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SweetSue's Class Notes
- Thread starter SweetSue
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- #902
I promised him before he passed that I’d make this understandable. It’s time. I’ll start working it tomorrow.
CajunCelt, post: 2490854
How CCO Kills Cancer
I'm asked this daily, so here goes:
In every cell there is a family of interconvertible sphingolipids that specifically manage the life and death of that cell. This profile of factors is called the "Sphingolipid Rheostat." If ceramide (a signaling metabolite of sphingosine-1- phosphate) is high, then cell death (apoptosis) is imminent. If ceramide is low, the cell will be strong in its vitality.
Very simply, when THC connects to the CB1 or CB2 cannabinoid receptor site on the cancer cell, it causes an increase in ceramide synthesis which drives cell death. A normal healthy cell does not produce ceramide in the presence of THC, thus is not affected by the cannabinoid.
The cancer cell dies, not because of cytotoxic chemicals, but because of a tiny little shift in the mitochondria. Within most cells there is a cell nucleus, numerous mitochondria (hundreds to thousands), and various other organelles in the cytoplasm. the purpose of the mitochondria is to produce energy (ATP) for cell use. As ceramide starts to accumulate, turning up the Sphingolipid Rheostat, it increases the mitochondrial membrane pore permeability to cytochrome c, a critical protein in energy synthesis. Cytochrome c is pushed out of the mitochondria, killing the source of energy for the cell.
Ceramide also causes genotoxic stress in the cancer cell nucleus generating a protein called p53, whose job it is to disrupt calcium metabolism in the mitochondria. If this weren't enough, ceramide disrupts the cellular lysosome, the cell's digestive system that provides nutrients for all cell functions. Ceramide, and other sphingolipids, actively inhibit pro-survival pathways in the cell leaving no possibility at all of cancer cell survival.
The key to this process is the accumulation of ceramide in the system. This means taking therapeutic amounts of cannabinoid extract, steadily, over a period of time, keeping metabolic pressure on this cancer cell death pathway.
How did this pathway come to be? Why is it that the body can take a simple plant enzyme and use it for healing in many different physiological systems? This endocannabinoid system exists in all animal life, just waiting for it's matched exocannabinoid activator.
This is interesting. Our own endocannabinoid system covers all cells and nerves; it is the messenger of information flowing between our immune system andthe central nervous system (CNS). It is responsible for neuroprotection, and micro- manages the immune system. This is the primary control system that maintains homeostasis; our well being.
Just out of curiosity, how does the work get done at the cellular level, and where does the body make the endocannabinoids? Here we see that endocannabinoids have their origin in nerve cells right at the synapse. When the body is compromised through illness or injury it calls insistently to the endocannabinoid system and directs the immune system to bring healing. If these homeostatic systems are weakened, it should be no surprise that exocannabinoids perform the same function. It helps the body in the most natural way possible.
To see how this works we visualize the cannabinoid as a three dimensional molecule, where one part of the molecule is configured to fit the nerve or immune cell receptor site just like a key in a lock. There are at least two types of cannabinoid receptor sites, CB1 (CNS) and CB2 (immune). In general CB1 activates the CNS messaging system, and CB2 activates the immune system, but it's much more complex than this. Both THC and anandamide activate both receptor sites. Other cannabinoids activate one or the other receptor sites. Among the strains of Cannabis, C. sativa tends toward the CB1 receptor, and C. indica tends toward CB2. So sativa is more neuroactive, and indica is more immunoactive. Another factor here is that sativa is dominated by THC cannabinoids, and indica is predominately CBD (cannabidiol).
It is known that THC and CBD are biomimetic to anandamide, that is, the body can use both interchangeably. Thus, when stress, injury, or illness demand more from endogenous anandamide than can be produced by the body, its mimetic exocannabinoids are activated. If the stress is transitory, then the treatment can be transitory. If the demand is sustained, such as in cancer, then treatment needs to provide sustained pressure of the modulating agent on the homeostatic systems.
Typically CBD gravitates to the densely packed CB2 receptors in the spleen, home to the body's immune system. From there, immune cells seek out and destroy cancer cells. Interestingly, it has been shown that THC and CBD cannabinoids have the ability to kill cancer cells directly without going through immune intermediaries. THC and CBD hijack the lipoxygenase pathway to directly inhibit tumor growth. As a side note, it has been discovered that CBD inhibits anandamide reuptake. Here we see that cannabidiol helps the body preserve its own natural endocannabinoid by inhibiting the enzyme that breaks down anandamide.
This post touches lightly on a few essential concepts. Mostly I would like to leave you with an appreciation that nature has designed the perfect medicine that fits exactly with our own immune system of receptors and signaling metabolites to provide rapid and complete immune response for systemic integrity and metabolic homeostasis.
CajunCelt, post: 2490854
How CCO Kills Cancer
I'm asked this daily, so here goes:
In every cell there is a family of interconvertible sphingolipids that specifically manage the life and death of that cell. This profile of factors is called the "Sphingolipid Rheostat." If ceramide (a signaling metabolite of sphingosine-1- phosphate) is high, then cell death (apoptosis) is imminent. If ceramide is low, the cell will be strong in its vitality.
Very simply, when THC connects to the CB1 or CB2 cannabinoid receptor site on the cancer cell, it causes an increase in ceramide synthesis which drives cell death. A normal healthy cell does not produce ceramide in the presence of THC, thus is not affected by the cannabinoid.
The cancer cell dies, not because of cytotoxic chemicals, but because of a tiny little shift in the mitochondria. Within most cells there is a cell nucleus, numerous mitochondria (hundreds to thousands), and various other organelles in the cytoplasm. the purpose of the mitochondria is to produce energy (ATP) for cell use. As ceramide starts to accumulate, turning up the Sphingolipid Rheostat, it increases the mitochondrial membrane pore permeability to cytochrome c, a critical protein in energy synthesis. Cytochrome c is pushed out of the mitochondria, killing the source of energy for the cell.
Ceramide also causes genotoxic stress in the cancer cell nucleus generating a protein called p53, whose job it is to disrupt calcium metabolism in the mitochondria. If this weren't enough, ceramide disrupts the cellular lysosome, the cell's digestive system that provides nutrients for all cell functions. Ceramide, and other sphingolipids, actively inhibit pro-survival pathways in the cell leaving no possibility at all of cancer cell survival.
The key to this process is the accumulation of ceramide in the system. This means taking therapeutic amounts of cannabinoid extract, steadily, over a period of time, keeping metabolic pressure on this cancer cell death pathway.
How did this pathway come to be? Why is it that the body can take a simple plant enzyme and use it for healing in many different physiological systems? This endocannabinoid system exists in all animal life, just waiting for it's matched exocannabinoid activator.
This is interesting. Our own endocannabinoid system covers all cells and nerves; it is the messenger of information flowing between our immune system andthe central nervous system (CNS). It is responsible for neuroprotection, and micro- manages the immune system. This is the primary control system that maintains homeostasis; our well being.
Just out of curiosity, how does the work get done at the cellular level, and where does the body make the endocannabinoids? Here we see that endocannabinoids have their origin in nerve cells right at the synapse. When the body is compromised through illness or injury it calls insistently to the endocannabinoid system and directs the immune system to bring healing. If these homeostatic systems are weakened, it should be no surprise that exocannabinoids perform the same function. It helps the body in the most natural way possible.
To see how this works we visualize the cannabinoid as a three dimensional molecule, where one part of the molecule is configured to fit the nerve or immune cell receptor site just like a key in a lock. There are at least two types of cannabinoid receptor sites, CB1 (CNS) and CB2 (immune). In general CB1 activates the CNS messaging system, and CB2 activates the immune system, but it's much more complex than this. Both THC and anandamide activate both receptor sites. Other cannabinoids activate one or the other receptor sites. Among the strains of Cannabis, C. sativa tends toward the CB1 receptor, and C. indica tends toward CB2. So sativa is more neuroactive, and indica is more immunoactive. Another factor here is that sativa is dominated by THC cannabinoids, and indica is predominately CBD (cannabidiol).
It is known that THC and CBD are biomimetic to anandamide, that is, the body can use both interchangeably. Thus, when stress, injury, or illness demand more from endogenous anandamide than can be produced by the body, its mimetic exocannabinoids are activated. If the stress is transitory, then the treatment can be transitory. If the demand is sustained, such as in cancer, then treatment needs to provide sustained pressure of the modulating agent on the homeostatic systems.
Typically CBD gravitates to the densely packed CB2 receptors in the spleen, home to the body's immune system. From there, immune cells seek out and destroy cancer cells. Interestingly, it has been shown that THC and CBD cannabinoids have the ability to kill cancer cells directly without going through immune intermediaries. THC and CBD hijack the lipoxygenase pathway to directly inhibit tumor growth. As a side note, it has been discovered that CBD inhibits anandamide reuptake. Here we see that cannabidiol helps the body preserve its own natural endocannabinoid by inhibiting the enzyme that breaks down anandamide.
This post touches lightly on a few essential concepts. Mostly I would like to leave you with an appreciation that nature has designed the perfect medicine that fits exactly with our own immune system of receptors and signaling metabolites to provide rapid and complete immune response for systemic integrity and metabolic homeostasis.
- Thread starter
- #903
Lipid raft
From Wikipedia, the free encyclopedia
Lipid raft organization, region (1) is standard lipid bilateral, while region (2) is a lipid raft.
The plasma membranes of cells contain combinations of glycosphingolipids, cholesterol and protei receptors organized in glycolipoprotein lipid microdomains termed lipid rafts. Their existence in cellular membranes remains somewhat controversial. It has been proposed that they are specialized membrane micro domains which compartmentalize cellular processes by serving as organizing centers for the assembly of signalling molecules, allowing a closer interaction of protein receptors and their effectors to promote kinetic ally favorable interactions necessary for the signal transduction. Lipid rafts influence membrane fluidity and membrane protein trafficking, thereby regulating neurotransmission and receptor trafficking. Lipid rafts are more ordered and tightly packed than the surrounding bilateral, but float freely within the membrane bilateral. Although more common in the cell membrane, lipid rafts have also been reported in other parts of the cell, such as the Golgi apparatus and lysosomes.
Sphingolipids are a class of lipids containing a backbone of sphingoid bases, a set of aliphatic amino alcohols that includes sphingosine. ... Sphingolipidoses, or disorders of sphingolipid metabolism, have particular impact on neural tissue. A sphingolipid with an R group consisting of a hydrogen atom only is a ceramide.
From Wikipedia, the free encyclopedia
Lipid raft organization, region (1) is standard lipid bilateral, while region (2) is a lipid raft.
The plasma membranes of cells contain combinations of glycosphingolipids, cholesterol and protei receptors organized in glycolipoprotein lipid microdomains termed lipid rafts. Their existence in cellular membranes remains somewhat controversial. It has been proposed that they are specialized membrane micro domains which compartmentalize cellular processes by serving as organizing centers for the assembly of signalling molecules, allowing a closer interaction of protein receptors and their effectors to promote kinetic ally favorable interactions necessary for the signal transduction. Lipid rafts influence membrane fluidity and membrane protein trafficking, thereby regulating neurotransmission and receptor trafficking. Lipid rafts are more ordered and tightly packed than the surrounding bilateral, but float freely within the membrane bilateral. Although more common in the cell membrane, lipid rafts have also been reported in other parts of the cell, such as the Golgi apparatus and lysosomes.
Sphingolipids are a class of lipids containing a backbone of sphingoid bases, a set of aliphatic amino alcohols that includes sphingosine. ... Sphingolipidoses, or disorders of sphingolipid metabolism, have particular impact on neural tissue. A sphingolipid with an R group consisting of a hydrogen atom only is a ceramide.
- Thread starter
- #904
REVIEW ARTICLE
Front. Cell Dev. Biol., 19 September 2019 | Diverse Facets of Sphingolipid Involvement in Bacterial Infections
Diverse Facets of Sphingolipid Involvement in Bacterial Infections
Tobias C. Kunz and
Vera Kozjak-Pavlovic*
Introduction
Sphingolipids belong to a class of lipids defined by their amino-alcohol backbone. They were considered merely to be ubiquitous components of the eukaryotic cell membrane, shown to play a critical role in the formation of membrane microdomains called lipid rafts that are important for cell signaling (Simons and Ikonen, 1997). However, in the past decades, it has been revealed that many sphingolipids are bioactive lipids that regulate a large subset of cellular functions, such as apoptosis or autophagy (Cuvillier et al., 1996; Harvald et al., 2015). Although sphingolipids vary greatly in their structure and function, their synthesis and degradation are mediated by common synthetic and catabolic pathways. Sphingolipids can be synthesized de novo, by the hydrolysis of sphingomyelin, or through the salvage pathway, by recovery of sphingosine from complex sphingolipids (Figure 1). In all cases the result is the synthesis of ceramide, which represents the starting point for the creation of complex sphingolipids and thus is involved in many regulating processes within the cell. The metabolism of sphingolipids has been extensively reviewed by Gault et al. (2010). Ceramide itself regulates growth and development and promotes cell survival and division (Mencarelli and Martinez-Martinez, 2013).
The de novo biosynthesis of ceramide starts at the endoplasmic reticulum (ER) with an enzyme called serine palmitoyltransferase. This enzyme catalyzes the condensation of serine and fatty acid-CoA to 3-ketosphinganine. Afterward, 3-ketosphinganine gets reduced by 3-ketosphinganine reductase and then is processed by dihydroceramide synthase to dihydroceramide. In the final step of the de novo ceramide biosynthesis, a dihydroceramide desaturase introduces a double bond to create ceramide (Perry, 2002; Menaldino et al., 2003; Figure 1).
Constitutive degradation of sphingolipids and glycosphingolipids takes place in the late endosomes and lysosomes at acidic pH to form sphingosine (Riboni et al., 1997; Kolter and Sandhoff, 2005). The oligosaccharide chains of glycosphingolipids are stepwise removed by the release of monosaccharide units through exohydrolases. In the salvage pathway, long-chain sphingoid bases are broken down to sphingosine, which is reacylated to form ceramide by an enzyme called ceramide synthase. Thus, ceramide synthase family members probably trap free sphingosine released from the lysosome at the surface of the ER or in ER-associated membranes. The salvage pathway is estimated to contribute to 50–90% of sphingolipid biosynthesis (Gillard et al., 1998; Tettamanti et al., 2003).
During the generation of ceramide from sphingosine, ceramide synthases add different fatty acyl chains at the C2-amino group of the sphingosine backbone, resulting in numerous and diverse sphingolipids. Variations in the chain length of ceramide acyl chains are linked to potentially altered membrane bilayer dynamics or differential signaling properties by recruitment of different binding partners. This topic has previously been reviewed by Grösch et al. (2012). However, the effect of different length of acyl chains on ceramide properties and function is poorly understood and needs further investigation.
Ceramide exerts a specific function in mitochondria, where the increase in ceramide has been linked to the induction of apoptosis. Ceramide pool in mitochondria seems to be regulated by the localized activity of ceramide synthase, sphingomyelinases, and neutral ceramidase. However, another source of mitochondrial ceramide could be the ER, due to the proximity and close interaction of these two organelles (Hernández-Corbacho et al., 2017).
Apart from ceramide, sphingosine-1-phosphate (S1P) has been shown to be a potent signaling molecule. It is linked to the regulation of mitochondrial function (Bajwa et al., 2015), gene expression (Davaille et al., 2000), and ER stress (Lépine et al., 2011). Moreover, it was implicated in the regulation of important processes such as apoptosis, autophagy, and cell proliferation (Harvald et al., 2015). S1P is synthesized by the sphingosine kinase-1 and -2 (SPHK1/2) by phosphorylation of sphingosine and degraded by the S1P phosphatase (SGPP) or lyase (SGPL1) to sphingosine or hexadecenal and phosphoethanolamine, respectively (Figure 1). While SPHK1 is mainly associated with cell survival (Sarkar et al., 2005), SPHK2 has been shown to influence mitochondrial function and homeostasis. It has also been involved in regulation of histone deacetylases and thereby in suppression of cell growth and promotion of apoptosis (Liu et al., 2003). SGPP and SGPL1 ensure balanced levels of S1P and other sphingolipid intermediates that may control cell growth and death. The upregulation of SGPL1 results in an accumulation of hexadecenal, which was shown to be cytotoxic (James and Zoeller, 1997).
Front. Cell Dev. Biol., 19 September 2019 | Diverse Facets of Sphingolipid Involvement in Bacterial Infections
Diverse Facets of Sphingolipid Involvement in Bacterial Infections
- Department of Microbiology, Biocenter, University of Würzburg, Würzburg, Germany
Introduction
Sphingolipids belong to a class of lipids defined by their amino-alcohol backbone. They were considered merely to be ubiquitous components of the eukaryotic cell membrane, shown to play a critical role in the formation of membrane microdomains called lipid rafts that are important for cell signaling (Simons and Ikonen, 1997). However, in the past decades, it has been revealed that many sphingolipids are bioactive lipids that regulate a large subset of cellular functions, such as apoptosis or autophagy (Cuvillier et al., 1996; Harvald et al., 2015). Although sphingolipids vary greatly in their structure and function, their synthesis and degradation are mediated by common synthetic and catabolic pathways. Sphingolipids can be synthesized de novo, by the hydrolysis of sphingomyelin, or through the salvage pathway, by recovery of sphingosine from complex sphingolipids (Figure 1). In all cases the result is the synthesis of ceramide, which represents the starting point for the creation of complex sphingolipids and thus is involved in many regulating processes within the cell. The metabolism of sphingolipids has been extensively reviewed by Gault et al. (2010). Ceramide itself regulates growth and development and promotes cell survival and division (Mencarelli and Martinez-Martinez, 2013).
The de novo biosynthesis of ceramide starts at the endoplasmic reticulum (ER) with an enzyme called serine palmitoyltransferase. This enzyme catalyzes the condensation of serine and fatty acid-CoA to 3-ketosphinganine. Afterward, 3-ketosphinganine gets reduced by 3-ketosphinganine reductase and then is processed by dihydroceramide synthase to dihydroceramide. In the final step of the de novo ceramide biosynthesis, a dihydroceramide desaturase introduces a double bond to create ceramide (Perry, 2002; Menaldino et al., 2003; Figure 1).
Constitutive degradation of sphingolipids and glycosphingolipids takes place in the late endosomes and lysosomes at acidic pH to form sphingosine (Riboni et al., 1997; Kolter and Sandhoff, 2005). The oligosaccharide chains of glycosphingolipids are stepwise removed by the release of monosaccharide units through exohydrolases. In the salvage pathway, long-chain sphingoid bases are broken down to sphingosine, which is reacylated to form ceramide by an enzyme called ceramide synthase. Thus, ceramide synthase family members probably trap free sphingosine released from the lysosome at the surface of the ER or in ER-associated membranes. The salvage pathway is estimated to contribute to 50–90% of sphingolipid biosynthesis (Gillard et al., 1998; Tettamanti et al., 2003).
During the generation of ceramide from sphingosine, ceramide synthases add different fatty acyl chains at the C2-amino group of the sphingosine backbone, resulting in numerous and diverse sphingolipids. Variations in the chain length of ceramide acyl chains are linked to potentially altered membrane bilayer dynamics or differential signaling properties by recruitment of different binding partners. This topic has previously been reviewed by Grösch et al. (2012). However, the effect of different length of acyl chains on ceramide properties and function is poorly understood and needs further investigation.
Ceramide exerts a specific function in mitochondria, where the increase in ceramide has been linked to the induction of apoptosis. Ceramide pool in mitochondria seems to be regulated by the localized activity of ceramide synthase, sphingomyelinases, and neutral ceramidase. However, another source of mitochondrial ceramide could be the ER, due to the proximity and close interaction of these two organelles (Hernández-Corbacho et al., 2017).
Apart from ceramide, sphingosine-1-phosphate (S1P) has been shown to be a potent signaling molecule. It is linked to the regulation of mitochondrial function (Bajwa et al., 2015), gene expression (Davaille et al., 2000), and ER stress (Lépine et al., 2011). Moreover, it was implicated in the regulation of important processes such as apoptosis, autophagy, and cell proliferation (Harvald et al., 2015). S1P is synthesized by the sphingosine kinase-1 and -2 (SPHK1/2) by phosphorylation of sphingosine and degraded by the S1P phosphatase (SGPP) or lyase (SGPL1) to sphingosine or hexadecenal and phosphoethanolamine, respectively (Figure 1). While SPHK1 is mainly associated with cell survival (Sarkar et al., 2005), SPHK2 has been shown to influence mitochondrial function and homeostasis. It has also been involved in regulation of histone deacetylases and thereby in suppression of cell growth and promotion of apoptosis (Liu et al., 2003). SGPP and SGPL1 ensure balanced levels of S1P and other sphingolipid intermediates that may control cell growth and death. The upregulation of SGPL1 results in an accumulation of hexadecenal, which was shown to be cytotoxic (James and Zoeller, 1997).
I have often wondered why folks using CCO or other forms of cannabis therapy still die of cancer. There must be more to it than CCO kills cancer.
- Thread starter
- #906
Over the years of study I’ve come to the idea that it’s really expectation. When all the medical staff are telling you it’s gonna kill you it can be nearly impossible to override that with “The hell it will!” Your body and brain are really one, and the body has a memory of feelings stored that it uses to preset the next anticipated moment with peptides.
It takes a strong will to get beyond what oncology “knows” and step into the seemingly miraculous. When your body has been torn down so much I can see how it could be insurmountable to keep going with the belief everyone tells you is airy-fairy.
So what killed Cajun was a lack of ingrained faith that it would work rather than the fact that maybe it doesn't? You think the blame for Cajun's death falls on some psychological failing on his part?
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- #908
I know it does, uncomfortable as that thought may be, and he admitted it himself in our conversations. He put everyone else's needs and the sense that he owed them something of himself to make up for past behavior he was less than proud of being a part of. He accepted that the black cloud he knew he allowed to follow him was of his own making, and he actually promised me he'd seek some professional guidance.
He never got to taking care of his emotional health.
Cajun had a history he carried like a weight. You can't convince someone you care deeply for to put that weight down if they won't forgive themselves, no matter how much you care. He told me himself that his lack of action would likely kill him in the end. He laughed about it at the time. The closing of his dream Cannabis oncology practice on top of his neglect of his personal protocol made for a perfect storm to help him transition right off the planet.
Right out of our lives. Right out of pain he'd lived with for so many years.
Your thoughts drive your biology. There's really no way past that truth. Cajun was an expert on the ECS, and he understood that better than most of us. He got to say his family goodbyes before he passed. That's something of a solace.
He taught me that we are eternal beings, and reinforced my belief that the stories we tell ourselves are the most important ones when we speak of health maintenance.
- Thread starter
- #909
From "Hemp: A New Crop With New Uses for North America" (Ernest Small and David Marcus)
I believe this is from 2002.
Analysis of commercial Cannabis product potential for NA (in decreasing value)
Seeds
I believe this is from 2002.
Analysis of commercial Cannabis product potential for NA (in decreasing value)
Seeds
- Confectionary, baked goods
- Salad oil
- Body care "cosmetics"
- Animal food (whole seed for birds, press cake for mammalian livestock)
- Gamma-linoleic acid dietary supplements
- Speciality industrial oils
- Plastic-molded products
- Speciality papers
- Construction fiberboard
- Biodegradable landscape matting & plant culture products
- Coarse textiles (carpets, upholstery)
- Fine textiles
- Animal bedding
- Thermal insulation
- Construction (fiberboard, plaster board, etc.)
- Medicinal cannabinoids
- Essential oil (for flavor and perfume)
- Insect repellent
- Alcohol
- Fuel
- Silage
- Thread starter
- #910
Continuing the study of Fundamentals of Cannabis:
From "Hemp: A New Crop With New Uses for North America" (Ernest Small and David Marcus)
Basic Categories Of Cannabis And Their Field Architecture
Cannabis sativa
From "Hemp: A New Crop With New Uses for North America" (Ernest Small and David Marcus)
Basic Categories Of Cannabis And Their Field Architecture
Cannabis sativa
- annual wind-pollinated plant
- normally dioecious
- (of a plant or invertebrate animal) having the male and female reproductive organs in separate individuals.
- and dimorphic
- occurring in or representing two distinct forms
- SHIT! It won't let me edit on this iPad.
- I think when I get so frustrated that it drives me to tears it's time to walk away and dance with abandon.
- Thread starter
- #911
Continuing the study of Fundamentals of Cannabis:
From "Hemp: A New Crop With New Uses for North America" (Ernest Small and David Marcus)
Basic Categories Of Cannabis And Their Field Architecture
Cannabis sativa
Productive benefits of fems:
Hybrid seed is expensive to produce. Really? I can see it's time-consuming, but with a system in place I'd think this cost could be controlled. Cannabis is a seed-making monster, from what I've witnessed.
Staminate plants (males)
Cannabis is a prolific pollinator
A "perigonal bract" (floral bract) subtends each female flower, and grows to envelop the fruit
Trichomes (small, secretory, resin-producing glands) cover the epidermis of most of the plant, from soil level to tip
Root structure:
Stems are
Although stem is often woody, the species is always referred to as herb or forb (a herbaceous flowering plant other than a grass.)
Plants vary enormously in height
Photo from collections of Harvard University.
Cannabis sativa: Morphology
1. Flowering branch of male plant. 2. Flowering branch of female plant. 3. Seedling. 4. Leaflet. 5. Cluster of male flowers. 6. Female flower, enclosed by perigonal bract. 7. Mature fruit, enclosed by perigonal bract. 8. Seed (achene), showing wide face. 9. Seed, showing narrow face. 10. Stalked secretory gland. 11. Top of sessile secretory gland. 12. Long section of cystolith hair (note calcium carbonate concertion at base).
I just couldn't stop with such bad energy. Now I'm feeling better, and I'm satisfied with this part. Enough for tonight. Time for a celebratory buzz before bed. 
From "Hemp: A New Crop With New Uses for North America" (Ernest Small and David Marcus)
Basic Categories Of Cannabis And Their Field Architecture
Cannabis sativa
- annual wind-pollinated plant
- normally dioecious
- (of a plant or invertebrate animal) having the male and female reproductive organs in separate individuals.
- and dimorphic
- occurring in or representing two distinct forms
- sometimes monoecious
- (of a plant or invertebrate animal) having both the male and female reproductive organs in the same individual; hermaphrodite.
- mostly modern European cultivars
- can also result in occasional males and hermaphrodites
Productive benefits of fems:
- -uniformity
- few males to take up space, so you get more grain (bud? He's talking about hemp here, but we now use hemp for medicines, and it's the buds you want for meds.)
Hybrid seed is expensive to produce. Really? I can see it's time-consuming, but with a system in place I'd think this cost could be controlled. Cannabis is a seed-making monster, from what I've witnessed.
Staminate plants (males)
- tend to be 10-15% taller than pistillates (females)
- are usually less robust than females
Cannabis is a prolific pollinator
- you'll need a 5 km isolation distance to assure a pure foundation seed crop
A "perigonal bract" (floral bract) subtends each female flower, and grows to envelop the fruit
- subtends: (of a bract) extend under (a flower) so as to support or enfold it.
Trichomes (small, secretory, resin-producing glands) cover the epidermis of most of the plant, from soil level to tip
- trichomes are most concentrated and contain the most oil in the flower bracts
- it's the essential oil in those glands we want with euphoric cultivars
Root structure:
- laterally-branched taproot
- generally 30-60 cm deep
- can be up to 2.5 m in loose soil
- roots grow very near the surface
- will be more branched in wet soils
- extensive root systems allow hemp to tap into deep supplies of nutrients and water
Stems are
- erect
- furrowed
- usually branched
- woody interior
- may be hollow in the internodes
Although stem is often woody, the species is always referred to as herb or forb (a herbaceous flowering plant other than a grass.)
Plants vary enormously in height
- depending on genetics and environment
- typically 1-5 m (12 m heights have been recorded)
Cannabis sativa: Morphology
1. Flowering branch of male plant. 2. Flowering branch of female plant. 3. Seedling. 4. Leaflet. 5. Cluster of male flowers. 6. Female flower, enclosed by perigonal bract. 7. Mature fruit, enclosed by perigonal bract. 8. Seed (achene), showing wide face. 9. Seed, showing narrow face. 10. Stalked secretory gland. 11. Top of sessile secretory gland. 12. Long section of cystolith hair (note calcium carbonate concertion at base).
I just couldn't stop with such bad energy.
Now I'm feeling better, and I'm satisfied with this part. Enough for tonight. Time for a celebratory buzz before bed. 
Derbybud
Well-Known Member
Another dance is in order.
- Thread starter
- #913
Derbybud
Well-Known Member
Best thing for ya. Have a great evening Sue.
- Thread starter
- #915
- Thread starter
- #916
History Of Cannabis
Note: All five owned slaves to work those crops. Cannabis (hemp) was extremely labor intensive to process.
Among the largest slave-holding states were the ones growing hemp
Pick up here tomorrow.
- At least 8,500 yrs of continuious use by Chinese (around 2737 BC)
- Chinese pharmacopeia not written until 100 yrs BC
- Introduced into Europe and Asia between 1000 and 2000 BCE
- People needed goods and slaves.
- Ships needed sail and ropes to supply both.
- Hemp ropes and sails were superior quality, as was the durable nature of hemp cloth and paper, among other uses.
- S. America in Chile (1545)
- N. America in Port Royal, Acadia (1606)
- Legislated household growing in VA (1619)
Note: All five owned slaves to work those crops. Cannabis (hemp) was extremely labor intensive to process.
- George Washington (for clothing and to repair fishing nets)
- Thomas Jefferson
- James Madison
- Benjamin Franklin
- Henry Clay (Ashland in KY grew hemp as primary crop)
- An aggressive advocate for protections for hemp
Among the largest slave-holding states were the ones growing hemp
- VA and MD prior to US independence
- KY, IL, MO following behind
Pick up here tomorrow.
- Thread starter
- #917
Fear drives this world right now, and the human brain is hard-wired to make decisions from a point of pleasure. The bolding in huge letters is of my own making. When we overlook major parts of the study we do a disservice to the hard-working researchers.
Contrary to what Aurelius Data wants to believe, I don’t read this study to say that THC is what’s doing the ultimate damage, and may be the reason cannabis-using patients survive.
We have so much bad science being bantered about in the pandemic scare it turns my stomach.
COVID-19 Patients Should Avoid THC
Source
COVID-19 Patients Should Avoid THC
Studies Find Potential Harmful Side Effects of Cannabis on Infected Coronavirus Patients
MISSOULA, Mont., March 19, 2020 (GLOBE NEWSWIRE) --
Aurelius Data, the first global patient perception big data company in plant-based medicines, cautions the public against the potential harmful side effects that can come from consuming cannabis products with Tetrahydrocannabinol (THC) if a patient is infected with COVID-19.
“We know that the epidemiology of COVID-19 is similar to the influenza virus and has a similar disease presentation. And we know that in studies1 where THC was administered to mice with influenza, we saw an increase in viral loads and a decrease in the immune system to fight off the virus. It stands to reason that the same would hold true for Coronavirus and THC consumption could diminish the immune system of someone infected with the virus,” said Aurelius Data CEO Julie Armstrong.
More research is required to accurately map the relationship between the immune and endocannabinoid systems, but it's well established that CBD helps to modulate autoimmune and inflammatory responses.
“Although no clinical trials exist showing poorer outcomes in patients infected with COVID-19 who use therapeutic or recreational cannabis, the data from pre-human studies urge caution for these individuals in the face of the current viral epidemic,” notes Barry Mennen, MD, a clinician who utilizes medical cannabis in his primary care practice.
Source
'It’s a good news, bad news story': Cannabis researcher clears the air on COVID-19 and THC
COVID-19 Patients Should Avoid THC” is the headline of a news release published by Aurelius Data last month. It was reported on widely, but when a doctor reached out to express some reservations about the conclusions of that interpretation of the cited studies, we contacted one of the world’s leading researchers of cannabis and the immune system, Norbert Kaminski, to find out more.
Kaminski, the director of the Institute for Integrative Toxicology at Michigan State University, prefaced his interview with The GrowthOp by saying he is not advocating that “people self-medicate with cannabis or cannabinoids” during the pandemic, but he says Aurelius is telling only part of the story.
When it comes to people who have coronavirus, Kaminski says ingesting THC is a double-edged sword.
As a professor in pharmacology and toxicology and a pioneering cannabis researcher, Kaminski has studied the effects of cannabis on the immune system since 1990. His lab at Michigan State was the first in the world to identify and characterize cannabinoid receptors within the immune system.
One of the studies cited in the review paper that informed the press released involved Kaminski and his colleagues experimenting with THC and the H1N1 influenza virus on mice. Two types of mice were used in the study, wild mice and genetically engineered mice without cannabinoid receptors. Both sets of mice were administered THC and the flu virus. Kaminski says the mice without cannabinoid receptors had far worse symptoms.
“They were more gaunt, less mobile, there were significantly greater adverse effects,” Kaminski says. What that study showed was that THC was tempering the immune response. “The genetically engineered mice did not respond to THC and they did not respond to the molecules that are normally produced in the body that work through those receptors and that’s why those animals showed much more severe issues,” Kaminski explains.
“It showed that there’s a balance. If you have a too severe immune response, the tissue damage that occurs can potentially be life-threatening and that’s what’s actually happening in coronavirus infected people, their immune system responds so well that it’s actually causing severe injury to their airways.”
Patients that end up in a severe respiratory symptomatic stage are at the highest risk of permanent lung damage. When coronavirus becomes that advanced, your own immune system becomes a danger as it goes into overdrive to fight off the invading virus. The longer and more aggressive that response, the more likely there will be damage to healthy lung tissue, or even death.
Dr. Randy Cron, a pediatric rheumatologist and professor at the University of Alabama, told the New York Times that once an invading virus is defeated, the immune system is hard-wired to shut off. But in some cases of coronavirus, the immune system keeps fighting, even when the virus is no longer a threat.
“It continues to release cytokines that keep the body on an exhausting full alert,” the article reads. “In their misguided bid to keep the body safe, these cytokines attack multiple organs including the lungs and liver, and may eventually lead to death. In these people, it’s their body’s response, rather than the virus, that ultimately causes harm.”
What Kaminiski’s team demonstrated was that when mice were infected with the H1N1 virus and then treated with THC, the ability to clear the virus was impaired. But — and this is the part that was overlooked by Aurelius Data, he says — the amount of damage that was caused in the lungs by the immune system to clear the pathogen was decreased.
This is the very effect needed to stop the destruction of lung tissue that’s killing COVID-19 patients.
“It’s a good news, bad news story,” Kaminski says. “The good news is that as the immune system gears up and destroys those cells it’s destroying the pathogen. The bad news is that if the response is too severe, the tissue damage that occurs can then compromise the ability of the lungs to do their job, which is primarily gas exchange.”
He also says that it’s important to keep in mind that the studies are on mice, and mice are not human.
Julie Armstrong, the CEO and co-founder of Aurelius Data, says that she has heard the “mouse” criticism since publishing the release, but she stands by it.
“I know you’re not a mouse, but viruses virus regardless of the host,” she says. “They can infect anything. Having the mouse as the host really doesn’t make a difference. It’s a mammal, we’re a mammal. The virus doesn’t care what the host is.”
Armstrong says CBD alone is “probably pretty safe, but we do know that THC is a problem.”
“Unless the symptoms that you’re treating with THC are more harmful than COVID, the suggestion still stands.”
Kaminski says the takeaway is that more clinical trials are needed. We simply do not know enough yet about coronavirus, and we’re still just scratching the surface when it comes to cannabis.
“I wouldn’t recommend anybody who has coronavirus take THC or smoke cannabis,” Kaminski says, before explaining that there is growing interest in treating severe cases of coronavirus with anti-inflammatory medications that could potentially decrease the severity of the immune system’s response.
So what he’s saying is we should use other anti-inflammatory drugs that have dangerous side-effects because we’re misrepresenting what’s going on in the study instead of finding the right doses for THC?
And yet the government is pushing an unproven and dangerous drug because the country is run by a narcissist no one seems capable of controlling.
“It’s that balance between having a strong enough immune response to eliminate the pathogen but not so strong that basically the response ends up killing you because you have massive tissue injury,” he says. “I think there is promise for some of the anti-inflammatory properties of these cannabinoids for therapeutic use
God help us all.
Contrary to what Aurelius Data wants to believe, I don’t read this study to say that THC is what’s doing the ultimate damage, and may be the reason cannabis-using patients survive.
We have so much bad science being bantered about in the pandemic scare it turns my stomach.
COVID-19 Patients Should Avoid THC
Source
COVID-19 Patients Should Avoid THC
Studies Find Potential Harmful Side Effects of Cannabis on Infected Coronavirus Patients
MISSOULA, Mont., March 19, 2020 (GLOBE NEWSWIRE) --
Aurelius Data, the first global patient perception big data company in plant-based medicines, cautions the public against the potential harmful side effects that can come from consuming cannabis products with Tetrahydrocannabinol (THC) if a patient is infected with COVID-19.
“We know that the epidemiology of COVID-19 is similar to the influenza virus and has a similar disease presentation. And we know that in studies1 where THC was administered to mice with influenza, we saw an increase in viral loads and a decrease in the immune system to fight off the virus. It stands to reason that the same would hold true for Coronavirus and THC consumption could diminish the immune system of someone infected with the virus,” said Aurelius Data CEO Julie Armstrong.
More research is required to accurately map the relationship between the immune and endocannabinoid systems, but it's well established that CBD helps to modulate autoimmune and inflammatory responses.
“Although no clinical trials exist showing poorer outcomes in patients infected with COVID-19 who use therapeutic or recreational cannabis, the data from pre-human studies urge caution for these individuals in the face of the current viral epidemic,” notes Barry Mennen, MD, a clinician who utilizes medical cannabis in his primary care practice.
Source
'It’s a good news, bad news story': Cannabis researcher clears the air on COVID-19 and THC
COVID-19 Patients Should Avoid THC” is the headline of a news release published by Aurelius Data last month. It was reported on widely, but when a doctor reached out to express some reservations about the conclusions of that interpretation of the cited studies, we contacted one of the world’s leading researchers of cannabis and the immune system, Norbert Kaminski, to find out more.
Kaminski, the director of the Institute for Integrative Toxicology at Michigan State University, prefaced his interview with The GrowthOp by saying he is not advocating that “people self-medicate with cannabis or cannabinoids” during the pandemic, but he says Aurelius is telling only part of the story.
When it comes to people who have coronavirus, Kaminski says ingesting THC is a double-edged sword.
As a professor in pharmacology and toxicology and a pioneering cannabis researcher, Kaminski has studied the effects of cannabis on the immune system since 1990. His lab at Michigan State was the first in the world to identify and characterize cannabinoid receptors within the immune system.
One of the studies cited in the review paper that informed the press released involved Kaminski and his colleagues experimenting with THC and the H1N1 influenza virus on mice. Two types of mice were used in the study, wild mice and genetically engineered mice without cannabinoid receptors. Both sets of mice were administered THC and the flu virus. Kaminski says the mice without cannabinoid receptors had far worse symptoms.
“They were more gaunt, less mobile, there were significantly greater adverse effects,” Kaminski says. What that study showed was that THC was tempering the immune response. “The genetically engineered mice did not respond to THC and they did not respond to the molecules that are normally produced in the body that work through those receptors and that’s why those animals showed much more severe issues,” Kaminski explains.
“It showed that there’s a balance. If you have a too severe immune response, the tissue damage that occurs can potentially be life-threatening and that’s what’s actually happening in coronavirus infected people, their immune system responds so well that it’s actually causing severe injury to their airways.”
Patients that end up in a severe respiratory symptomatic stage are at the highest risk of permanent lung damage. When coronavirus becomes that advanced, your own immune system becomes a danger as it goes into overdrive to fight off the invading virus. The longer and more aggressive that response, the more likely there will be damage to healthy lung tissue, or even death.
Dr. Randy Cron, a pediatric rheumatologist and professor at the University of Alabama, told the New York Times that once an invading virus is defeated, the immune system is hard-wired to shut off. But in some cases of coronavirus, the immune system keeps fighting, even when the virus is no longer a threat.
“It continues to release cytokines that keep the body on an exhausting full alert,” the article reads. “In their misguided bid to keep the body safe, these cytokines attack multiple organs including the lungs and liver, and may eventually lead to death. In these people, it’s their body’s response, rather than the virus, that ultimately causes harm.”
What Kaminiski’s team demonstrated was that when mice were infected with the H1N1 virus and then treated with THC, the ability to clear the virus was impaired. But — and this is the part that was overlooked by Aurelius Data, he says — the amount of damage that was caused in the lungs by the immune system to clear the pathogen was decreased.
This is the very effect needed to stop the destruction of lung tissue that’s killing COVID-19 patients.
“It’s a good news, bad news story,” Kaminski says. “The good news is that as the immune system gears up and destroys those cells it’s destroying the pathogen. The bad news is that if the response is too severe, the tissue damage that occurs can then compromise the ability of the lungs to do their job, which is primarily gas exchange.”
He also says that it’s important to keep in mind that the studies are on mice, and mice are not human.
Julie Armstrong, the CEO and co-founder of Aurelius Data, says that she has heard the “mouse” criticism since publishing the release, but she stands by it.
“I know you’re not a mouse, but viruses virus regardless of the host,” she says. “They can infect anything. Having the mouse as the host really doesn’t make a difference. It’s a mammal, we’re a mammal. The virus doesn’t care what the host is.”
Armstrong says CBD alone is “probably pretty safe, but we do know that THC is a problem.”
“Unless the symptoms that you’re treating with THC are more harmful than COVID, the suggestion still stands.”
Kaminski says the takeaway is that more clinical trials are needed. We simply do not know enough yet about coronavirus, and we’re still just scratching the surface when it comes to cannabis.
“I wouldn’t recommend anybody who has coronavirus take THC or smoke cannabis,” Kaminski says, before explaining that there is growing interest in treating severe cases of coronavirus with anti-inflammatory medications that could potentially decrease the severity of the immune system’s response.
So what he’s saying is we should use other anti-inflammatory drugs that have dangerous side-effects because we’re misrepresenting what’s going on in the study instead of finding the right doses for THC?
And yet the government is pushing an unproven and dangerous drug because the country is run by a narcissist no one seems capable of controlling.
“It’s that balance between having a strong enough immune response to eliminate the pathogen but not so strong that basically the response ends up killing you because you have massive tissue injury,” he says. “I think there is promise for some of the anti-inflammatory properties of these cannabinoids for therapeutic use
God help us all.
- Thread starter
- #918
I promised Cajun I’d do this one day. Today is step one: annotation.
How Concentrated Cannabis Oil Kills Cancer
CajunCelt said:
“I'm asked this daily, so here goes:
In every cell there is a family of interconvertible sphingolipids
Interconvertible sphingolipids - sphingolipids that can convert from one to the other.
that specifically manage the life and death of that cell. This profile of factors is called the "Sphingolipid Rheostat." If ceramide (a signaling metabolite of sphingosine-1- phosphate) is high, then cell death (apoptosis) is imminent. If ceramide is low, the cell will be strong in its vitality.”
The Sphingolipid Rheostat is the process by which sphingolipids can interchange with one another.
“Very simply, when THC connects to the CB1 or CB2 cannabinoid receptor site on the cancer cell, it causes an increase in ceramide synthesis which drives cell death. A normal healthy cell does not produce ceramide in the presence of THC, thus is not affected by the cannabinoid.”
THC connects with eCBR on cancer cell
”The cancer cell dies, not because of cytotoxic chemicals, but because of a tiny little shift in the mitochondria. Within most cells there is a cell nucleus, numerous mitochondria (hundreds to thousands), and various other organelles in the cytoplasm. The purpose of the mitochondria is to produce energy (ATP) for cell use.
As ceramide starts to accumulate, turning up the Sphingolipid Rheostat, it increases the mitochondrial membrane pore permeability to cytochrome c, a critical protein in energy synthesis. Cytochrome c is pushed out of the mitochondria, killing the source of energy for the cell.”
It’s, not the chemical assault that kills the cell.
“Ceramide also causes genotoxic stress in the cancer cell nucleus generating a protein called p53, whose job it is to disrupt calcium metabolism in the mitochondria. If this weren't enough, ceramide disrupts the cellular lysosome, the cell's digestive system that provides nutrients for all cell functions. Ceramide, and other sphingolipids, actively inhibit pro-survival pathways in the cell leaving no possibility at all of cancer cell survival.9
Ceramide also causes genotoxic stress (genetic stress that is toxic)
Ceramide and other sphingolipids work to inhibit ways the cancer cell uses to stay alive.
“The key to this process is the accumulation of ceramide in the system. This means taking therapeutic amounts of cannabinoid extract, steadily, over a period of time, keeping metabolic pressure on this cancer cell death pathway.”
The key to success is the constant and steady inflow of cannabis extracts (oils)
“How did this pathway come to be? Why is it that the body can take a simple plant enzyme and use it for healing in many different physiological systems? This endocannabinoid system exists in all animal life, just waiting for it's matched exocannabinoid activator.
Why have a programmed cellular self-destruct signaling system across the animal kingdom?
This is interesting. Our own endocannabinoid system covers all cells and nerves; it is the messenger of information flowing between our immune system and the central nervous system (CNS). It is responsible for neuroprotection, and micro- manages the immune system. This is the primary control system that maintains homeostasis; our well being.”
Almost every one of the trillions of cells that make up you responds to the signaling action of cannabinoids.
“Just out of curiosity, how does the work get done at the cellular level, and where does the body make the endocannabinoids? Here we see that endocannabinoids have their origin in nerve cells right at the synapse. When the body is compromised through illness or injury it calls insistently to the endocannabinoid system and directs the immune system to bring healing. If these homeostatic systems are weakened, it should be no surprise that exocannabinoids perform the same function. It helps the body in the most natural way possible.”
Questions:
When compromised the cells signal the ECS for healing to begin
If the homeostatic ECS is deficient we can use exocannabinoids (from outside the body)
“To see how this works we visualize the cannabinoid as a three dimensional molecule, where one part of the molecule is configured to fit the nerve or immune cell receptor site just like a key in a lock. There are at least two types of cannabinoid receptor sites, CB1 (CNS) and CB2 (immune). In general CB1 activates the CNS messaging system, and CB2 activates the immune system, but it's much more complex than this.
Both THC and anandamide activate both receptor sites. Other cannabinoids activate one or the other receptor sites. Among the strains of Cannabis, C. sativa tends toward the CB1 receptor, and C. indica tends toward CB2. So sativa is more neuroactive, and indica is more immunoactive. Another factor here is that sativa is dominated by THC cannabinoids, and indica is predominately CBD (cannabidiol).”
How does this work?
There are two identified endocannabinoid receptors identified
For most part
Current knowledge is that the receptors are not limited to these domains and can turn up where needed.
Cannabis chemovars (strains)
Note: It’s much more complex than this. It’s the terpenes making those differences in signaling, IMHO.
“It is known that THC and CBD are biomimetic to anandamide, that is, the body can use both interchangeably. Thus, when stress, injury, or illness demand more from endogenous anandamide than can be produced by the body, its mimetic endocannabinoids are activated. If the stress is transitory, then the treatment can be transitory. If the demand is sustained, such as in cancer, then treatment needs to provide sustained pressure of the modulating agent on the homeostatic systems.”
THC and anandamide are essentially interchangeable from a cellular signaling perspective
“Typically CBD gravitates to the densely packed CB2 receptors in the spleen, home to the body's immune system. From there, immune cells seek out and destroy cancer cells. Interestingly, it has been shown that THC and CBD cannabinoids have the ability to kill cancer cells directly without going through immune intermediaries. THC and CBD hijack the lipoxygenase pathway to directly inhibit tumor growth. As a side note, it has been discovered that CBD inhibits anandamide reuptake. Here we see that cannabidiol helps the body preserve its own natural endocannabinoid by inhibiting the enzyme that breaks down anandamide.”
Typically CBD activates CB2
Both THC and CBD kill cancer cells without the immune response
CBD also inhibits anandamide reuptake
LThis post touches lightly on a few essential concepts. Mostly I would like to leave you with an appreciation that nature has designed the perfect medicine that fits exactly with our own immune system of receptors and signaling metabolites to provide rapid and complete immune response for systemic integrity and metabolic homeostasis.l
What Cajun wants you to take away is that cannabis is Nature’s wonderful response to your body’s need for signals that
How Concentrated Cannabis Oil Kills Cancer
CajunCelt said:
“I'm asked this daily, so here goes:
In every cell there is a family of interconvertible sphingolipids
Interconvertible sphingolipids - sphingolipids that can convert from one to the other.
that specifically manage the life and death of that cell. This profile of factors is called the "Sphingolipid Rheostat." If ceramide (a signaling metabolite of sphingosine-1- phosphate) is high, then cell death (apoptosis) is imminent. If ceramide is low, the cell will be strong in its vitality.”
The Sphingolipid Rheostat is the process by which sphingolipids can interchange with one another.
- All cells are programmed for death.
- Sphingosine -1- phosphate has a metabolite (ceramide) that acts as a signal for cell death.
- Cell death in this suicidal manner is referred to as apoptosis.
- If ceramide production is high, cell death is imminent.
- If ceramide production is low, the cell is strong and vital.
“Very simply, when THC connects to the CB1 or CB2 cannabinoid receptor site on the cancer cell, it causes an increase in ceramide synthesis which drives cell death. A normal healthy cell does not produce ceramide in the presence of THC, thus is not affected by the cannabinoid.”
THC connects with eCBR on cancer cell
- Ceramide is created, leading to cell death
- Normal, healthy cells don’t produce ceramide when signalled by an eCBR ligand (THC has no terminal effects on healthy cells).
”The cancer cell dies, not because of cytotoxic chemicals, but because of a tiny little shift in the mitochondria. Within most cells there is a cell nucleus, numerous mitochondria (hundreds to thousands), and various other organelles in the cytoplasm. The purpose of the mitochondria is to produce energy (ATP) for cell use.
As ceramide starts to accumulate, turning up the Sphingolipid Rheostat, it increases the mitochondrial membrane pore permeability to cytochrome c, a critical protein in energy synthesis. Cytochrome c is pushed out of the mitochondria, killing the source of energy for the cell.”
It’s, not the chemical assault that kills the cell.
- There’s a tiny shift in the mitochondria.
- Most cells have a nucleus with hundreds to thousands of mitochondria and other organelles in the cytoplasm.
- The purpose of the mitochondria is to produce ATP, which cells use for energy.
- Ceramide begins to accumulate.
- The Sphingolipid Rheostat turns up.
- Mitochondrial membrane permeability to cytochrome C increases.
- Cytochrome C is a critical protein to the synthesizing of energy.
- It’s pushed from the mitochondria.
- As a result, the cell’s energy source is disrupted and the cell dies.
“Ceramide also causes genotoxic stress in the cancer cell nucleus generating a protein called p53, whose job it is to disrupt calcium metabolism in the mitochondria. If this weren't enough, ceramide disrupts the cellular lysosome, the cell's digestive system that provides nutrients for all cell functions. Ceramide, and other sphingolipids, actively inhibit pro-survival pathways in the cell leaving no possibility at all of cancer cell survival.9
Ceramide also causes genotoxic stress (genetic stress that is toxic)
- It generates creation of p53
- Its job is to disrupt calcium metabolism in mitochondria.
- Ceramide also disrupts cellular lysosome.
- Lysosome is the cell’s digestive system.
- Provides nutrients for all cell functions.
Ceramide and other sphingolipids work to inhibit ways the cancer cell uses to stay alive.
- leaving no possible way for the cancer cell to survive.
“The key to this process is the accumulation of ceramide in the system. This means taking therapeutic amounts of cannabinoid extract, steadily, over a period of time, keeping metabolic pressure on this cancer cell death pathway.”
The key to success is the constant and steady inflow of cannabis extracts (oils)
- keeps constant pressure on the pathway to this cancer cell’s death
“How did this pathway come to be? Why is it that the body can take a simple plant enzyme and use it for healing in many different physiological systems? This endocannabinoid system exists in all animal life, just waiting for it's matched exocannabinoid activator.
Why have a programmed cellular self-destruct signaling system across the animal kingdom?
- a system that accepts exogenous signaling molecules nonetheless
This is interesting. Our own endocannabinoid system covers all cells and nerves; it is the messenger of information flowing between our immune system and the central nervous system (CNS). It is responsible for neuroprotection, and micro- manages the immune system. This is the primary control system that maintains homeostasis; our well being.”
Almost every one of the trillions of cells that make up you responds to the signaling action of cannabinoids.
- the system exists to balance the CND with the immune system
- responsible for
- neuroprotection
- micro-management of immune response
- homeostasis (well-being)
“Just out of curiosity, how does the work get done at the cellular level, and where does the body make the endocannabinoids? Here we see that endocannabinoids have their origin in nerve cells right at the synapse. When the body is compromised through illness or injury it calls insistently to the endocannabinoid system and directs the immune system to bring healing. If these homeostatic systems are weakened, it should be no surprise that exocannabinoids perform the same function. It helps the body in the most natural way possible.”
Questions:
- What’s happening at the cellular level?
- Where do cannabinoids actually come from?
- they originate right at the synapse of the nerve cell
- the point where electrical impulse jumps from one neuron to another
- they originate right at the synapse of the nerve cell
When compromised the cells signal the ECS for healing to begin
- during injury or illness
- calling in the immune system to get busy
If the homeostatic ECS is deficient we can use exocannabinoids (from outside the body)
- exocannabinoids support healing in a natural way
“To see how this works we visualize the cannabinoid as a three dimensional molecule, where one part of the molecule is configured to fit the nerve or immune cell receptor site just like a key in a lock. There are at least two types of cannabinoid receptor sites, CB1 (CNS) and CB2 (immune). In general CB1 activates the CNS messaging system, and CB2 activates the immune system, but it's much more complex than this.
Both THC and anandamide activate both receptor sites. Other cannabinoids activate one or the other receptor sites. Among the strains of Cannabis, C. sativa tends toward the CB1 receptor, and C. indica tends toward CB2. So sativa is more neuroactive, and indica is more immunoactive. Another factor here is that sativa is dominated by THC cannabinoids, and indica is predominately CBD (cannabidiol).”
How does this work?
- visualize cannabinoids in 3 dimensions
- one part has attachment for cannabinoid receptors
- attachment is configured to activate a particular receptor
- on either nerve or immune cells
- it’s more of a bump than a lock in place with exocannabinoids
- other molecules are now identified as also activating eCBRs
There are two identified endocannabinoid receptors identified
- CB1 (CNS)
- CB2 (immune)
For most part
- CB1 is active in CNS
- CB2 signals change in immune cells
Current knowledge is that the receptors are not limited to these domains and can turn up where needed.
- Both THC and anandamide activate both known eCBRs
- other cannabinoids are also activators of eCBRs
Cannabis chemovars (strains)
- sativas most active with eCB1
- more neuroactive
- tend to be higher in THC This isn’t true, to my understanding. Indicas have typically been higher in THC.
- indicas appear to activate mostly eCB2
- more immunoactive
- tend to have more CBD A changing reality.
Note: It’s much more complex than this. It’s the terpenes making those differences in signaling, IMHO.
- Indicas tend to have more b-caryophyllene, which activates CB2.
- It’s b-caryophyllene, not CBD that was making the difference when Cajun wrote this.
“It is known that THC and CBD are biomimetic to anandamide, that is, the body can use both interchangeably. Thus, when stress, injury, or illness demand more from endogenous anandamide than can be produced by the body, its mimetic endocannabinoids are activated. If the stress is transitory, then the treatment can be transitory. If the demand is sustained, such as in cancer, then treatment needs to provide sustained pressure of the modulating agent on the homeostatic systems.”
THC and anandamide are essentially interchangeable from a cellular signaling perspective
- the body gets stressed, injured, ill
- calls for anandamide go out
- stress levels determine response timelines
- transitory stress = transitory response
- chronic stress (i.e. cancer) = sustained pressure (continual response of the ECS) from cannabinoids
“Typically CBD gravitates to the densely packed CB2 receptors in the spleen, home to the body's immune system. From there, immune cells seek out and destroy cancer cells. Interestingly, it has been shown that THC and CBD cannabinoids have the ability to kill cancer cells directly without going through immune intermediaries. THC and CBD hijack the lipoxygenase pathway to directly inhibit tumor growth. As a side note, it has been discovered that CBD inhibits anandamide reuptake. Here we see that cannabidiol helps the body preserve its own natural endocannabinoid by inhibiting the enzyme that breaks down anandamide.”
Typically CBD activates CB2
- gravitates to spleen
- home of body’s immune system
- densely packed with eCB2
- immune cells radiate out through body from spleen
Both THC and CBD kill cancer cells without the immune response
- they both hijack the lipoxygenase pathway
- the pathway that inhibits tumor growth
CBD also inhibits anandamide reuptake
- helps the body preserve anandamide by interfering with the enzyme that degrades anandamide
- Cannabinoids are created by taking lipids from the cell membrane and having enzymes configure them and other components into cannabinoids.
- The cannabinoid swims backward in the stream (made of oil when everything swimming around them going in the other direction is water-based) and hits the receptor with its signal.
- At the end of the signaling process cannabinoids are eliminated by disassembly, and critical parts are absorbed back into the cell membrane for future use.
LThis post touches lightly on a few essential concepts. Mostly I would like to leave you with an appreciation that nature has designed the perfect medicine that fits exactly with our own immune system of receptors and signaling metabolites to provide rapid and complete immune response for systemic integrity and metabolic homeostasis.l
What Cajun wants you to take away is that cannabis is Nature’s wonderful response to your body’s need for signals that
- mirror your body’s own signaling molecules
- provide rapid, complete immune response
- support cellular homeostasis
- Thread starter
- #919
A little formatting of the original post, to make it easier to digest.
How Concentrated Cannabis Oil Kills Cancer
CajunCelt said:
“I'm asked this daily, so here goes:
In every cell there is a family of interconvertible sphingolipids that specifically manage the life and death of that cell. This profile of factors is called the "Sphingolipid Rheostat." If ceramide (a signaling metabolite of sphingosine-1- phosphate) is high, then cell death (apoptosis) is imminent. If ceramide is low, the cell will be strong in its vitality.
Very simply, when THC connects to the CB1 or CB2 cannabinoid receptor site on the cancer cell, it causes an increase in ceramide synthesis which drives cell death. A normal healthy cell does not produce ceramide in the presence of THC, thus is not affected by the cannabinoid.
The cancer cell dies, not because of cytotoxic chemicals, but because of a tiny little shift in the mitochondria. Within most cells there is a cell nucleus, numerous mitochondria (hundreds to thousands), and various other organelles in the cytoplasm.
The purpose of the mitochondria is to produce energy (ATP) for cell use. As ceramide starts to accumulate, turning up the Sphingolipid Rheostat, it increases the mitochondrial membrane pore permeability to cytochrome c, a critical protein in energy synthesis. Cytochrome c is pushed out of the mitochondria, killing the source of energy for the cell.
Ceramide also causes genotoxic stress in the cancer cell nucleus generating a protein called p53, whose job it is to disrupt calcium metabolism in the mitochondria.
If this weren't enough, ceramide disrupts the cellular lysosome, the cell's digestive system that provides nutrients for all cell functions. Ceramide, and other sphingolipids, actively inhibit pro-survival pathways in the cell leaving no possibility at all of cancer cell survival.
The key to this process is the accumulation of ceramide in the system. This means taking therapeutic amounts of cannabinoid extract, steadily, over a period of time, keeping metabolic pressure on this cancer cell death pathway.
How did this pathway come to be? Why is it that the body can take a simple plant enzyme and use it for healing in many different physiological systems? This endocannabinoid system exists in all animal life, just waiting for it's matched exocannabinoid activator.
This is interesting. Our own endocannabinoid system covers all cells and nerves; it is the messenger of information flowing between our immune system and the central nervous system (CNS). It is responsible for neuroprotection, and micro- manages the immune system. This is the primary control system that maintains homeostasis; our well being.
Just out of curiosity, how does the work get done at the cellular level, and where does the body make the endocannabinoids? Here we see that endocannabinoids have their origin in nerve cells right at the synapse. When the body is compromised through illness or injury it calls insistently to the endocannabinoid system and directs the immune system to bring healing. If these homeostatic systems are weakened, it should be no surprise that exocannabinoids perform the same function. It helps the body in the most natural way possible.
To see how this works we visualize the cannabinoid as a three dimensional molecule, where one part of the molecule is configured to fit the nerve or immune cell receptor site just like a key in a lock. There are at least two types of cannabinoid receptor sites, CB1 (CNS) and CB2 (immune). In general CB1 activates the CNS messaging system, and CB2 activates the immune system, but it's much more complex than this.
Both THC and anandamide activate both receptor sites. Other cannabinoids activate one or the other receptor sites. Among the strains of Cannabis, C. sativa tends toward the CB1 receptor, and C. indica tends toward CB2. So sativa is more neuroactive, and indica is more immunoactive. Another factor here is that sativa is dominated by THC cannabinoids, and indica is predominately CBD (cannabidiol).
It is known that THC and CBD are biomimetic to anandamide, that is, the body can use both interchangeably. Thus, when stress, injury, or illness demand more from endogenous anandamide than can be produced by the body, its mimetic endocannabinoids are activated. If the stress is transitory, then the treatment can be transitory. If the demand is sustained, such as in cancer, then treatment needs to provide sustained pressure of the modulating agent on the homeostatic systems.
Typically CBD gravitates to the densely packed CB2 receptors in the spleen, home to the body's immune system. From there, immune cells seek out and destroy cancer cells.
Interestingly, it has been shown that THC and CBD cannabinoids have the ability to kill cancer cells directly without going through immune intermediaries. THC and CBD hijack the lipoxygenase pathway to directly inhibit tumor growth. As a side note, it has been discovered that CBD inhibits anandamide reuptake. Here we see that cannabidiol helps the body preserve its own natural endocannabinoid by inhibiting the enzyme that breaks down anandamide.
This post touches lightly on a few essential concepts. Mostly I would like to leave you with an appreciation that nature has designed the perfect medicine that fits exactly with our own immune system of receptors and signaling metabolites to provide rapid and complete immune response for systemic integrity and metabolic homeostasis.”
How Concentrated Cannabis Oil Kills Cancer
CajunCelt said:
“I'm asked this daily, so here goes:
In every cell there is a family of interconvertible sphingolipids that specifically manage the life and death of that cell. This profile of factors is called the "Sphingolipid Rheostat." If ceramide (a signaling metabolite of sphingosine-1- phosphate) is high, then cell death (apoptosis) is imminent. If ceramide is low, the cell will be strong in its vitality.
Very simply, when THC connects to the CB1 or CB2 cannabinoid receptor site on the cancer cell, it causes an increase in ceramide synthesis which drives cell death. A normal healthy cell does not produce ceramide in the presence of THC, thus is not affected by the cannabinoid.
The cancer cell dies, not because of cytotoxic chemicals, but because of a tiny little shift in the mitochondria. Within most cells there is a cell nucleus, numerous mitochondria (hundreds to thousands), and various other organelles in the cytoplasm.
The purpose of the mitochondria is to produce energy (ATP) for cell use. As ceramide starts to accumulate, turning up the Sphingolipid Rheostat, it increases the mitochondrial membrane pore permeability to cytochrome c, a critical protein in energy synthesis. Cytochrome c is pushed out of the mitochondria, killing the source of energy for the cell.
Ceramide also causes genotoxic stress in the cancer cell nucleus generating a protein called p53, whose job it is to disrupt calcium metabolism in the mitochondria.
If this weren't enough, ceramide disrupts the cellular lysosome, the cell's digestive system that provides nutrients for all cell functions. Ceramide, and other sphingolipids, actively inhibit pro-survival pathways in the cell leaving no possibility at all of cancer cell survival.
The key to this process is the accumulation of ceramide in the system. This means taking therapeutic amounts of cannabinoid extract, steadily, over a period of time, keeping metabolic pressure on this cancer cell death pathway.
How did this pathway come to be? Why is it that the body can take a simple plant enzyme and use it for healing in many different physiological systems? This endocannabinoid system exists in all animal life, just waiting for it's matched exocannabinoid activator.
This is interesting. Our own endocannabinoid system covers all cells and nerves; it is the messenger of information flowing between our immune system and the central nervous system (CNS). It is responsible for neuroprotection, and micro- manages the immune system. This is the primary control system that maintains homeostasis; our well being.
Just out of curiosity, how does the work get done at the cellular level, and where does the body make the endocannabinoids? Here we see that endocannabinoids have their origin in nerve cells right at the synapse. When the body is compromised through illness or injury it calls insistently to the endocannabinoid system and directs the immune system to bring healing. If these homeostatic systems are weakened, it should be no surprise that exocannabinoids perform the same function. It helps the body in the most natural way possible.
To see how this works we visualize the cannabinoid as a three dimensional molecule, where one part of the molecule is configured to fit the nerve or immune cell receptor site just like a key in a lock. There are at least two types of cannabinoid receptor sites, CB1 (CNS) and CB2 (immune). In general CB1 activates the CNS messaging system, and CB2 activates the immune system, but it's much more complex than this.
Both THC and anandamide activate both receptor sites. Other cannabinoids activate one or the other receptor sites. Among the strains of Cannabis, C. sativa tends toward the CB1 receptor, and C. indica tends toward CB2. So sativa is more neuroactive, and indica is more immunoactive. Another factor here is that sativa is dominated by THC cannabinoids, and indica is predominately CBD (cannabidiol).
It is known that THC and CBD are biomimetic to anandamide, that is, the body can use both interchangeably. Thus, when stress, injury, or illness demand more from endogenous anandamide than can be produced by the body, its mimetic endocannabinoids are activated. If the stress is transitory, then the treatment can be transitory. If the demand is sustained, such as in cancer, then treatment needs to provide sustained pressure of the modulating agent on the homeostatic systems.
Typically CBD gravitates to the densely packed CB2 receptors in the spleen, home to the body's immune system. From there, immune cells seek out and destroy cancer cells.
Interestingly, it has been shown that THC and CBD cannabinoids have the ability to kill cancer cells directly without going through immune intermediaries. THC and CBD hijack the lipoxygenase pathway to directly inhibit tumor growth. As a side note, it has been discovered that CBD inhibits anandamide reuptake. Here we see that cannabidiol helps the body preserve its own natural endocannabinoid by inhibiting the enzyme that breaks down anandamide.
This post touches lightly on a few essential concepts. Mostly I would like to leave you with an appreciation that nature has designed the perfect medicine that fits exactly with our own immune system of receptors and signaling metabolites to provide rapid and complete immune response for systemic integrity and metabolic homeostasis.”
- Thread starter
- #920
History of Cannabis with Dr. Bearman - Green Flower Media course, Fundamentals of Cannabis
Shared that his father was a freshman at U of Minnesota School of Pharmacy in 1928 he had to prepare a tincture of cannabis
- had to be careful because alcohol was illegal at the time
- two years later Aslinger started his organization, in direct conflict of previous statements about cannabis being safe for society
- one year after that they passed the legislation to make cannabis illegal
-physicians at the time were writing millions of prescriptions for preparations containing cannabis
1927 edition of Remington's Textbook of Pharmacy
- pgs 999-1000 gives instructions on making tincture of cannabis
- useful as analgesic and tranquilizer
-most common use for current recommendations are chronic pain and anxiety
Used as medicine for thousands of years
- cannabis one of the earliest cultivated plants (10,000 - 12,000 yrs ago)
- Chinese claim first pharmacopeia written in 2737 BC (oral)
- oldest known hard copy in 100 AD -100 BC and contained cannabis
- by Shen Nung, 2nd Emperor and God of Agriculture and Pharmacy
- tested different herbs and wrote of them in the pharmacopoeia
Ancients used cannabis for many things we use it for today
- the ECS hasn't changed, and the plant constituents haven't changed, so of course the meds still work the same way
- used as analgesic, childbirth anesthetic, treating migraines, indigestion, insomnia
Ayurvedic medicine has oldest pharmacopeia
- first use was probably tea w/dairy product to carry cannabinoids (fat soluable)
- tea was made from leaves, roots, buds
- oldest hard copy of Ayurvedic pharmacopeia is 1100-1700 BCE
During Dark Ages you could be burned at the stake as a witch for using herbs as medicine (Faith should heal you)
- this killed off a lot of midwives (the idea of original sin fueled this mania)
The 19th century
- French (Napoleon) invasion of Egypt introduced cannabis into France
- both rec and medicinal use
- in 19th century the largest volume of medical info on cannabis was in French
- 1939: Dr. O'Shaughnessy traipsed across India with the telegraph installation
- he did animal and human trials
1850-1942 cannabis was listed in the USP
1890s Sr. Joshua Reynolds, personal physician to Q. Victoria, prescribed cannabis for her menstrual cramps
- wrote in The Lancet of the positive responses
1892 Sr. William Osler (one of founders of John Hopskins and founder of modern medicine)
- in first textbook of internal medicine: cannabis was best treatment for migraine
Most drug companies at the time produced patented cannabis medicines until 1942
- often tinctures
- cannabis was third-most prescribed medicine at this time (alcohol and opium beat it out) over 3,000,000 a year
- replaced by aspirin
Why replace it with aspirin?
- cannabis fat-soluable, couldn't be used in a syringe
The year after cannabis was removed from the USP Dr. Fish nine also said that cannabis was best treatment for migraine
- It's notable to me that from then on he vilified the plant and kept research from occurring. One wonders how much investment he had in pharmaceuticals.
- Dr. Russo tried to get funding for study of migraine treatment with cannabis and has been stonewalled 4 times in a row by the US govt.
- They're only interested in proving negative effects.
In 1920s three different canna cigarettes were marketed (cannabis is both an anti-inflammatory and bronchodilator, like Advair))
- Cannadonna (Australia)
- Cigares De Joy (France)
- Grimault (India/US)
From popular to pariah (progressives took over)
1897 aspirin
1902 Collier's article
1909 Sikhs vilified by SF chronicle
1910 Flexner Report (damaged holistic medicine for decades)
1910 Mexican Revolution (when white Americans went crazy)
1900-30 Cult of Modernism
1914 Harrison Narcotic Tax Act
1916 Schlichten Decorticator
1930 Aslinger manned head of BNDD
1930s Propagandized the word "marijuana"
1935 Did Lamont DuPont lobby Oliphant?
Plant-based medicines can't be standardized, cannabis probably less so than many others, with its rich entourage.
- plants are complicated arrangements of multiple molecules
- coffee has 880 molecules, cannabis 512, tomatoes 380
Our country has wasted trillions of dollars and destroyed countless lives here and abroad because Henry Aslinger and Henry Randolph Hearst waged a racist war against Mexicans and blacks.
- Aslinger created a problem where none existed and kept the fight funded all along.
The Marijuana Tax act may have been propagated by the petrochemical industry.
- the concern was competition from hemp for synthetic fabrics in the pipeline
- Ford was developing a Model T to run on ethanol
- the tax act demonized cannabis
Hearst was concerned about hemp's impact on his paper and pulp investments
- he funded the yellow journalism that went on for decades
Dr. William Woodward (Chief Legal officer of the AMA in early 30s)
- lobbied for relief of the act
- couldn't find any evidence anywhere to back up Anslinger's outlandish claims
- pleaded the case for medical value
- they told him to go home
In 1938 Popular Mechanics wrote "Hemp: The Billion-Dollar Crop."
- also that year Food, Cosmetic and Drug Act grandfathered in cannabis
- this act was what gave fed govt authority to approve safety of all foods and drugs
1941 cannabis was thrown out of the USP
- treated like a new drug ever since
In 1940s there were still cannabis champions in authority
In 1947 modern medicine began to take hold
- 1949 Ramsey and Davis began to look at THC for treating epilepsy (great success)
- wrote article in 1949 suggesting more research be done
- 65+ years later, here we are.
1954 "The Marijuana Bugaboo Revisited" by Col. Phased in Military Medicine
1957 last legal hemp harvested
1964 Mechoulam characterized structure of THC
1968 Dr. Melanie Dreher studied mothers in Jamaica
- determined cannabis in pregnancy to be beneficial to unborn child's later development
- did better in school
- reached developmental landmarks earlier than children who's mothers didn't partake
1970 Controlled Substances Act passed (Thank you Nixon)
- one year after Supreme Court ruled the Marijuana Tax Act unconstitutional
- we had one free year 1969-1970
- cannabis in Schedule One, (Marinol is listed today in Schedule Three)
- act required a study, the study said legalize, Nixon started the War On Drugs and threw cannabis to the top of the list
1972 Nixon Marijuana Commisdion
1974 Robert Randall became the first Federal medical cannabis patient
- he is considered the beginning of the modern movement to legalize cannabis
- 15 individuals were the participants
- 1978 start of IND Program
1985 Marinol approved (synthetic THC)
- has one cannabinoid
- cannabis has over 66 cannabinoids (about 512 constituents in cannabis)
1988 DEA Chief ALJ recommends rescheduling cannabis
- found cannabis to be one of the most therapeutic agents available to man
- recommended reducing to Schedule II
- recommendation denied by DEA Director John Law
1996 Prop 215 passes in California
- physican could recommend cannabis
Arizona initiative blocked by uncooperative state legislature
1997 House of Lords Science and Technology Committee Report
- report on potential for cannabis as medicine
- report was through review of the medicinal use over ages
- paved the way for GW Pharma and Sativex
1999 GW Pharma studies commence
- studying tinctures
- for relief of muscle spasms, neurological pain of MS
1999 Entourage effect postulated by Mechoulam
- the interplay of constituents
- the sum is greater than the individual parts
1999 IOM Report Marijuana and Medicine assessing the science base
At 21:48 there's a list of books.
- Drugs Are Not The Devil's Tools, Dr. Bearman: (has a website)
- Yields And Dosages, Chris Conrad
- Pot Book, Julie Holland, MD
- Cannabinomic, Christopher Fichtner, MD
- American Herbal Pharmacopeia - Cannabis Inflorescence Revised 2014
- HerbalGram Number 97, April 2013
Shared that his father was a freshman at U of Minnesota School of Pharmacy in 1928 he had to prepare a tincture of cannabis
- had to be careful because alcohol was illegal at the time
- two years later Aslinger started his organization, in direct conflict of previous statements about cannabis being safe for society
- one year after that they passed the legislation to make cannabis illegal
-physicians at the time were writing millions of prescriptions for preparations containing cannabis
1927 edition of Remington's Textbook of Pharmacy
- pgs 999-1000 gives instructions on making tincture of cannabis
- useful as analgesic and tranquilizer
-most common use for current recommendations are chronic pain and anxiety
Used as medicine for thousands of years
- cannabis one of the earliest cultivated plants (10,000 - 12,000 yrs ago)
- Chinese claim first pharmacopeia written in 2737 BC (oral)
- oldest known hard copy in 100 AD -100 BC and contained cannabis
- by Shen Nung, 2nd Emperor and God of Agriculture and Pharmacy
- tested different herbs and wrote of them in the pharmacopoeia
Ancients used cannabis for many things we use it for today
- the ECS hasn't changed, and the plant constituents haven't changed, so of course the meds still work the same way
- used as analgesic, childbirth anesthetic, treating migraines, indigestion, insomnia
Ayurvedic medicine has oldest pharmacopeia
- first use was probably tea w/dairy product to carry cannabinoids (fat soluable)
- tea was made from leaves, roots, buds
- oldest hard copy of Ayurvedic pharmacopeia is 1100-1700 BCE
During Dark Ages you could be burned at the stake as a witch for using herbs as medicine (Faith should heal you)
- this killed off a lot of midwives (the idea of original sin fueled this mania)
The 19th century
- French (Napoleon) invasion of Egypt introduced cannabis into France
- both rec and medicinal use
- in 19th century the largest volume of medical info on cannabis was in French
- 1939: Dr. O'Shaughnessy traipsed across India with the telegraph installation
- he did animal and human trials
1850-1942 cannabis was listed in the USP
1890s Sr. Joshua Reynolds, personal physician to Q. Victoria, prescribed cannabis for her menstrual cramps
- wrote in The Lancet of the positive responses
1892 Sr. William Osler (one of founders of John Hopskins and founder of modern medicine)
- in first textbook of internal medicine: cannabis was best treatment for migraine
Most drug companies at the time produced patented cannabis medicines until 1942
- often tinctures
- cannabis was third-most prescribed medicine at this time (alcohol and opium beat it out) over 3,000,000 a year
- replaced by aspirin
Why replace it with aspirin?
- cannabis fat-soluable, couldn't be used in a syringe
The year after cannabis was removed from the USP Dr. Fish nine also said that cannabis was best treatment for migraine
- It's notable to me that from then on he vilified the plant and kept research from occurring. One wonders how much investment he had in pharmaceuticals.
- Dr. Russo tried to get funding for study of migraine treatment with cannabis and has been stonewalled 4 times in a row by the US govt.
- They're only interested in proving negative effects.
In 1920s three different canna cigarettes were marketed (cannabis is both an anti-inflammatory and bronchodilator, like Advair))
- Cannadonna (Australia)
- Cigares De Joy (France)
- Grimault (India/US)
From popular to pariah (progressives took over)
1897 aspirin
1902 Collier's article
1909 Sikhs vilified by SF chronicle
1910 Flexner Report (damaged holistic medicine for decades)
1910 Mexican Revolution (when white Americans went crazy)
1900-30 Cult of Modernism
1914 Harrison Narcotic Tax Act
1916 Schlichten Decorticator
1930 Aslinger manned head of BNDD
1930s Propagandized the word "marijuana"
1935 Did Lamont DuPont lobby Oliphant?
Plant-based medicines can't be standardized, cannabis probably less so than many others, with its rich entourage.
- plants are complicated arrangements of multiple molecules
- coffee has 880 molecules, cannabis 512, tomatoes 380
Our country has wasted trillions of dollars and destroyed countless lives here and abroad because Henry Aslinger and Henry Randolph Hearst waged a racist war against Mexicans and blacks.
- Aslinger created a problem where none existed and kept the fight funded all along.
The Marijuana Tax act may have been propagated by the petrochemical industry.
- the concern was competition from hemp for synthetic fabrics in the pipeline
- Ford was developing a Model T to run on ethanol
- the tax act demonized cannabis
Hearst was concerned about hemp's impact on his paper and pulp investments
- he funded the yellow journalism that went on for decades
Dr. William Woodward (Chief Legal officer of the AMA in early 30s)
- lobbied for relief of the act
- couldn't find any evidence anywhere to back up Anslinger's outlandish claims
- pleaded the case for medical value
- they told him to go home
In 1938 Popular Mechanics wrote "Hemp: The Billion-Dollar Crop."
- also that year Food, Cosmetic and Drug Act grandfathered in cannabis
- this act was what gave fed govt authority to approve safety of all foods and drugs
1941 cannabis was thrown out of the USP
- treated like a new drug ever since
In 1940s there were still cannabis champions in authority
In 1947 modern medicine began to take hold
- 1949 Ramsey and Davis began to look at THC for treating epilepsy (great success)
- wrote article in 1949 suggesting more research be done
- 65+ years later, here we are.
1954 "The Marijuana Bugaboo Revisited" by Col. Phased in Military Medicine
1957 last legal hemp harvested
1964 Mechoulam characterized structure of THC
1968 Dr. Melanie Dreher studied mothers in Jamaica
- determined cannabis in pregnancy to be beneficial to unborn child's later development
- did better in school
- reached developmental landmarks earlier than children who's mothers didn't partake
1970 Controlled Substances Act passed (Thank you Nixon)
- one year after Supreme Court ruled the Marijuana Tax Act unconstitutional
- we had one free year 1969-1970
- cannabis in Schedule One, (Marinol is listed today in Schedule Three)
- act required a study, the study said legalize, Nixon started the War On Drugs and threw cannabis to the top of the list
1972 Nixon Marijuana Commisdion
1974 Robert Randall became the first Federal medical cannabis patient
- he is considered the beginning of the modern movement to legalize cannabis
- 15 individuals were the participants
- 1978 start of IND Program
1985 Marinol approved (synthetic THC)
- has one cannabinoid
- cannabis has over 66 cannabinoids (about 512 constituents in cannabis)
1988 DEA Chief ALJ recommends rescheduling cannabis
- found cannabis to be one of the most therapeutic agents available to man
- recommended reducing to Schedule II
- recommendation denied by DEA Director John Law
1996 Prop 215 passes in California
- physican could recommend cannabis
Arizona initiative blocked by uncooperative state legislature
1997 House of Lords Science and Technology Committee Report
- report on potential for cannabis as medicine
- report was through review of the medicinal use over ages
- paved the way for GW Pharma and Sativex
1999 GW Pharma studies commence
- studying tinctures
- for relief of muscle spasms, neurological pain of MS
1999 Entourage effect postulated by Mechoulam
- the interplay of constituents
- the sum is greater than the individual parts
1999 IOM Report Marijuana and Medicine assessing the science base
At 21:48 there's a list of books.
- Drugs Are Not The Devil's Tools, Dr. Bearman: (has a website)
- Yields And Dosages, Chris Conrad
- Pot Book, Julie Holland, MD
- Cannabinomic, Christopher Fichtner, MD
- American Herbal Pharmacopeia - Cannabis Inflorescence Revised 2014
- HerbalGram Number 97, April 2013