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RECENT interesting findings

Pate worked for me for 2 decades we ran several grow outs in my greenhouse he designed that tried to prove that UVB improved Cannabis in any way. We could not, We used 3 different clones one CBD and two drug varieties we had 4 examples of each each of the 3 clones they were set up so the first set of three were 1 meter from the UVB lights, the next set was 3 meters, the next set was 6 meters, and the last set was a control with no UVB. They were all in 10 liter pots the same size, about 3 feet when started, with the same soil and watering. The closest to the lights got badly fried, the second set was lightly fried, the third set, not really harmed and the 4th set looked the same as controls. We ran the lights first in veg then in flowering. We used GC-FID to measure the cannabinoids and terpenes and weighed the total biomass, and flowers and stems and leaf fraction of the dry plants after harvest.
RCC and I did organoleptic analysis on the two drug varieties Skunk #1 and a Thai?, the no UVB plants were the best. The closest row to the lights were much less weight and resin, the second row was lightly harmed in a similar way. None of the UVB plants had any more cannabinoids or terpenes or more weight. I did try.
-SamS

very informative. Im wondering if you used any meter to measure the UVB you were getting at those distances. Is it possible that the plants were already receiving UVB through the greenhouse ?

Also could there have been an issue with hardening off the plants to uv exposure?
 
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Sam_Skunkman

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Yes we used the correct UVB lights and we had a good UV meter.
Glass in a greenhouse stops 95% of the UVB.
What issue with harding off? If I stick a plant started in the greenhouse outdoors where there is UVB I do not see any negative effects, except if it is colder outdoors. Even with the work it was only the ones that were to close and maybe got to much UVB that were harmed, but none got any benefit at any UVB level.
-SamS


very informative. Im wondering if you used any meter to measure the UVB you were getting at those distances. Is it possible that the plants were already receiving UVB through the greenhouse ?

Also could there have been an issue with hardening off the plants to uv exposure?
 
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Sam_Skunkman

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A powerful article that reveals the propyl cannabinoids inheritance. Many of the parental plants used in this study were selected by me for this purpose, more then a decade ago some closer to two decades or more. At: sci-hub.cc
Enjoy....
-SamS

The inheritance of chemical phenotype in Cannabis sativa L. (V): regulation of the propyl-/pentyl cannabinoid ratio, completion of a genetic model
E. P. M. de Meijer . K. M. Hammond
Euphytica
DOI 10.1007/s10681-016-1721-3
 
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Phaeton

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I did indoor studies for a year using varying UVB levels correlated to elevation.

Control plants with zero UVB to plants receiving the equivalent of 20,000'. Plants in simulated conditions matching the top of Denali died in less than three days.

I limited exposure to levels stunting growth up to 20%. Subjectively the "creeper" effect of the smoke increased with UVB exposure. Extracting and weighing showed no change in the percentages of THC.

UVB has been used at all stages of growth since the testing in 2006-2007. The subjective tests have been consistent in informal testing done on visitors to the garden.
Something is happening, it is not THC, but the positive effects are noted by almost every user questioned on how their high is.

This falls under anecdotes, but I thought I would add it in anyhow.
 

oldchuck

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This falls under anecdotes, but I thought I would add it in anyhow.

Not really, Phaeton. I think your work does contribute some science. I don't know exactly what but you have done some interesting experiments. Not being sure just what you have demonstrated suggests you have reached a good place. Science is rarely completely sure about anything and a good scientist pushes on to find out more. Your science seems to me at least as good as most sociology.
 

Sam_Skunkman

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https://www.ncbi.nlm.nih.gov/pubmed/27285147

Current Status and Prospects for Cannabidiol Preparations as New Therapeutic Agents
Fasinu PS, Phillips S, ElSohly MA, Walker LA
Pharmacotherapy · June 10, 2016
DOI: 10.1002/phar.1780

Abstract
There is growing pressure for states and the federal government to legalize the use of cannabis products for medical purposes in the United States. Sixteen states have legalized (or decriminalized possession of) products high in cannabidiol (CBD) and with restricted Δ9 -tetrahydrocannabinol (Δ9 -THC) content. In most of these states, the intent is for use in refractory epileptic seizures in children, but in a few states, the indications are broader. The objectives of this review are to provide an overview of the pharmacology and toxicology of CBD; to summarize some of the regulatory, safety, and cultural issues relevant to the further exploitation of its antiepileptic or other pharmacologic activities; and to assess the current status and prospects for clinical development of CBD and CBD-rich preparations for medical use in the United States. Unlike Δ9 -THC, CBD elicits its pharmacologic effects without exerting any significant intrinsic activity on the cannabinoid receptors (CB1 and CB2 ), whose activation results in the psychotropic effects characteristic of Δ9 -THC, and CBD possesses several pharmacologic activities that give it a high potential for therapeutic use. CBD exhibits neuroprotective, antiepileptic, anxiolytic, antipsychotic, and antiinflammatory properties. In combination with Δ9 -THC, CBD has received regulatory approvals in several European countries and is currently under study in U.S. Food and Drug Administration-registered trials in the United States. A number of states have passed legislation to allow for the use of CBD-rich, limited Δ9 -THC-content preparations of cannabis for certain pathologic conditions. CBD is currently being studied in several clinical trials and is at different stages of clinical development for various medical indications. Judging from clinical findings reported so far, CBD and CBD-enriched preparations have great potential utility, but uncertainties regarding sourcing, long-term safety, abuse potential, and regulatory dilemmas remain.
 

Betterhaff

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^^Baby steps I guess but why do they continue dwelling on the long term effects crap.

Curious back to when Cannabis was part of the Pharmacopeia. A lot of the medicines were tinctures made with Cannabis Indica, I suppose with an ethanol base. I wonder what the concentrations of THC and/or CBD were...although those compounds had yet to be discovered.
 

oldchuck

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Sam, how do you rate the science in the "Current Status" paper above? I have no access to nih studies beyond the abstract. Have you read it? I am particularly interested in the statement: "Unlike Δ9 -THC, CBD elicits its pharmacologic effects without exerting any significant intrinsic activity on the cannabinoid receptors (CB1 and CB2 )" I had never heard this. Is it true?
 

oldchuck

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Curious back to when Cannabis was part of the Pharmacopeia. A lot of the medicines were tinctures made with Cannabis Indica, I suppose with an ethanol base. I wonder what the concentrations of THC and/or CBD were...although those compounds had yet to be discovered.

What they were then calling Cannabis Indica is what you would most likely call a "Sativa." There is no way of telling what they actually used. I suspect they produced a very erratic product.
 

Betterhaff

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What they were then calling Cannabis Indica is what you would most likely call a "Sativa." There is no way of telling what they actually used. I suspect they produced a very erratic product.
Probably but it was part of the Pharmacopeia for some 80 years.
 

Sam_Skunkman

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Yes true, this has been known for at least 5-6 years that CBD does not bind to the CB1 & CB2 but it does modulate them. Look at my post #79. The paper will be on sci-hub.cc in a few days I bet.

-SamS


Sam, how do you rate the science in the "Current Status" paper above? I have no access to nih studies beyond the abstract. Have you read it? I am particularly interested in the statement: "Unlike Δ9 -THC, CBD elicits its pharmacologic effects without exerting any significant intrinsic activity on the cannabinoid receptors (CB1 and CB2 )" I had never heard this. Is it true?
 
^^ Sam is correct again.. It apparently acts on an "orphan cannabinoid receptor" GPR55 while having negligble affinity for CB1 and CB2 receptors. From my understanding it works as allosteric modulator of CB2 with studies suggesting it could increase THC levels. This, however, was at doses (in mice) most would never receive with natural cannabis. It apparently also modulates opioid receptors as well.

A question Sam, I have also experienced equivalent doses of CBD with THC to completely negate the psychoactive effects. The only thing I notice is crystal clear vision and a sense of general wellbeing but without any real high. Has any research pointed in any direction to explain the apparent antagonism CBD has on d9THC
 
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Sam_Skunkman

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^^ Sam is correct again.. It apparently acts on an "orphan cannabinoid receptor" GPR55 while having negligble affinity for CB1 and CB2 receptors. From my understanding it works as allosteric modulator of CB2 with studies suggesting it could increase THC levels. This, however, was at doses (in mice) most would never receive with natural cannabis. It apparently also modulates opioid receptors as well.

A question Sam, I have also experienced equivalent doses of CBD with THC to completely negate the psychoactive effects. The only thing I notice is crystal clear vision and a sense of general wellbeing but without any real high. Has any research pointed in any direction to explain the apparent antagonism CBD has on d9THC

Check out post #75 & #79, 41.

-SamS
 

oldchuck

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^^ Sam is correct again.. It apparently acts on an "orphan cannabinoid receptor" GPR55 while having negligble affinity for CB1 and CB2 receptors. From my understanding it works as allosteric modulator of CB2 with studies suggesting it could increase THC levels. This, however, was at doses (in mice) most would never receive with natural cannabis. It apparently also modulates opioid receptors as well.

A question Sam, I have also experienced equivalent doses of CBD with THC to completely negate the psychoactive effects. The only thing I notice is crystal clear vision and a sense of general wellbeing but without any real high. Has any research pointed in any direction to explain the apparent antagonism CBD has on d9THC

I have not heard of an orphan cannabinoid receptor. I'll have to look that one up.

Regarding your experience, Weed, my experience of a more balanced ratio has been the same. All a matter of how you define it I suppose but I consider that clarity actually to be a "psychoactive" effect. A remarkable calm much to be valued.
 

oldchuck

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Thank you, Sam. Now I am wondering what differences there might be among "binding to", "activating" and "modulating." All seems like pretty much the same thing to me.
 

Ollie

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Thank you, Sam. Now I am wondering what differences there might be among "binding to", "activating" and "modulating." All seems like pretty much the same thing to me.
Binding to = Which locker does the key fits
Activating = Turning something on or off
Modulating = Like a light dimmer, however the dimming effect is not solely determined by the single Cannabinoid, but rather works in ensemble with(not limited to) Terpenes, which create vast and different modulating effects.

That is why the difference in the Cannabis is so diverse, due to the "endless" possibilities of combinations.
 

Sam_Skunkman

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We all may need this when you get to be older?

http://journal.frontiersin.org.sci-hub.cc/article/10.3389/fnins.2016.00243/full

Front. Neurosci., 31 May 2016 | http://dx.doi.org.sci-hub.cc/10.3389/fnins.2016.00243
CB2 Cannabinoid Receptor As Potential Target against Alzheimer's Disease

Ester Aso1,2* and Isidro Ferrer1,2*
1Institut de Neuropatologia, Servei d'Anatomia Patològica, Bellvitge Biomedical Research Institute (IDIBELL)-Hospital Universitari de Bellvitge, Universitat de Barcelona, L'Hospitalet de Llobregat, Spain
2CIBERNED - Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas, Instituto Carlos III, Madrid, Spain
The CB2 receptor is one of the components of the endogenous cannabinoid system, a complex network of signaling molecules and receptors involved in the homeostatic control of several physiological functions. Accumulated evidence suggests a role for CB2 receptors in Alzheimer's disease (AD) and indicates their potential as a therapeutic target against this neurodegenerative disease. Levels of CB2 receptors are significantly increased in post-mortem AD brains, mainly in microglia surrounding senile plaques, and their expression levels correlate with the amounts of Aβ42 and β-amyloid plaque deposition. Moreover, several studies on animal models of AD have demonstrated that specific CB2 receptor agonists, which are devoid of psychoactive effects, reduce AD-like pathology, resulting in attenuation of the inflammation associated with the disease but also modulating Aβ and tau aberrant processing, among other effects. CB2 receptor activation also improves cognitive impairment in animal models of AD. This review discusses available data regarding the role of CB2 receptors in AD and the potential usefulness of specific agonists of these receptors against AD.


http://www.nature.com/articles/npjamd201612

Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids
Antonio Currais, Oswald Quehenberger, Aaron M Armando, Daniel Daugherty, Pam Maher & David Schubert

npj Aging and Mechanisms of Disease 2, Article number: 16012 (2016)
doi:10.1038/npjamd.2016.12
Alzheimer's disease Neurodegeneration
05 January 2016
The beta amyloid (Aβ) and other aggregating proteins in the brain increase with age and are frequently found within neurons. The mechanistic relationship between intracellular amyloid, aging and neurodegeneration is not, however, well understood. We use a proteotoxicity model based upon the inducible expression of Aβ in a human central nervous system nerve cell line to characterize a distinct form of nerve cell death caused by intracellular Aβ. It is shown that intracellular Aβ initiates a toxic inflammatory response leading to the cell's demise. Aβ induces the expression of multiple proinflammatory genes and an increase in both arachidonic acid and eicosanoids, including prostaglandins that are neuroprotective and leukotrienes that potentiate death. Cannabinoids such as tetrahydrocannabinol stimulate the removal of intraneuronal Aβ, block the inflammatory response, and are protective. Altogether these data show that there is a complex and likely autocatalytic inflammatory response within nerve cells caused by the accumulation of intracellular Aβ, and that this early form of proteotoxicity can be blocked by the activation of cannabinoid receptors.
 
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oldchuck

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I am already older, Sam. I'm not in danger from Alzheimer's but am fully aware of the benefits of Cannabis for older people. This is actually the group, I think, that could derive the most benefit from the plant. That is, if it was as cheap as it could be and freely available to anyone.
 

Sam_Skunkman

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https://www.researchgate.net/public..._and_Bronze_Age_trans-continental_connections
Cannabis in Eurasia: origin of human use and Bronze Age trans-continental connections
Vegetation History and Archaeobotany · June 2016
DOI: 10.1007/s00334-016-0579-6
A systematic review of archaeological and palaeoenvironmental records of cannabis (fibres, pollen, achenes and imprints of achenes) reveals its complex history in Eurasia. A multiregional origin of human use of the plant is proposed, considering the more or less contemporaneous appearance of cannabis records in two distal parts (Europe and East Asia) of the continent. A marked increase in cannabis achene records from East Asia between ca. 5,000 and 4,000 cal bp might be associated with the establishment of a trans-Eurasian exchange/migration network through the steppe zone, influenced by the more intensive exploitation of cannabis achenes popular in Eastern Europe pastoralist communities. The role of the Hexi Corridor region as a hub for an East Asian spread of domesticated plants, animals and cultural elements originally from Southwest Asia and Europe is highlighted. More systematic, interdisciplinary and well-dated data, especially from South Russia and Central Asia, are necessary to address the unresolved issues in understanding the complex history of human cannabis utilisation.

And one for phdilly,

https://peerj.com/preprints/1553/
Genome-wide analyses reveal clustering in Cannabis cultivars: the ancient domestication trilogy of a panacea
Philippe Henry ​
In the present research, I used an open access data set (Medicinal Genomics) consisting of nearly 200'000 genome-wide single nucleotide polymorphisms (SNPs) typed in 28 cannabis accessions to shed light on the plant's underlying genetic structure. Genome-wide loadings were used to sequentially cull less informative markers. The process involved reducing the number of SNPs to 100K, 10K, 1K, 100 until I identified a set of 42 highly informative SNPs that I present here. The two first principal components, encompass over 3/4 of the genetic variation present in the dataset (PCA1 = 48.6%, PCA2= 26.3%). This set of diagnostic SNPs is then used to identify clusters into which cannabis accession segregate. I identified three clear and consistent clusters; reflective of the ancient domestication trilogy of the genus Cannabis.
 
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