system — but both are found throughout the body, explaining the ECS's breadth of clinical relevance.
The ECS is critically important clinically:
ECS deficiency/dysfunction may cause disease (CED theory)
For diseases without direct ECS pathology: target symptoms (pain, nausea, spasticity) and inflammatory pathways
Research is expanding rapidly — we must continue to translate ECS physiology into improved clinical outcomes.
54–55 — References / Thank You
54–55 — References / Thank You
Acknowledge the scientific foundation: Mechoulam, Devane, Pertwee, Russo, Di Marzo, and the many teams cited throughout.
Contact: drterel.newton@trulieve.com
Invite questions.
Closing statement: "The endocannabinoid system is not a niche topic for cannabis advocates. It is a foundational physiological system that every clinician should understand. Our patients deserve better than a medicine that ignores a system that governs pain, mood, immunity, metabolism, and neurological health. Thank you."
2
2
Title and Presenter Information Welcome the audience and introduce the topic of Understanding Cannabis Use Disorders. State your full credentials as Terel Newton MD, board-certified anesthesiologist and interventional pain specialist, with AI in healthcare certifications from MIT and additional certifications in progress. Highlight your role as Medical Director at Trulieve Florida, the largest U.S. dispensary network with over 160 locations. Mention the conference context from Morehouse School of Medicine and note the visual collage of clinical, dispensary, and lab settings to set a professional tone for the module.
Disclaimers and Disclosures Clearly state all professional roles including consultant and medical advisor on opioid alternatives, state medical director at Trulieve Florida, and research interests in medical cannabis for chronic pain and mental health. Emphasize no remuneration for this presentation, federal Schedule I status of cannabis, varying state laws, and that many discussed medicines lack FDA approval. Reassure the audience this is an educational module focused on clinical and public health perspectives without commercial bias.
Module Overview Outline the two-part structure: Part 1 covers Cannabis Use Disorder (CUD) including diagnostic criteria, epidemiology, burden, risk factors, and evidence-based interventions; Part 2 addresses Cannabinoid Hyperemesis Syndrome (CHS) with clinical presentation, diagnostic criteria, pathophysiology, and management approaches. Stress the module’s focus on rising accessibility and normalization of cannabis from both clinical practice and public health viewpoints to frame the entire session.
Learning Objectives Review the three core objectives: analyze the public health and safety implications of CUD in diverse populations; critically evaluate policies and research related to cannabis use disorders; and determine signs, symptoms, and evidence-based strategies for managing both CUD and CHS. Tie these to real-world application in patient care, policy, and prevention.
Required Resources Direct attention to the three key systematic reviews and studies listed: the 2024 Brain Sciences review by Ghafouri et al. on CUD treatments across the lifespan; the 2022 Medical Principles and Practice review by Senderovich et al. on CHS management options; and the 2025 IJERPH article by Seabrook et al. on CHS in youth with clinical and public health insights. Encourage participants to reference these for deeper evidence after the session.
Disclosures Reiterate the educational nature of the module developed without commercial influence. Briefly restate your roles as medical director of the largest U.S. dispensary, practicing physician, and AI in healthcare student, while confirming no dispensary products will be discussed, no financial exchanges, and no conflicts of interest related to the content.
Part 1: Cannabis Use Disorder (CUD) Transition smoothly into the first major section by noting that CUD represents a growing clinical challenge amid increasing cannabis availability. Set the stage for case-based learning and diagnostic foundations that follow.
Case Study: Adolescent with CUD Present the 16-year-old profile including daily vaping and edibles, symptoms of morning irritability, missed assignments, and family conflict, plus CUD features such as tolerance, withdrawal, craving, role failures, and hazardous use. Describe the intervention of motivational enhancement therapy (MET)/cognitive behavioral therapy (CBT) plus contingency management at clinic and home, resulting in longer abstinence with supporting odds ratio evidence (OR 1.16; 95% CI 1.02–1.32). Highlight the clinical pearl that adolescents respond well to family engagement and rewards.
Abbreviations from Ghafouri et al., 2024 (CUD Review) Quickly review key abbreviations grouped by clinical conditions, psychosocial interventions (highlighting CBT, MI, MET, CM, ACRA, MDFT, PNC-txt), pharmacological approaches (CB1, NAC, nabiximols, dronabinol), measurement/outcomes, and study design. Explain these will appear throughout the evidence sections to aid clarity without reading every item verbatim.
Case Study: Young Adult with CUD Share the 22-year-old profile with 4–6 times daily use, symptoms of poor sleep, depressed mood, and relationship strain. Detail the 4-week text-delivered peer network counseling (PNC-txt) intervention yielding 80% negative urine screens versus 53% in controls, plus reduced cravings and cannabis problems. Emphasize the clinical pearl on scalable tech-based, peer-oriented programs for campus or young adult settings.
Case Discussion: Why These Interventions Work Explain the behavioral economics behind contingency management (immediate rewards countering delayed gratification from abstinence, positive reinforcement, especially effective in developing brains). Discuss mechanisms of text-based interventions (peer norms, low-friction delivery, timely support, easy scaling). Conclude that matching interventions to developmental stage drives better outcomes in both cases.
Mapping Cases to DSM-5 Domains Walk through the table linking impaired control, social impairment, risky use, and pharmacologic criteria to each case. Note that both demonstrate multiple domains indicating moderate-to-severe CUD, reinforcing how real patients meet diagnostic thresholds across categories.
DSM-5/DSM-5-TR Cannabis Use Disorder Criteria Detail the requirement of 2 or more criteria within 12 months across impaired control (4 items), social impairment (3 items), risky use (2 items), and pharmacologic (2 items). Clearly explain severity levels: 2–3 mild, 4–5 moderate, 6 or more severe. Reference the American Psychiatric Association as the source and stress the importance of these criteria in clinical assessment.
CUD Prevalence: United States Present the statistics: approximately 1.5% of U.S. adults meet CUD criteria; over 35% of 12th graders report past-year use; and 192 million global annual users per UNODC. Position cannabis as the third most common psychoactive substance after alcohol and tobacco to underscore its public health scale.
Risk of Progression to CUD Use the pie charts to highlight risks: 1 in 10 regular users, 1 in 6 adolescent-onset users, and 25–50% of daily users develop CUD. Stress that early onset and high frequency are the strongest predictors, framing prevention opportunities.
Public Safety Implications of CUD Cover the key concerns with the visual of an accident scene: impaired driving and motor vehicle accidents, rising cannabis-related emergency department visits, decreased school attendance and achievement, and workplace safety risks from impaired judgment and reaction time.
Functional Impact of CUD Break down impacts by domain: educational (lower attainment, cognitive deficits, higher dropout), occupational (absenteeism, reduced productivity, employment disruptions), and social (relationship strain, reduced engagement, isolation from non-using peers). Emphasize broader social and economic consequences beyond individual health.
Psychiatric Associations with CUD Discuss increased risks of depression, anxiety, psychosis (especially high-potency products), self-harm, and violence in comorbid groups. Explain the bidirectional relationships: cannabis triggering symptoms in vulnerable individuals, psychiatric issues leading to self-medication, and shared genetic/environmental factors. Use the brain image to illustrate complexity.
Policy Context and CUD Address legalization impacts (increased accessibility, normalization, decreased perceived risk, product diversification) and resulting public health challenges (rising ED visits, increased CHS cases, youth exposure, regulatory gaps in potency). Note how the legal landscape creates new demands for messaging and clinical practice.
Potency Shift: A Key Risk Factor Highlight the 400% increase in THC content from 3% in the 1980s to 15–30% in modern products. Link this rise to higher rates of adverse effects including psychosis and CUD, using the lab visual to reinforce the modern context.
Neurodevelopmental Risk Factors Focus on prefrontal cortex maturation continuing until approximately age 25 and its vulnerability to cannabis, affecting executive function, decision-making, and impulse control. List adolescent risks: memory deficits, attention problems, executive impairment, and potential permanent brain structure changes. Reference the linked frontal lobe resource.
Route & Formulation Risk Factors Describe high-risk delivery methods: concentrates/dabs (60–90% THC, rapid onset), high-THC vapes (discreet, frequent use potential), and edibles (delayed onset leading to overconsumption and prolonged effects). Explain how these increase CUD and adverse effect risks with the product images.
Psychosocial Risk Factors Differentiate by age: for adolescents and young adults (peer influence, social reinforcement, identity development, risk-taking, stress management); for adults and older adults (self-medication, chronic condition coping, sleep/pain issues, established patterns). Note these factors drive both initiation and maintenance across the lifespan.
Medical Comorbidity Risk Factors Cover pain conditions driving symptom management use, sleep disorders prompting cannabis as a sleep aid, and polypharmacy risks in older adults. Stress the need for integrated treatment approaches in complex clinical pictures.
Social Determinants as Risk Factors Outline key factors: stress from economic hardship/discrimination/trauma, dispensary density in vulnerable areas, community normalization, targeted marketing post-legalization, and barriers to healthcare/prevention. Use the dispensary street scene to illustrate environmental influences.
Cannabis Withdrawal Profile Present the timeline: onset 24–72 hours (irritability, anxiety, sleep issues); peak at ~1 week (intensified mood, sleep, appetite problems); resolution 1–2 weeks (acute symptoms fade, some linger). List common symptoms and note this profile informs clinical management.
Screening Tips for CUD Advise using open-ended questions (“Tell me about your cannabis use”), non-stigmatizing tone, the hot shower question to flag possible CHS, and assessing frequency/amount/setting/reasons. Emphasize that effective screening builds the foundation for intervention.
Psychosocial Interventions: The Mainstay of Treatment State that psychosocial approaches form the core, with pharmacotherapy as adjunct only. Highlight evidence-based options: motivational interviewing for motivation, CBT for coping and thought patterns, contingency management for incentives (strongest evidence in adolescents).
Family & School Interventions Outline the four approaches: parent training (monitoring/communication/boundaries), family therapy (addressing dynamics), school-based programs (prevention/early intervention), and combined parent training plus contingency management for better teen abstinence. Stress family and school engagement for adolescents.
Digital Interventions Discuss PNC-txt (4-week text peer counseling: 80% negative urine vs 53% control, reduced cravings/problems) and eCHECKUP (online feedback reducing use days/hours). Highlight scalability, accessibility, and low cost for young adults.
Pharmacologic Interventions Reiterate these are adjuncts only. Review NAC (modest withdrawal relief, mixed results), gabapentin (possible withdrawal reduction, limited relapse prevention), and CB1 agonists (reduce withdrawal but side effects limit use). Note the key limitation of no robust relapse-prevention pharmacologics.
Interventions for Older Adults Cover brief maintenance check-ups for short-term abstinence, medication monitoring for interactions, addressing comorbidities (pain/sleep/mood), and age-appropriate motivational approaches focused on health impacts.
Relapse Prevention Strategies Detail the four pillars: trigger plans for high-risk situations, sleep normalization, mood care for depression/anxiety, and peer substitution via non-using networks/activities. Emphasize addressing biological, psychological, and social factors comprehensively.
Measurable Treatment Goals Explain objective measures (urine screens, days abstinent, grams/day) and functional outcomes (academic/occupational performance, relationships, mental health, quality of life). Use the topiramate trial example to show how goals guide progress and adjustments.
Matching Interventions to Life Stage Summarize tailoring: adolescents (family, contingency management, school support); young adults (digital, peer, campus programs); older adults (adjunct meds, check-ups, comorbidity management). Stress improved effectiveness when matched to developmental stage and context.
Transition to CHS Bridge to Part 2 by noting the paradoxical shift from CUD to Cannabinoid Hyperemesis Syndrome, a distinct clinical entity linked to chronic use, setting up the second half of the module.
Part 2: Cannabinoid Hyperemesis Syndrome (CHS) Introduce Part 2 by recapping the module overview and noting CHS as an emerging paradoxical condition tied to heavy, prolonged cannabis use, often under-recognized in clinical settings.
Case Study: CHS (Youth/Adult Presentation) Present the case of recurrent ED visits with unrevealing labs/CT and ineffective antiemetics. Detail diagnosis via Rome IV criteria for CHS and outcome of complete resolution with cannabis cessation. Deliver the clinical pearl to always ask about cannabis use in unexplained cyclic vomiting.
39–42. Clinical Presentation of CHS
Describe the three phases (prodromal, hyperemetic, recovery) with emphasis on morning nausea, abdominal discomfort, anxiety in prodromal phase while appetite is preserved, followed by intense persistent vomiting, severe pain, and dehydration in the hyperemetic phase. Use visuals to differentiate from other vomiting syndromes.
Prodromal Phase of CHS Highlight early subtle signs: morning nausea, abdominal discomfort, anxiety, preserved appetite, continued cannabis use as self-medication. Stress this phase can last months to years and is often missed.
44–47. Diagnostic Criteria for CHS
Review Rome IV criteria including episodic vomiting, relief with hot showers/baths, resolution with cannabis cessation, and exclusion of other causes. Note the importance of detailed history to avoid unnecessary testing.
Hyperemetic Phase of CHS Detail acute features: intense vomiting (often >5 episodes/hour), severe abdominal pain, dehydration, electrolyte abnormalities, weight loss, and compulsive hot bathing behavior for relief.
49–52. Pathophysiology of CHS
Explain proposed mechanisms involving CB1 receptor downregulation with chronic exposure, altered hypothalamic thermoregulation, and gastrointestinal motility changes leading to the paradoxical hyperemesis despite cannabis’s usual antiemetic properties. Reference genetic and dose-response factors.
53–58. Management Approaches for CHS
Outline primary treatment as complete cannabis cessation (the only curative approach). Discuss supportive care (IV fluids, antiemetics like haloperidol or capsaicin cream for symptom relief, benzodiazepines for anxiety), avoidance of opioids, and follow-up with counseling for CUD. Note behavioral and motivational strategies to support abstinence.
59–62. Public Health and Youth Implications of CHS
Cover rising incidence in adolescents and young adults, ED burden, diagnostic delays, and prevention messaging around potency and frequency. Reference the 2025 Seabrook et al. study for youth-specific insights.
63–71. Additional Topics, Integration, and Clinical Pearls
Integrate CUD and CHS management across lifespans, discuss policy implications for screening and education, review evidence from Senderovich et al. 2022, and share practical pearls for emergency and primary care settings.
Closing Summary and Q&A Summarize key takeaways from both parts: early recognition of CUD and CHS, evidence-based psychosocial interventions as mainstay, cannabis cessation as cornerstone for CHS, and the need for tailored, non-stigmatizing care. Open the floor for questions, thank the audience, and reference the required resources for further reading.
FRIDAY – Pre-Conference
Aaron Bloom — CEO, DocMJ — Moderator, Sustainable Cannabis Practice
Brad Hunt — Risk Consultant — Navigating Cannabis Wrongful Acts
Dan McNeff — CEO, Legally Mine — Asset Protection & Tax Strategies
Peggy Koller — Founder — Cannabis Practice Becomes Forensic Case
Jennifer Makris — Founder — Bridging Cannabis Care and Business
SATURDAY – Opening Session
Gene Jones — Executive Director — Welcome Address
Dr. William Troutt — Medical Director — Moderator, Opening Session
Ron Watson — President — Florida Cannabis Legislative Update
Dr. Bonni Goldstein — CEO — Presentation TBD
Dr. Derrick DeSilva — Medical Director — Peptides in Cannabinoid System
SATURDAY – Session I (Research)
Dr. Catalina Lopez-Quintero — UF Professor — Real-World Cannabis Research
Dr. Juan Pérez-Carreno — PhD Candidate — Epidemiology Research Insights
Dr. Md Mahmudul Hasan — UF Professor — Pharmaceutical Outcomes Research
Dr. Karina Villalba — UCF Professor — Population Health Cannabis Data
SATURDAY – Session II (Clinical)
Dr. Michelle Beasley — Physician — Moderator, Precision Cannabis (invited)
Sabrina Fayaz — Program Director — Cannabinoid Dosing Strategies
Dr. Joseph Rosado — Physician — Safety, Dosing, Clinical Framework
Dr. Lihi Bar-Lev Schleider — Researcher — Deprescribing Cannabis Outcomes
Dr. Deondra Asike — Pain Specialist — Cannabinoids in Chronic Pain
SATURDAY – Session III (FAMU / MMERI)
GP Mendie — AVP Research — MMERI Program Leadership
Dr. Mandip Sachdeva — Professor — Cannabis Quality and Safety
Dr. Jamal Brown — PharmD — Pharmacy Practice Education
Michelle Wilson — Associate Director — MMERI Program Development
Anthony Washington — Outreach Coordinator — Statewide Cannabis Education
SUNDAY – Session IV (OMMU)
Todd Schimpf — Communications Manager — OMMU Regulatory Update
Cassie Hurley — IT Manager — OMMU Systems and Compliance
SUNDAY – Session V (Business / Practice Growth)
Scheril Murray Powell — Attorney — Moderator, Modern Cannabis Practice
Dr. Kelly King — Founder — Successful Cannabis Practice
Nick Garulay — CEO — Engineering Compliance Infrastructure
Emily Carew — COO — Education for Retention Growth
Alex Johnson — Founder — Clinic Models Driving Performance
Stew Baskin — Consultant — Smarter Benefits Lower Costs
✅ UPDATED — ALL GROUPS COMBINED (FMCCE + CLAB + Cannabase)
✅ UPDATED — ALL GROUPS COMBINED (FMCCE + CLAB + Cannabase)
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CLAB (44)
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🔹 CLAB Leadership Board (Tag-Ready)
🔹 CLAB Leadership Board (Tag-Ready)
@Amanda — Partner, Cannabis Law — Legal Leadership
@Beej — Owner — Retail Operations
@Chris — Audit & Assurance Partner — Financial Oversight
@Christa — Retail Marketing — Brand Strategy
@Christian — Training Director — Retail Education
@Cody — Founder — Cannabis Retail Development
@Corey — Event Partnerships — Industry Engagement
@Crafton — Marketing Director — Cannabis Branding
@Dana — Chief Business Development — Strategic Growth
@Daniel — Founder — Consulting Strategy
@Adam — CEO — Wellness Practice Leadership
@Roz — Founder — Minority Cannabis Advocacy
@Eric — President — Insurance Leadership
@Eric — Project Manager — Construction Operations
@Eric — Operations Director — Retail Execution
@Gregg — Vice President — Supply Chain Leadership
@Javier — Founder — Retail Innovation
@Jen — Business Consultant — Cannabis Finance
@Jillian — Co-Founder — Community Growth
@Joel — Franchise Owner — Financial Operations
@John — CEO — Creative Leadership
@Jon — Partner — Cannabis Legal Strategy
@Karen — Executive Director — NORML Advocacy
@Krysta — CEO — Networking Platform Growth
@Matthew — Partner — Retail Strategy
@Michelle — Regional Manager — Outreach Programs
@Tom — CEO — Retail Expansion
@Randy — CEO — Cultivation Leadership
@Renee — Strategic Partnerships — Business Development
@Rhonda — SVP Banking — Financial Services
@PJ — Executive Director — Association Leadership
@Rob — Founder — Indigenous Cannabis Advocacy
@Sam — President — Architecture Consulting
@Sammy — Shareholder — Investment Strategy
@Scott — Sales Director — Retail Distribution
@Stephen — Chief Strategy Officer — Product Innovation
@Stewart — Consultant — Workforce Solutions
@Todd — Regional Manager — Retail Operations
@Toros — Business Development — Credit Union Strategy
@Vijay — Partner — Legal Advisory
@Zach — Partner — Legal Services
@Connor — Business Development — Retail Technology
@Masha — Growth & Education — Laboratory Expansion
Technology for Neuropathy
Teaching Opioid Alternatives
Breast Cancer & Med Cannabis (Basic)
Breast Cancer & Med Cannabis (Advanced)
Live Class: Learn w/ AI
Live Class: Learn w/ AI
Live Class
Live Class
FUTURES ... 2nd Sunday | ORL Cars & Coffee
FUTURES ... 2nd Sunday | ORL Cars & Coffee
if (t < 93000) return DayRegime.PreMarket;
if (t < 95000) return DayRegime.OpeningDrive;
if (t < 110000) return DayRegime.MidMorningTrend;
if (t < 120000) return DayRegime.LateMorning;
if (t < 133000) return DayRegime.Lunch;
if (t < 143000) return DayRegime.EarlyAfternoon;
if (t < 154500) return DayRegime.PowerHour;
Below is a professional breakdown of the U.S. index futures trading day (e.g., YM / ES) segmented by time, behavior, and dominant pattern tendencies.This assumes regular U.S. equity session (RTH): 9:30 AM – 4:00 PM ET.
I. Pre-Market Structure (6:00 – 9:29 AM ET)1️⃣ Early Pre-Market (6:00 – 8:20)Character:Thin liquidityOvernight inventory positioningGlobex range developmentCommon Patterns:Range buildingOvernight high/low testsVWAP reversionFalse breakouts due to thin liquidityEdge Type:Mean reversionOvernight structure plays
2️⃣ News Window (8:30 – 9:15)(Economic releases: CPI, NFP, GDP, etc.)Character:Sudden volatility expansionLiquidity vacuum movesRapid repricingCommon Patterns:News spike & retraceNews spike & continuationLiquidity grab through overnight high/lowEdge Type:Fade the spike (if rejection)Acceptance breakout if volume confirms
II. Opening Drive Phase (9:30 – ~9:50)This is the most structurally important part of the day.1️⃣ Opening Drive (OD)Time: 9:30–9:40 (sometimes extends to 9:50)Character:Institutional imbalanceLarge program ordersHigh volatilityWide range candlesPatterns Seen:Straight-line impulse moveGap-and-goOpening trend continuationOpening range breakout (ORB)Stop-run through overnight high/lowSubtypes:Drive & HoldDrive & PullbackDrive & ReverseEdge Type:Momentum breakoutPullback continuationLiquidity sweep + reclaim
2️⃣ Opening ReversalTime: 9:35–10:00Character:Early traders trappedCounter-move against opening spikePatterns:Gap fillSweep of opening extremeDouble top/bottom off first pushEdge Type:Reversal entry at exhaustionVWAP reversion
III. Expansion & Structure Phase (9:50 – 11:00)After opening volatility stabilizes.1️⃣ Trend Continuation WindowTime: 9:50–10:30Character:Structured pullbacksHigher lows / lower highs formingTrend clarity improvesPatterns:Ascending support compressionFlag formationsEMA/SMA pullback entriesVWAP trend holdsEdge Type:Pullback addsStructured scalingBreakout from compressionThis is often where A+ trend days form.
2️⃣ Mid-Morning Liquidity ExpansionTime: 10:00–10:30Common for:Second impulse legHigh-of-day or low-of-day formationAlgo-driven stop sweep near 00 / 25 / 50 levelsEdge Type:Acceptance breakoutLiquidity sweep continuation
IV. Late Morning Transition (11:00 – 12:00)Character:Volume dropsRange compressionRotational behavior increasesPatterns:VWAP ping-pongNarrow range coilFalse breakoutsChop around round numbersEdge Type:Mean reversionSmall scalpsAvoid large scaling
V. Midday / Lunch Session (12:00 – 1:30)Character:Lowest liquidity of the dayAlgorithmic micro-rotationsNo strong initiative order flowPatterns:Tight rangesStop hunts around small intraday levelsSlow grind channelsEdge Type:PatienceLight size onlyAvoid scaling aggressivelyMost large traders reduce size here.
VI. Early Afternoon Repricing (1:30 – 2:30)Liquidity starts returning.1️⃣ Early Afternoon PushTime: 1:30–2:00Character:Repricing toward morning extremesTest of VWAP or daily high/lowPatterns:Trend resumptionRange breakoutFailed breakdown/breakout
2️⃣ Power Hour Initiation (2:00 – 2:30)Often begins directional bias.Patterns:Break of morning rangeGamma-driven movesStrong acceptance beyond key levelsEdge Type:Momentum re-entryStructured adds
VII. Power Hour (2:30 – 3:45)High-probability expansion window.Character:Institutional positioningHedging flowsTrend acceleration or reversalPatterns:Late-day trend continuationSqueeze movesVWAP reclaim + expansionClose imbalance setupEdge Type:Aggressive scalingHold runnersBreakout continuation
VIII. Closing Auction (3:45 – 4:00)Character:Imbalance-driven volatilityFast directional burstsLarge closing printsPatterns:Final squeezeReversal flushClose-only imbalance moveEdge Type:Fast scalpsNot ideal for large new swing entries
Summary View of the Trading DayPhaseTimeBehaviorBest Strategy TypePre-Market6:00–9:29Range / prepMean reversionOpening Drive9:30–9:50ImbalanceMomentumExpansion9:50–11:00Structured trendPullback scalingLate Morning11:00–12:00RotationLight scalpsLunch12:00–1:30CompressionAvoid sizeEarly Afternoon1:30–2:30RepricingBreakoutsPower Hour2:30–3:45ExpansionAggressive scalingClose3:45–4:00ImbalanceFast trades
If you’d like next, I can:Map each time segment to A+/A/B trade grading.Explain which periods statistically support 80–100 contract scaling.Or show how to program ODMAR2 to adjust behavior based on time-of-day regime.
To the author, Javier ...
Thank you for “The Power 100.” I'm honored to be mentioned along other great authors, advocates, and pioneers that paved the way and continue to contribute to an amazing and unique industry. Congratulations to everyone mentioned and those who continue to make progress for communities and patients This piece reflects integrity, context, and respect for the architects of this movement.
- Dr. Newton
MEDICAL CANNABIS STUDIES & AWARENESS MONTHS
MEDICAL CANNABIS STUDIES & AWARENESS MONTHS
Here are some 2025-2026 medical cannabis studies you may find interesting
Here are some 2025-2026 medical cannabis studies you may find interesting
1. April 2025: Global Consensus on Oncological Pain
1. April 2025: Global Consensus on Oncological Pain
Study: Meta-analysis of medical cannabis outcomes and associations with cancer
Numbers: Meta-analysis of hundreds of studies (sentiment analysis of over 2,500 data points).
Ratio & Route: Multi-modal analysis; prioritized oral and sublingual routes for maintenance and vaporization for acute breakthrough pain.
Results: Found clinical support for medical cannabis in cancer care is 31.38x stronger than opposition.
2. May 2025: Breakthrough in Seizure Freedom
2. May 2025: Breakthrough in Seizure Freedom
Study: 19 patients report seizure freedom with medical cannabis oil treatment
Numbers: 19 patients (15 pediatric, 4 adult) with drug-resistant epilepsy.
Ratio & Route: Full-spectrum CBD-rich oils (typically 20:1 to 25:1 CBD:THC) administered sublingually/orally.
Results: Median of 245 days of total seizure freedom; 3 patients successfully weaned off all other anti-seizure medications.
URL: https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2025.1570531/full
3. June 2025: Florida State Registry (CCORC) Annual Findings
3. June 2025: Florida State Registry (CCORC) Annual Findings
Study: Proceedings of the 2025 Cannabis Clinical Outcomes Research Conference
Numbers: Registry-level data from 930,000+ active Florida patients.
Ratio & Route: Diverse Florida-specific routes including flower (inhalation) and low-THC oils (oral).
Results: Significant statewide reduction in opioid prescriptions; established high safety profile for Florida's geriatric demographic.
4. July 2025: Hospitalization Rates and Quality of Life
4. July 2025: Hospitalization Rates and Quality of Life
Study: Medical Cannabis Use and Healthcare Utilization Among Patients with Chronic Pain
Numbers: Causal inference study using data from a multi-state certifying body (Leafwell).
Ratio & Route: Various dispensary-grade products used over a 12-month period.
Results: 3.2% reduction in ER visits and 2.0% reduction in urgent care visits; fewer "unhealthy days" per month reported.
5. August 2025: Same-Day PTSD Relief for Veterans
5. August 2025: Same-Day PTSD Relief for Veterans
Study: Daily Associations Between Cannabis Use and PTSD Symptoms in Military Veterans
Numbers: 74 military veterans with service-connected PTSD.
Ratio & Route: Ad-libitum (self-managed) use; typically high-THC flower or 1:1 ratios.
Results: Same-day cannabis use significantly lowered symptom severity and "negative affect" spikes.
URL: https://www.sciencedirect.com/science/article/abs/pii/S0165178125002744, and https://www.marijuanamoment.net/using-marijuana-helps-military-veterans-experience-lower-ptsd-symptoms-on-days-they-use-it-federally-funded-study-shows/
6. September 2025: Opioid-Sparing Synergy
6. September 2025: Opioid-Sparing Synergy
Study: CMCR Investigators' Meeting: Opioid-sparing Effects of Cannabinoids
Numbers: Preclinical and preliminary clinical patient data.
Ratio & Route: CBD vapor and THC:CBD combinations.
Results: Vaporized CBD decreased opioid intake without the reinforcing "reward" behavior found in high-THC products.
URL: https://www.cmcr.ucsd.edu/index.php/news-2/homeblog/464-cmcr-investigators-meeting-september-2025
7. October 2025: Alzheimer's Disease Microdosing
7. October 2025: Alzheimer's Disease Microdosing
Study: A randomized clinical trial of low-dose cannabis extract in Alzheimer's disease
Numbers: Phase 2 trial of elderly patients (ages 60–80).
Ratio & Route: 1.4:1 THC:CBD oral extract; micro-dose of 0.35mg THC / 0.24mg CBD daily.
Results: Significantly higher MMSE (cognitive) scores at 26 weeks compared to placebo group.
8. December 2025: Sustained Opioid Reduction (JAMA)
8. December 2025: Sustained Opioid Reduction (JAMA)
Study: Medical cannabis and opioid receipt among adults with chronic pain
Numbers: 204 participants tracked prospectively for 18 months.
Ratio & Route: Clinician-certified medical cannabis via oral, sublingual, and inhaled routes.
Results: 22% reduction in daily opioid MME; a 30-day cannabis supply was linked to 3.53 fewer MME per day.
9. January 2026: Early Integration for Pancreatic Cancer
9. January 2026: Early Integration for Pancreatic Cancer
Study: Pilot Randomized Trial of Medical Cannabis (CanPan)
Numbers: 34 patients with advanced pancreatic cancer.
Ratio & Route: Standard-of-care cannabis (patient's choice); median dose of 7.3 mg THC daily.
Results: 70% improvement in sleep and 44% improvement in pain; early access yielded better outcomes than delayed access.
10. January 2026: Endometriosis and Quality of Life
10. January 2026: Endometriosis and Quality of Life
Study: Cannabis Formulations Associated With Reduced Pain in Endometriosis Patients
Numbers: 28 patients (New Zealand cohort) and 63 patients (UK Medical Cannabis Registry).
Ratio & Route: CBD-dominant oils or balanced THC:CBD flower/oil.
Results: Significant drop in "worst pain" (from 7.62 to 5.38) and massive improvement in EHP-30 health scores.
Here are some of the Medical Awareness Months related to Florida MMJ Qualified Conditions
Here are some of the Medical Awareness Months related to Florida MMJ Qualified Conditions
January
January
Glaucoma
Organizations: Glaucoma Research Foundation; American Academy of Ophthalmology
February
February
General wellness, mobility, chronic pain (adaptive sports education)
' Roll-up' initiative to sport adaptive sports athletes
March
March
Multiple sclerosis; colorectal cancer; traumatic brain injury; spasticity; neuropathic pain
Organizations: National Multiple Sclerosis Society; Colorectal Cancer Alliance
April
April
Parkinson’s disease; autism spectrum disorder (symptom-based)
Organizations: Parkinson’s Foundation; Michael J. Fox Foundation; Neuro Challenge Foundation
May
May
Arthritis; fibromyalgia; chronic musculoskeletal pain; senior health
Organizations: Arthritis Foundation; Administration for Community Living
June
June
PTSD; anxiety disorders; migraine
Organizations: National Center for PTSD; American Migraine Foundation
July
July
General seizure education; chronic pain (7/10 oil-education anchor only)
Organizations: Americans for Safe Access
August
August
Crohn’s disease; inflammatory bowel disease; GI disorders; nausea; appetite loss
Organizations: Crohn’s & Colitis Foundation; International Foundation for Gastrointestinal Disorders
September
September
Prostate cancer; chronic pain; neuropathy
Organizations: Prostate Cancer Foundation; U.S. Pain Foundation
October
October
Breast cancer; cancer supportive care; chemotherapy-induced nausea; neuropathy
Organizations: Susan G. Komen; American Cancer Society
November
November
Epilepsy / seizure disorders; lung cancer; hospice & palliative care; terminal illness
Organizations: Epilepsy Foundation; National Hospice and Palliative Care Organization
December
December
HIV/AIDS; cachexia; chronic pain; sleep disturbance
Organizations: Centers for Disease Control and Prevention; HIV.gov
Key date: December 1 – World AIDS Day
Let me know if you have any questions about any of these studies, other research or the awareness months.
Dr Newton
EVENTS CALENDAR
MARCH
Sat 21 ATL (NAACP) Health Panel
Fri 27-30 S. Florida
APRIL
Fri 3 Tampa (WTOs)
ATL Cannabase
Sun ORL CarsnCoffee - 2nd Sunday.
MAY
End FMCCE
JUNE
JULY
11th SAT NEWTONVILLE, NJ.
===
Here’s the class schedule:
Monday & Wednesday | 8–9 PM ET – Post Market Analysis
Tuesday & Thursday | 9:30–10 AM ET – Live Market Performance (Recording available)
Jax - 3/6, [3/13=Mbeo], 3/20 , 3/27 (Telehealth 10am), 4/3, 4/24
HEALTH AWARENESS MONTHS
HEALTH AWARENESS MONTHS
HEALTH AWARENESS MONTHS
HEALTH AWARENESS MONTHS
JAN — Cervical Cancer / Thyroid / Glaucoma / Migraine
JAN — Cervical Cancer / Thyroid / Glaucoma / Migraine
Cervical CA: 600 K global │ 13 K US yearly. CBD + curcumin reduce inflammation; folate, zinc, and AHCC boost immunity and HPV clearance.
Thyroid: 200 M global │ 20 M US. CBD stabilizes hormones; iodine + selenium support metabolism and stress resilience.
Glaucoma: 80 M global │ 3 M US. THC lowers eye pressure; omega-3 + laser protect vision.
Migraine: MOVED TO JUNE
FEB — Heart Disease / Cancer / PTSD / Fibromyalgia
FEB — Heart Disease / Cancer / PTSD / Fibromyalgia
Heart: 550 M global │ 697 K US deaths yearly. CBD + omega-3 lower BP; CoQ10 + turmeric improve vascular tone.
Cancer: 20 M global │ 1.9 M US. THC/CBD ease chemo pain; IV vit C + hyperthermia improve recovery.
PTSD: 350 M global │ 13 M US. CBN + ketamine calm fear circuitry; EMDR builds resilience.
Fibromyalgia: 100 M global. CBD, 5-HTP, and magnesium improve sleep and reduce central sensitization.
MAR — Brain Injury / Colorectal CA / MS / Anxiety
MAR — Brain Injury / Colorectal CA / MS / Anxiety
TBI: 69 M global │ 1.5 M US. CBD + omega-3 repair neurons; ketamine + rehab enhance neuroplasticity.
CRC: 1.9 M global │ 150 K US. Curcumin + fiber reduce tumor growth; cannabis eases abdominal pain.
MS: 2.8 M global. CBD/THC mix reduces spasticity; vitamin D + B12 enhance myelin repair.
Anxiety: 301 M global │ 42 M US. CBD + mindfulness reduce cortisol; adaptogens like ashwagandha stabilize mood.
APR — Autism / Alcohol Abuse / Epilepsy / Financial Stress
APR — Autism / Alcohol Abuse / Epilepsy / Financial Stress
Autism: 75 M global │ 1 in 36 US kids. CBD eases anxiety; B6 + magnesium aid cognition.
Alcohol use: 283 M global │ 140 K US deaths. IV B-complex detox + cannabis reduce cravings.
Epilepsy: MOVED TO NOVEMBER
Financial anxiety: 200 M global. Budget therapy + journaling reduce pain flare frequency and insomnia.
MAY — Mental Health / Arthritis / Back Pain / Burnout
MAY — Mental Health / Arthritis / Back Pain / Burnout
Depression: 300 M global │ 21 M US. Ketamine + omega-3 elevate mood; magnesium + CBD aid serotonin.
Arthritis: 350 M global │ 53 M US. PRP + CBG relieve joints; curcumin + collagen rebuild cartilage.
Back Pain: 619 M global │ 65 M US. CBD + epidural steroids relieve inflammation; posture therapy prevents relapse.
Burnout: 400 M global. Adaptogens + mindfulness + B12 restore energy.
JUN — Men's Health / MIGRAINE / ED / Sleep
JUN — Men's Health / MIGRAINE / ED / Sleep
Prostate: 1.4 M global │ 288 K US. Saw palmetto + zinc improve flow; CBD + low-dose THC reduce pain.
Migraine: 1 B global │ 39 M US. Botox + CBD block pain; magnesium + riboflavin reduce triggers.
ED: 320 M global. PRP + shockwave restore circulation; L-arginine boosts nitric oxide.
Insomnia: 1 B global │ 70 M US. CBN + melatonin restore REM; magnesium glycinate calms nerves.
JUL — Minority Mental Health / Skin Cancer / PTSD / Burnout
JUL — Minority Mental Health / Skin Cancer / PTSD / Burnout
PTSD: 350 M global │ 13 M US. Ketamine infusions reset trauma pathways; CBN + CBD aid rest.
Skin Cancer: 1 M global │ 5.5 M US. Topical CBD + vitamin D reduce UV-induced DNA damage.
Burnout: 400 M global. Omega-3, mindfulness, and social support prevent physician fatigue.
AUG — Immunization / Psoriasis / Autoimmune / Chronic Fatigue
AUG — Immunization / Psoriasis / Autoimmune / Chronic Fatigue
Psoriasis: 125 M global │ 7.5 M US. CBD + turmeric calm inflammation; UVB phototherapy enhances skin renewal.
Lupus: 5 M global │ 200 K US. Omega-3 + CBD lower flares; vitamin D + CoQ10 aid immunity.
Chronic Fatigue: 150 M global. NAD+ IVs + adaptogens restore mitochondrial energy.
SEP — Chronic Pain / Prostate CA / Neuropathy / Addiction
SEP — Chronic Pain / Prostate CA / Neuropathy / Addiction
Chronic Pain: 1.5 B global │ 50 M US. THC/CBD ↓ opioid need > 60%; nerve blocks + acupuncture improve function.
Prostate CA: 1.4 M global │ 288 K US. CBD reduces bone pain; lycopene + vit D support prevention.
Neuropathy: 240 M global. Alpha-lipoic acid + CBG + IV B12 repair nerves.
Addiction: 200 M global. Cannabis + ketamine-assisted therapy improve long-term recovery.
OCT — Breast CA / Depression / Osteoporosis / Financial Toxicity
OCT — Breast CA / Depression / Osteoporosis / Financial Toxicity
Breast CA: 2.3 M global │ 300 K US. CBD + CBG relieve chemo pain; omega-3 aid tissue repair.
Depression: 300 M global │ 21 M US. Ketamine + 5-HTP lift mood; mindfulness builds resilience.
Osteoporosis: 500 M global │ 10 M US. PRP + vitamin K2 + weight training increase bone density.
Financial toxicity: 80% cancer patients affected — budgeting + advocacy reduce distress.
NOV — Lung CA / Diabetes / COPD / EPILEPSY / Pain Crisis
NOV — Lung CA / Diabetes / COPD / EPILEPSY / Pain Crisis
Lung CA: 2.2 M global │ 234 K US. CBD + vit C IV reduce fatigue; THC aids appetite and mood.
Diabetes: 540 M global │ 38 M US. CBG + berberine enhance glucose control; magnesium supports insulin.
COPD: 390 M global │ 16 M US. Nebulized CBD + breathing rehab improve oxygenation.
Epilepsy: 65 M global │ 3 M US. CBD (Epidiolex) FDA-approved; ketogenic diet aids seizure control.
Pain crisis: 1.5 B global. Multimodal pain + cannabis reduce ER visits.
DEC — HIV/AIDS / Road Injury / Insomnia / Holiday Stress
DEC — HIV/AIDS / Road Injury / Insomnia / Holiday Stress
HIV: 39 M global │ 1.2 M US. CBD ↑ appetite; B-complex + omega-3 boost immunity.
Traffic injury: 1.3 M global deaths │ 46 K US. Post-injury PRP + CBD ↓ opioid reliance.
Insomnia: 1 B global │ 70 M US. CBN + magnesium improve rest.
Holiday stress: Mindfulness + CBD tea ↓ cortisol; gratitude resets the brain.
AWARENESS MONTHS (Empathy & Perspective)
Aug – Immunization, Psoriasis, National Wellness, Pain-Free Posture Awareness, Musculoskeletal Health
Sep – Healthy Aging, Pain Awareness, Suicide Prevention, Cholesterol, Yoga, Fall Prevention
Oct – Emotional Wellness, Breast Cancer, Liver Awareness, Health Literacy, Ergonomics Awareness (Workplace Pain Prevention), Bone & Joint Health, First week = Mental Illness Awareness Week (NAMI), 10th - Depression Screening Day,
Nov – Alzheimer’s, Diabetes, Lung Cancer, Family Caregivers, Sleep Comfort, TMJ Awareness, Sciatica Awareness, National Family Health History Awareness
Dec – Handwashing Awareness Month, Safe Toys & Gifts
Jan – Healthy Weight, Mental Wellness, Glaucoma, Thyroid, Cervical Health, Rheumatoid Arthritis
Feb – American Heart, Cancer Prevention, Black Hx Month
Mar – Nutrition, Kidney Cancer, Colorectal Cancer, Sleep Awareness, Autoimmune Disease Awareness, TBI, MULTIPLE SCLEROSIS - NMSS
Apr – Stress Awareness, Autism Awareness, Minority Health, Parkinson’s, IBS, Injury Prevention, Joint Health
May – Mental Health, Arthritis, Stroke, Osteoporosis, Women's Health, Physical Fitness & Sports Injury Prevention, Fibromyalgia Awareness
Jun – Brain Awareness, Men's Health, PTSD, Migraine, Alzheimer’s & Dementia, National Safety Month (Injury Prevention), Spine Health Work Safety Month
Jul – Healthy Vision, UV Safety, Minority Mental Health, Chronic Disease Management, Scoliosis Awareness
========
HIPAA/Privacy:
Data Privacy Day (January 28): Highlights protecting patient information and HIPAA Privacy Rule compliance.
Health Information Professionals (HIP) Week (March/April): Honors HIM professionals and underscores HIPAA best practices.
Cybersecurity Awareness Month (October): Stresses HIPAA Security Rule adherence through cybersecurity initiatives.
Workplace Safety:
National Safety Month (June): Promotes overall workplace safety, including OSHA standards and injury prevention.
Patient Safety Awareness Week (March): Focuses on reducing errors and improving patient outcomes.
Infection Prevention Week (October): Emphasizes policies to prevent healthcare-associated infections.
Respiratory Protection Week (September): Reinforces the proper use of respirators and OSHA compliance.
Safe + Sound Week (August): Encourages implementing effective safety and health programs.
Fire Prevention Week (Week of October 9): Highlights fire safety measures and emergency evacuation plans.
Favorite Places in
Favorite Places in
Tampa - Aquarium, Attorney Strickland's new office, Trulieve, USF, Ybor,
Tampa - Aquarium, Attorney Strickland's new office, Trulieve, USF, Ybor,
Orlando - BOT, TulipsBlooms.org, Trulieve, Disney Parks, Rosen Centre, Mall at Millenia, Dr Massi's, Dr Mbeo's, MCO, IMG, Oh Que Bueno,
Orlando - BOT, TulipsBlooms.org, Trulieve, Disney Parks, Rosen Centre, Mall at Millenia, Dr Massi's, Dr Mbeo's, MCO, IMG, Oh Que Bueno,
Miami - Brightline, Trulieve, Gables Pain, MARC,
Miami - Brightline, Trulieve, Gables Pain, MARC,
Jax - My office, NWM, Town Center, Libraries, Avenues Mall
Jax - My office, NWM, Town Center, Libraries, Avenues Mall
' Do Every Day, All You Can Do That Day '
' Do Every Day, All You Can Do That Day '
- Dr Newton
- Dr Newton
↑ signal + ↓ noise → success
excel | enjoy growth systems | transfer focus | find genius zone audit | transfer | fill
produce energy | dream bigger | 1 project away |
Dr. Terel S. Newton, M.D.
Board-Certified Pain Specialist | Interventional Pain Consultant | Medical Cannabis Expert
Medical Director, Trulieve MMTC | Total Pain Relief LLC | Stepping Stones CRI
🌐 TerelNewton.com | 🔬 Research Interests
📧 DrTerelNewton@gmail.com | Terel.Newton@Trulieve.com
Languages: English | Spanish (Proficient)
"Advancing Pain Relief Through Innovation, Education, and Compassion."
GUEST SPEAKER: Multiple Conferences and events ...
ELEVATE ATL | BOOK STORE GALLERY
ATTENDED and/or PRESENTED...
FL - CANNABIS LAB, FSIPP, SPACE CON, SMOKEN YOGA
GA - WOMEN IN BIZ EXPO (ATL)
NEVADA - MJ BIZ CON, Blue-Ribbon Study Committee (Ga)
Dispensary Tours (Retail) = Medical Doctors/Clinic Staff, BCFCF, Tulips Blooms, Media Day, Grand Opening.
Dispensary Tours (Cultivation) = Universities, Educators/Research/Community Outreach, et al
SUPPORT ...
BOT CANNABIZIAC M4MM MMERI FMCCE FMA GMA
Disclaimer:
Information provided is for reference only and does not imply affiliation or endorsement with the mentioned individuals, companies, products, services, treatments, and websites. For informational purposes only - contact your medical provider for health and medical advice. Content accuracy, completeness, and timeliness are not guaranteed. Inclusion of information and websites does not constitute endorsement. Users should exercise caution when accessing external content. See your medical, legal, finance, tax, spiritual and other professionals for discussion, guidance, planning, recommendations and greater understanding of the risks, benefits, options and ability to apply any information to your situation.
GREAT PEOPLE TO WORK WITH ...FSU
GREAT PEOPLE TO WORK WITH ...FSU
Faculty Profiles
Faculty Profiles
Dr. Nicole Ennis, Ph.D. – Associate Professor and Vice Chair, Dept. of Behavioral Sciences & Social Medicine (BSSM). Dr. Ennis is a leading behavioral scientist with a focus on public health, substance use, and medical cannabis outcomes researchmed.fsu.edu. She has extensive experience developing and implementing interventions for people with chronic illnesses (e.g. HIV) and those affected by substance misusemed.fsu.edu. Notably, Dr. Ennis and collaborators have been at the forefront of studying medical marijuana’s effects – for example, examining how long-term medical cannabis use (alone or with opioids) impacts driving performance in older adultsmed.fsu.edu. Her work in this area has earned continuous funding from the National Institute on Drug Abuse (NIDA) and other agencies for over a decademed.fsu.edu. In recognition of her expertise, FSU’s president recently nominated Dr. Ennis to the Board of the Florida Consortium for Medical Marijuana Clinical Outcomes Research, a statewide research initiativemed.fsu.edu. This speaks to her openness and leadership in medical cannabis research, as well as alignment with Florida’s health priorities. Contact: nennis@fsu.edu (Department of BSSM, FSU College of Medicine)med.fsu.edu.
Dr. Heather A. Flynn, Ph.D. – Professor and Chair, Dept. of Behavioral Sciences & Social Medicine. Dr. Flynn is a senior faculty member and clinical psychologist specializing in mental health, behavioral health integration, and health services researchmed.fsu.edumed.fsu.edu. Under her leadership, the BSSM department has secured over $21 million in external grants (2015–2019) in mission-focused areas including chronic illness, mental health, substance use/addiction, and health policymed.fsu.edu. She has a proven NIH funding track record (e.g. perinatal depression research) and is a strong advocate for patient‐centered outcomes research and community-engaged studiesmed.fsu.edu. Importantly, Dr. Flynn has demonstrated openness to medical cannabis research – she co-authored a recent study on Florida medical cannabis patients’ health outcomes and opioid use reductionmed.fsu.edu. As department chair, she can lend significant institutional support and ensure any cannabis study aligns with FSU’s values of scientific rigor and public health impact. Contact: heather.flynn@med.fsu.edu (Chair, BSSM, FSU College of Medicine)med.fsu.edu.
Dr. Laura Reid Marks, Ph.D. – Associate Professor, Dept. of Behavioral Sciences & Social Medicine. Dr. Marks is a behavioral health researcher focusing on substance use, mental health, and health disparities in emerging adultsmed.fsu.eductbs.fsu.edu. She directs the G.R.O.W.T.H. research lab at FSU’s Center for Translational Behavioral Science, investigating how factors like discrimination and stress influence health behaviors. Her work includes studying young adults’ alcohol and cannabis use patterns – for instance, she recently published on perceived increases in alcohol and cannabis use among diverse college-aged adults during the pandemicmed.fsu.edu. This background shows her comfort with cannabis-related research questions (especially regarding vulnerable or underserved populations). Dr. Marks’s expertise in culturally tailored interventions and digital health (mHealth) toolsmed.fsu.edu could be valuable for innovative study designs (e.g. mobile health data collection from medical marijuana patients). She would likely champion projects examining cannabis in the context of mental health and health equity, aligning with NIH’s focus on disparity populations. Contact: laura.reidmarks@fsu.edu (Dept. of BSSM, FSU College of Medicine)ctbs.fsu.edu.
Collaboration Options
Collaboration Options
Joint Observational Study (MMJ Registry + FSU Networks): A collaborative observational study leveraging MMJOutcomes.org’s patient registry data and FSU’s clinical networks. This could involve prospectively tracking health outcomes (pain levels, opioid use, functional status, etc.) in patients using medical cannabis. FSU’s statewide clinical footprint (primary care and specialty clinics, plus the geriatric patient base) provides access to diverse patient populations, including older adults and rural patients – groups of high interest as Florida’s medical cannabis usage growsmed.fsu.edu. By pooling MMJOutcomes registry data with FSU clinical data, the study can yield real-world evidence on medical cannabis efficacy and safety (e.g. improvements in pain and quality of life, reduction in opioid dosagessciencedaily.comsciencedaily.com). This aligns with Florida’s public health priorities (addressing the opioid crisis through alternative pain therapies) and would likely earn institutional approval, as it builds on existing FSU strengths in community-based research and patient-centered outcomesmed.fsu.edu.
Co-authored Grant Proposal (Cannabis in Medicaid/Vulnerable Populations): A partnership to co-write a grant proposal focusing on evaluating medical cannabis outcomes in Florida’s Medicaid or other vulnerable populations. This could be a multidisciplinary project studying how cannabis therapy affects healthcare utilization, costs, or health metrics in low-income or minority patients (for example, examining if medical cannabis use correlates with reduced emergency visits or improved chronic pain management in Medicaid recipients). Such a proposal could target NIH (e.g. NIDA or NIMHD) or state funding. It would merge Dr. Ennis’s and Dr. Marks’s expertise in substance use and health disparities with Dr. Flynn’s experience in large-scale health services research. Strategically, this aligns with NIH funding trends encouraging research on cannabis as it relates to pain and opioid reductionmed.fsu.edu, and with Florida’s interest in evidence-based cannabis policy for its most vulnerable citizens. A well-crafted grant on this topic not only addresses pressing state health questions but also leverages FSU’s emphasis on health equity and policy-relevant research.
Cross-Institution Academic Publication (Cannabis Outcomes Review): A scholarly collaboration to produce a comprehensive review or policy paper on medical cannabis outcomes, co-authored by Dr. Newton and FSU faculty for a high-impact academic journal. Possible topics include a systematic review of clinical outcomes of medical cannabis in specific conditions (e.g. chronic pain, PTSD, or in older adults), or a review of policy and public health impacts of Florida’s medical marijuana program. Co-authoring such a paper would capitalize on FSU faculty’s subject-matter knowledge – Dr. Ennis’s work on driving and safety outcomesmed.fsu.edu, Dr. Marks’s insight into young adult usage patternsmed.fsu.edu, and Dr. Flynn’s perspective on mental health outcomes – combined with MMJOutcomes data and Dr. Newton’s registry findings. This publication could serve as a cornerstone for Florida’s thought leadership in cannabis research, and is in line with FSU’s academic mission to translate research into practice and policy. It also sets the stage for future joint projects, demonstrating a united front on cannabis outcomes research that would be well-received by both the university and state consortium.
GREAT PEOPLE TO WORK WITH ...FAMU
GREAT PEOPLE TO WORK WITH ...FAMU
FAMU Profiles
FAMU Profiles
Dr. G. P. Mendie (MMERI Executive Director)
https://www.famu.edu/administration/research/contact-us.php
Dr. Donald E. Palm III
https://www.famu.edu/_training-and-testing/backup-archived-pages/presidential-search/pdf/cv-DonaldPalm.pdf
(Also: https://news.famu.edu/2025/famu-coo-donald-palm-selected-for-news-service-of-florida-50-over-50-list.php)
Dr. Charles A. Weatherford
https://www.famu.edu/info/faculty-staff/profiles/cst/charles-weatherford.php
Dr. Mandip S. Sachdeva
https://pharmacy.famu.edu/research/research_laboratories/sachdeva-laboratory/index.php
Dr. Otis W. Kirksey
https://www.floridahealth.gov/provider-and-partner-resources/research/florida-health-grand-rounds/Bio-DrKirksey020821.pdf
(Also: https://events.diabetes.org/b/sp/otis-kirksey-1080
Dr. G.P. Mendie
Dr. G.P. Mendie
Official Profile: Executive Director of FAMU’s Medical Marijuana Education and Research Initiative (MMERI), listed on FAMU’s Division of Research contact pagefamu.edu. (This page provides his name, title, and email as the MMERI Executive Director.)
Official Image: A professional headshot is available via FAMU’s Service Excellence “Gallery of Distinction” (he was recognized as an Employee of the Quarter)famu.edu. Direct image URL: 640x480_G.P.-Mendie.jpg on FAMU’s site (the photo is embedded on the gallery page, but users can view/download it by accessing the image link).
Dr. Donald E. Palm
Dr. Donald E. Palm
Official Profile: Executive Vice President and Chief Operating Officer (COO) of FAMU. (No dedicated faculty profile page is published; however, FAMU’s news release announcing his recognition as a “50 Over 50” honoree serves as an official bionews.famu.edu.) This news article outlines Dr. Palm’s role and background at FAMU.
Official Image: A formal headshot of Dr. Palm is embedded in the FAMU News articlenews.famu.edu. Direct image URL: 1024x768_donald-palm.jpg on the FAMU News site (the image appears in the news story and can be saved from the page).
Dr. Charles Weatherford
Dr. Charles Weatherford
Official Profile: Vice President for Research at FAMU, and Professor of Physics. His official faculty profile page on FAMU’s website provides his biography and credentialsfamu.edufamu.edu. (This profile notes his roles, education, and accomplishments in research and academia at FAMU.)
Official Image: The profile includes an official headshot of Dr. Weatherfordfamu.edu. Direct image URL: 450x450_Dr.-Weatherford.jpg on the FAMU site (this is the image displayed on his faculty profile, which can be viewed or downloaded directly).
Dr. Mandip S. Sachdeva
Dr. Mandip S. Sachdeva
Official Profile: Professor of Pharmaceutical Sciences in the FAMU College of Pharmacy and Pharmaceutical Sciences (CoPPS). An official page on the CoPPS research site (Sachdeva Lab page) features his Biosketch and qualificationspharmacy.famu.edu. (This lab profile highlights his education, positions, and research focus at FAMU.)
Official Image: Dr. Sachdeva’s headshot is included in the CoPPS faculty/staff directorypharmacy.famu.edu. Direct image URL: Mandip-Sachdeva.jpg on the pharmacy.famu.edu server (the photo is shown in the directory listing and can be downloaded by accessing the image link).
Dr. Otis W. Kirksey
Dr. Otis W. Kirksey
Official Profile: N/A on FAMU site. Dr. Kirksey is a retired FAMU pharmacy faculty member (honored in 2020 as Professor Emeritus of Pharmacy Practice)floridahealth.gov. There is no current faculty profile on FAMU’s websites due to his retirement. (His contributions are noted in external publications, but no active FAMU page exists for him.)
Official Image: Not available. No official image or headshot is posted on FAMU’s current sites for Dr. Kirksey (as a retired faculty, he is not featured on current directories). Any photos of Dr. Kirksey appear on external sites (e.g. American Diabetes Association profiles), not on FAMU-hosted pages.
Vocab List - 1st 50
Monday & Wednesday | 8–9 PM ET – Post Market Analysis
Tuesday & Thursday | 9:30–10 AM ET – Live Market Performance
Absorption Passive limit orders neutralize aggressive orders, stopping continuation and signaling reversal.
ATR (Average True Range) Measures volatility and sets dynamic stop distances.
Bearish Engulfing Large red candle overtakes a smaller green one, signaling reversal.
Bid Stack Visible buy liquidity showing potential support depth.
Breakout Strong move above resistance with volume confirming trend ignition.
Breakdown Strong move below support triggering stops and continuation.
Compression Tight price clustering before explosive expansion.
Consolidation Sideways balance where buyers and sellers neutralize each other.
Continuation Trend resumes after pullback, confirming strong directional pressure.
Cumulative Delta Net aggressive buying vs selling revealing hidden positioning.
Demand Zone Area of prior institutional buying producing future bounces.
Delta Imbalance Heavy skew between buy and sell volume predicting directional moves.
Doji Indecision candle with equal open and close signaling potential shift.
Downtrend Sequence of lower highs and lower lows showing bearish control.
EMA (Exponential Moving Average) Fast-moving average defining short-term trend direction.
Engulfing Pattern Candle overtakes previous candle’s range signaling momentum takeover.
Expansion Volatility widening after compression, enabling strong trend legs.
Fair Value Gap (FVG) Inefficiency zone often retraced for balance.
Fib Retracement Key pullback levels (38.2, 50, 61.8) used for trend entries.
Fib Target Zone Common profit zones (100%, 127%, 161.8%).
First Pullback Entry High-probability early-trend entry after initial push.
Footprint Chart Displays bid–ask volume inside candles to expose imbalance.
Hammer Bullish reversal candle showing strong rejection of lows.
Hanging Man Bearish reversal candle after an uptrend with long lower wick.
Higher High New swing high confirming bullish structure.
Higher Low Rising trough confirming buyers stepping in earlier.
Imbalance Aggressive displacement leaving inefficient price areas later filled.
Impulse Leg Strong directional move used for Fib anchoring.
Inside Bar Candle fully inside previous bar signaling contraction.
Liquidity Grab Stop-triggering sweep beyond a key level before reversal.
Limit Order Passive order resting at a specific price.
MACD Momentum indicator showing trend acceleration or reversal.
Market Order Immediate execution consuming liquidity, indicating urgency.
Micro Pullback Very shallow retracement during strong trends showing dominance.
NQ/ES Futures Basics Highly liquid index futures used for intraday trend trading.
Order Block Institutional footprint of accumulation or distribution.
POC (Point of Control) Highest volume price acting as magnet and pivot.
Price Discovery Auction process establishing fair value.
Range Expansion Break from tight structure into larger price moves.
Range Contraction Tightening volatility showing indecision before move.
Rejection Wick Long wick showing strong denial of price continuation.
Reversal Trend turning after exhaustion and structural break.
RSI Momentum oscillator identifying overbought/oversold or divergence.
Scalping Framework Fast execution system targeting small high-frequency gains.
Slippage Worse-than-expected fill due to volatility or thin liquidity.
Stop Run Targeting of stop clusters to create volatility and fill liquidity.
Structure Break Major swing break confirming trend shift.
Supply Zone Region of previous institutional selling causing future resistance.
Support Price area where demand stops decline.
VWAP Volume-weighted fair value used for mean reversion and trend strength.
Advanced
Advanced
I. Master Alphabetical Glossary (High-Capital Scalping)
I. Master Alphabetical Glossary (High-Capital Scalping)
AAR – Aggressive Add Reclaim
Reclaim of key liquidity level after sweep with immediate displacement and confirming order flow, allowing confident size increase.
Example: Sweep PDL, reclaim with impulse + delta surge → add 30c.
ABR – Algo Break & Run
Algorithm-driven breakout with rapid expansion, minimal pullback, sustained velocity beyond structure.
Example: ORB break, stacked prints, 60-point run in two minutes.
AON – All-or-None Execution
Full-size order must fill entirely or not at all, preventing fragmented execution in thin liquidity.
Example: 75c AON above range high during expansion setup.
ATRX – ATR Expansion Event
Current range exceeds recent ATR average, signaling volatility expansion and institutional participation.
Example: 1m candle doubles 14ATR during VWAP break.
BDS – Bid Stack Absorption
Large resting bids absorb aggressive sellers, often preceding upside reversal or continuation.
Example: Repeated hits into bid at VWAP, price holds firm.
BRR – Break-Retest-Run
Break level, controlled pullback, renewed expansion confirming continuation.
Example: Break PDH → shallow pullback → bullish engulfing → scale 50c.
CBR – Continuation Breakout Re-entry
Secondary entry after breakout when pullback holds structure and momentum resumes.
Example: Pullback to breakout level with strong CLV → re-enter.
CD – Cumulative Delta
Running total of aggressive buying versus selling; confirms imbalance or divergence.
Example: Price flat, delta rising → bullish breakout pending.
CLV – Closing Location Value
Where candle closes within range; high close signals directional conviction.
Example: Marubozu close at high → continuation bias.
DLR – Deep Liquidity Raid
Stop sweep beyond obvious highs/lows before reversal or acceleration.
Example: Spike above ONH, immediate rejection wick.
DVP – Delta Volume Pulse
Sudden surge in aggressive order flow confirming expansion.
Example: +5,000 delta spike on breakout candle.
ELR – Extreme Liquidity Reversal
High-velocity reversal immediately after liquidity sweep.
Example: Stop purge above PDH → 80-point bearish impulse.
FBO – Failed Breakout
Break lacking follow-through, leading to sharp opposite move.
Example: Break high stalls, inside bar forms → short trigger.
FLS – First Liquidity Sweep
Initial stop run before structural move develops.
Example: Sweep range low, reclaim, build long.
HTF-A – Higher Timeframe Alignment
Lower timeframe entries aligned with 5m/15m/hourly structure bias.
Example: 1m breakout long with 15m bullish trend.
IMP – Impulse Leg
Strong directional displacement with minimal overlap, large bodies, strong volume.
Example: Three consecutive Marubozu, 100-point YM move.
LQZ – Liquidity Zone
Area containing clustered stops, equal highs/lows, visible resting liquidity.
Example: Equal highs above range attract breakout sweep.
LRR – Liquidity Reclaim & Run
Reclaim after sweep with sustained acceptance above/below level.
Example: Sweep PDL, reclaim VWAP, hold → expansion.
MEX – Momentum Exhaustion
Velocity decreases, wicks expand, delta diverges; trend fatigue signals exit.
Example: Higher highs with weakening volume.
MSS-X – Market Structure Shift with Expansion
Break in prior swing structure confirmed by displacement candle.
Example: Lower high breaks with volume expansion → trend shift.
OFI – Order Flow Imbalance
Significant disparity between aggressive buyers and sellers.
Example: 4:1 buy imbalance during breakout.
PVA – Price-Volume Acceleration
Simultaneous increase in price velocity and traded volume.
Example: Rapid 30-point move with doubled volume.
RLP – Reversal Liquidity Pocket
Tight consolidation after stop purge before reversal expansion.
Example: 3-candle base forms after sweep → long trigger.
SFA – Size Flow Acceleration
Increase in large-lot transactions supporting move.
Example: Block trades repeatedly lifting offer.
SPR – Stop-Purge Reversal
Aggressive stop sweep followed by immediate opposite expansion.
Example: Flush below range → bullish engulfing reversal.
TFX – Timeframe Expansion
Higher timeframe breakout aligns with lower timeframe trigger.
Example: 1m break aligns with 15m range break.
VEX – Volatility Expansion
Compression transitions into high-range breakout.
Example: Three narrow candles → explosive expansion bar.
VW-Dev – VWAP Deviation Extension
Significant stretch beyond VWAP deviation bands signaling continuation or exhaustion.
Example: +2 SD extension with divergence.
II. $50K+ Structured Execution Model (YM/NQ)
II. $50K+ Structured Execution Model (YM/NQ)
Capital Assumption
Capital Assumption
$50,000 account
Aggressive sizing model: 20–100 contracts (YM or NQ)
Target: 80–200+ points in expansion phase
Phase 1: Pre-Trade Qualification (All Must Align)
Phase 1: Pre-Trade Qualification (All Must Align)
HTF-A + TFX present
Liquidity event confirmed (FLS / DLR / LQZ interaction)
IMP or ATRX triggered
OFI + DVP confirmation
CLV strong in breakout direction
If 4/5 present → proceed.
Phase 2: Entry Protocol
Phase 2: Entry Protocol
Primary triggers:
• BRR
• MSS-X
• ABR
Execution:
Initial entry 25c
Add via AAR or CBR
Scale to 50c–100c only during VEX + SFA conditions
Phase 3: Risk Architecture
Phase 3: Risk Architecture
Initial stop: below structural reclaim (not fixed tick)
Max per-trade risk: 3–5% capital during expansion phase
Move to BE+ only after second impulse confirmation
Phase 4: Profit Model
Phase 4: Profit Model
YM example:
100 contracts × 100 points = 10,000 points
$5 per point = $50,000
NQ example:
50 contracts × 100 points
$20 per point = $100,000
Scaling logic:
Partial at 1R
Trail via TS under impulse lows
Final exit on MEX or VW-Dev divergence
Phase 5: Exit Triggers
Phase 5: Exit Triggers
• MEX
• Delta divergence
• Failure to hold reclaim
• Opposing SPR
• A TERELS-integrated version
• Or a statistical probability model for $50K setups
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