An attempt at a response to the beverage carve-out bill that benefits none of the actual "hemp" products or consumers. It's still in a draft phase looking for interested parties in government to take notice.
>On Sunday, leaders of the Senate Appropriations Committee released the text of a continuing resolution to extend funding for federal agencies through December 11, past the end of the current fiscal year on September 30.
>Included in the legislation are provisions that will also delay the planned prohibition on most hemp products until December 11—although there is a carve-out that will allow the immediately recriminalization on November 12 of synthetic cannabinoids “that are not capable of being naturally produced by a Cannabis sativa L. plant.
More time to figure out which of the bills being proposed wins out in the end.
I emptied out a Mighty dosing capsule to see what would happen if I put the exact same material that I normally vape into a cone and smoked it instead. The results: Almost indistinguishable effects from vaping the same material except I had a nasty smoke taste in my mouth for an hour afterwards. Having not smoked in years, it was almost as gross as if I had smoked a cigarette, but not as intense.
I don't understand why we still have threads full of people debating this in the second half of 2026. If you prefer to smoke, just go out and say you don't care about the difference in long term consequences of one method versus the other and go about your life without trying to influence other people to keep doing the same thing. It's quite literally not hurting you in any shape or form when somebody other than you switches from smoking to vaping, so why are people so adamant to mention every single time this comes up that DHV doesn't work for them, because they have sky-high tolerances?
If you cannot replicate others' experiences with a smaller amount of cannabis than you consume on the regular, who is holding you back from changing your own habits? You're essentially saying, "because I would have to smoke at least 1g at a time to feel anything, I couldn't benefit from the experience of a DHV, therefore they are shit and I have to keep reminding the community of that every time a newcomer comes around lest they might get the impression a DHV is a good purchase option."
Well then, what are you doing to solve that problem exactly? If your tolerance is too high, are you just going to continue going about your life assuming everyone else's is as well, and therefore DHVs are a worthless endeavor for the stoner community, or are you going to accept that perhaps you need to change your perspective and be more open of change when it comes to healthier consumption methods? I don't think anyone should be imagining a stoner utopia where you have to be "this high to enter" and the cutoff is above what a DHV can achieve.
Were that I had more space and another tent I could have kept these mutants alive to collect pollen. I already have a much larger male pollinating in my tent so these boys had to go. The asymmetry is pronounced in the growth of the one dominant side branch in each plant. The smaller plant is more asymmetric than the healthier specimen.
The stunted female in the center is just being left alive for now so I can gauge what the flower will look like on the others later. The other three females are all at day 50 and still in preflower. They are happily growing with no clear signs of reaching full flower soon. Obviously the dilemma is that unless warned adequately, most people would assume these are photoperiods and/or trash genetics, switch to 12/12, or give up. They are simply getting it from their great grandmother who was the biggest CBD autoflower I've seen so far.
Since I've also culled the males that stunted and only kept the better specimen of the late flowering (and now huge) males I expect the next generation to turn out like this as well. So the question is, if I can stabilize my cross and it keeps the 35+ days of veg growth and another 2-3 weeks after that of preflower, would people be turned away by that and just go with photoperiods instead because of the time investment?
A large draw/incentive of autoflowers over photoperiods is the faster turn around from start to finish. Removing that would leave the convenience of the steady time schedule and not much else I can think of at the moment. Just trying to ascertain whether this is too long of a life cycle for anyone to consider growing it.
So the double-sided seed was planted after I ripped out a male that flowered too early. Both halves sprouted. Unfortunately both are growing asymmetrically at the moment. The weaker one far more so than the stronger of the twins. I guess whatever causes a seed embryo to split into two seeds also has a strong likelihood of causing DNA damage/mutations? I'll try and keep them as healthy as I can so I can see how they turn out.
https://www.youtube.com/live/gTUFlqeSaH8?si=hAAXQKtizwSiBf-d&t=1890
It's not heartening to hear interviews like this from the "Face of the Hemp Industry". Apparently people like this, that refuse to differentiate when talking about THCa "hemp" that there also exists CBD flower that should have always been legalized, and still should be left legal for all people age 21+ are the face of the hemp industry.
Are any of the Hemp organizations providing counterpoints to people like this? Does anyone in the industry talk about how ridiculous it is that just because it's "smokeable" it would magically become illegal, meanwhile their higher profit extractions and THC beverages would be given their own carveout?
Switching from an industry that allowed bag appeal smokeable flower, to one that only allows for the most mass produced biomass extraction, is not a good move. That doesn't say, "we trust that hemp is safe medicine". If it's so fucking safe, why can't we stick it in our DHV? If it's so safe, why are we moving away from being able to see it before it's processed?
https://pmc.ncbi.nlm.nih.gov/articles/PMC9414986/
>Such thoroughly characterized chemotypes guarantee blinding in controlled studies by mimicking the sensory properties of hemp and may help to unravel the “entourage effect”. Capitalizing on the ability of cannabis to synthesize a large number of non-cannabinoid phenolic compounds, we here investigated, for the first time, the composition of the Ermo chemotype V and identified new compounds: two dihydrophenanthrenes and the methoxy-dihydrodenbinobin. All three compounds suppress pro-inflammatory leukotriene biosynthesis in activated macrophage subtypes by targeting 5-lipoxygenase, but substantially differ in their capacity to elevate the levels of specialized pro-resolving lipid mediators and their precursors in M2 macrophages. We conclude that the discovered compounds likely contribute to the anti-inflammatory properties of Cannabis sativa L. chemotype V and might promote inflammation resolution by promoting a lipid mediator class switch.
I stumbled across this while looking for something else as usual. It would seem that even if you grow cannabis genetics that do not produce glandular trichomes and thus do not produce cannabinoids, they still are a useful source of medicinal compounds elsewhere in the plant. Some of which were unknown prior to this study in 2022.
Now nobody is going to smoke, vape, or eat Type V, ever. This however adds more evidence to the pile that whole plant extractions or at least broader spectrum extractions are more beneficial than isolates and narrow spectrum concentrates. The Trade to Black podcast is on a loop lately with all the talk of "pharmaceutical grade CBD" being the next big thing to come out of hemp and medical marijuana. No longer will it be 98% pure made by unknown Chinese labs. Now it will be 99.9% pure made in America!
Okay... but what else are you adding back into these formulations? The researchers around the world are certainly thinking about health benefits. The original hemp cultivators and producers were certainly working towards that in 2018 and 2019 with all the whole plant CBD/hemp oils and tinctures on the market back then. Since then obviously we've seen "hemp" maligned by it's naming in loophole products that have nothing to do with hemp.
The last pharmaceutical product I saw containing hemp used a propriety blend of other plant extracted compounds. I'm afraid we might be entering an age where if anyone actually wants to help you get healthier, it's only behind the wall of secretive formulas and a heavy focus on the for profit aspect of their business model.
In 2026 I don't think a marketing campaign of "our products contain even less trace cannabinoids or other compounds than the competitor" may not sit as well with educated customers, whereas "we have a mystery blend of the good stuff and it's FDA approved" is just dumb enough for the audience of human beings we have today.
I think the future involves a whole lot of mixing and matching. People and the companies they run need to be more flexible about either encouraging customers to mix products, or providing their own blends that combine multiple chemotypes of the cannabis plant. In terms of pharmaceuticals, something much more complex than Epidiolex will be coming.
As an analogy, think of cannabis like a box of Lego pieces, hundreds of them all unique and different in some way. The more you reach into the box, the more you find. Yet the current climate is one where mainstream society is only playing with 2 to 4 of those pieces over and over and over again... Building the most generic structures you could possibly make.
I didn't completely rub all the purple skin off the bottom section from this orientation in the photo, but it's basically a yin yang of two smaller seeds fused together. I wonder if these don't normally show up on the market because they are too heavy and the sorting machines discard them? This came out of the last 2 grams of seeded bud from my personal breeding project.
https://www.mdpi.com/1424-8247/19/4/560
Background/Objectives: Rheumatoid arthritis (RA) is a chronic, inflammatory, autoimmune disease that primarily affects the joints. Current treatments aim to relieve pain and limit joint damage; however, many are associated with significant side effects or high costs. Neutrophils play a critical role in RA development and progression by driving synovial inflammation and tissue damage, yet no approved therapies directly target neutrophil-mediated pathogenic mechanisms. Cannabinoids have demonstrated anti-inflammatory potential. Although cannabinoids have been studied in RA, the direct modulation of neutrophil-driven mechanisms by purified CBG has not been systematically addressed. To harness the cannabinoid potential, we investigated the effects of the purified cannabinoid Cannabigerol (CBG) on neutrophil-mediated immune responses in RA. Methods: We assessed the effects of CBG on human blood isolated neutrophil cytokine secretion, signal transduction and migration as ex vivo models. In addition, collagen antibody-induced arthritis (CAIA) was applied in C57BL/6 wt mice, and immune-cell recruitment and cytokine secretion were examined after CBG treatment. Results: Ex vivo experiments demonstrated that CBG hampered the secretion of pro-inflammatory cytokines from human neutrophils in a dose-dependent manner (TNF-α and IL-6 by 68% and 72%, respectively). Furthermore, CBG downregulated inflammatory signal transduction, such as P38-MAPK, ERK1/2 and Akt phosphorylationpost neutrophil activation by 41%, 54% and 78%, respectively. Importantly, 60% of the CBG downregulation of IL-6 was consistent with the CB2 receptor axis in a selective way. In addition, CBG attenuated neutrophil migration toward IL-8 by 67%. To further evaluate CBG therapeutic capacity, we used CAIA as an in vivo model. CBG treatment resulted in improving mice arthritis clinical scores and body weight in comparison to RA-diseased mice. Moreover, CBG reduced leukocyte recruitment to the inflamed joints by 48%, primarily through the inhibition of neutrophil and monocyte cells to 27% and 49%, respectively. Additionally, CBG showed its anti-inflammatory effect by decreasing inflammatory cytokines like IL-6 and IL-1β by 98% and 60% in the blood. Also, CBG reduced MCP-1 and IL-1β cytokines in the joints by 22% and 38%, respectively. Conclusions: These results show that CBG has anti-inflammatory capacity and therapeutic potential in regulating neutrophil-mediated immunity in RA. These findings are preclinical and require further validation before therapeutic positioning.
. . .
Cannabinoids produce more than 100 naturally occurring chemicals, the most abundant of which are Δ-9-tetrahydrocannabinol (THC), cannabidiol (CBD), terpenes and flavonoids. THC and CBD bind with cannabinoid receptors (CB1 and CB2), which are present in the brain, immune system and many organs [20]. THC and CBD help to manage conditions ranging from chronic pain persistent inflammation, cancer, inflammatory bowel disease, and neurological disorders to even viral diseases such as Human Immunodeficiency virus (HIV) and SARS-CoV-2 [21]. Both THC and CBD exhibit promising therapeutic properties; however, impairments and the increased incidence of mental health diseases are associated with acute and chronic THC use, respectively, and significant side effects are associated with the chronic use of high-dose CBD [22]. Preclinical in vitro and in vivo studies show promising results regarding the anti-arthritic properties of cannabinoids, psychoactive and non-psychoactive alike [23]. Our previous studies demonstrated that a high-CBD extract (CBD-X) significantly reduced pro-inflammatory cytokine secretion in human-derived PBMCs, neutrophils and T cells [24]. More recent findings further show that CBD-X exerts anti-inflammatory effects in rheumatoid arthritis by inhibiting pro-inflammatory cytokine secretion, limiting immune-cell recruitment and attenuating inflammatory signal transduction [25]. However, CBD-X is an extract that has 37% CBD, 1.7% THC, 0.3% CBG and other unknown terpenes and flavonoids [25]. Therefore, we decided to focus our research on purified cannabinoids.
Cannabigerol (CBG) serves as the precursor molecule for the most abundant cannabinoids. While THC and CBD have been more widely studied than CBG, it has had increased attention due to the wide range of potential health benefits [26]. Studies indicate that CBG may have therapeutic potential in treating neurologic disorders (e.g., Huntington disease, Parkinson disease and multiple sclerosis) and inflammatory bowel disease, as well as having antibacterial activity [27]. Moreover, there are anti-inflammatory effects of CBG in rheumatoid arthritis synovial fibroblasts and peripheral blood mononuclear cell cultures [28]. Furthermore, research showed CBG has potential anti-inflammatory properties, including the diabetic kidney disease progression of rats subjected to a high-fat, high-sucrose diet [29].
CBG is a multi-target player that interacts with the endocannabinoid system and other key signaling pathways, such as CB1, CB2, transient receptor potential (TRP) channels and α2-adrenoceptor, potentially influencing inflammation, pain, neurodegeneration and other ailments. CB1 and CB2 are the two main types of cannabinoid receptors. Unlike THC and CBD, CBG does not bind directly to the CB1 receptors in the brain, which are responsible for the psychoactive effects of cannabis. CBG weakly agonizes the action of CB1 and partially acts as an agonist on CB2 receptor agonists [26]. Cannabinoid receptor 2 deficiency exacerbates inflammation and neutrophil recruitment [30]. The expression of the CB2 mRNA can be detected in neutrophils [31]. The CB2 receptor is primarily expressed only when there is active inflammation. Accordingly, CBG’s interaction with CB2 downregulates the inflammation [32]. Furthermore, CBG interacts with TRP channels, which play a crucial role in regulating the cytoplasmic calcium concentration from the extracellular sources as well as the calcium stored within the endoplasmic reticulum (ER). CBG serves as a strong agonist of TRPA1 and a weaker agonist of TRPV1, TRPV2 and TRPV4 while antagonizing TRPM8 (TRP melastatin type 8) [26]. CBG acts as a potent agonist of Peroxisome proliferator-activated receptor gamma (PPARγ), a transcription factor that suppresses NFκB or MAP kinases [33]. In addition, CBG is a potent serotonin 1A receptor (5-HT1A) antagonist, which is known to reduce the activity of NF-κB and the phosphorylation of its inhibitor α (IκB- α), resulting in a decrease in cytokine secretion [29].
Recent computational modeling indicates that CBG possesses a unique 3D conformational flexibility, characterized by ‘coiled’ and ‘stapled’ poses that are sterically distinct from the rigid bicyclic structure of CBD [34]. In addition, CBG exhibits affinity and activity characteristics between Δ9-THC and CBD at the cannabinoid receptors but appears to be unique in its interactions with the α-2 adrenoceptors, PPARγ and 5-HT1A [27].
However, CBG shows anti-inflammatory effects, but due to the lack of research, it is not widely used. Its physicochemical properties lead to considerable challenges, such as poor intestinal absorption, extensive first-pass metabolism, low bioavailability and variable brain penetration, all of which limit its effective application in clinical settings [35]. In addition, the regulatory status of cannabis, sources for cannabis and funding to support studies are difficult barriers to navigate [36].
There is growing interest in CBG and its promising therapeutic potential in treating immune-related diseases. Our aim in this study is to examine the regulatory effect of CBG in mitigating inflammatory RA disease severity through regulating neutrophil activity. We hypothesized that CBG through CB2 receptor mediation directly suppresses neutrophil activation and recruitment, thereby attenuating RA severity.
https://www.mdpi.com/1424-8247/19/4/560
Background/Objectives: Rheumatoid arthritis (RA) is a chronic, inflammatory, autoimmune disease that primarily affects the joints. Current treatments aim to relieve pain and limit joint damage; however, many are associated with significant side effects or high costs. Neutrophils play a critical role in RA development and progression by driving synovial inflammation and tissue damage, yet no approved therapies directly target neutrophil-mediated pathogenic mechanisms. Cannabinoids have demonstrated anti-inflammatory potential. Although cannabinoids have been studied in RA, the direct modulation of neutrophil-driven mechanisms by purified CBG has not been systematically addressed. To harness the cannabinoid potential, we investigated the effects of the purified cannabinoid Cannabigerol (CBG) on neutrophil-mediated immune responses in RA. Methods: We assessed the effects of CBG on human blood isolated neutrophil cytokine secretion, signal transduction and migration as ex vivo models. In addition, collagen antibody-induced arthritis (CAIA) was applied in C57BL/6 wt mice, and immune-cell recruitment and cytokine secretion were examined after CBG treatment. Results: Ex vivo experiments demonstrated that CBG hampered the secretion of pro-inflammatory cytokines from human neutrophils in a dose-dependent manner (TNF-α and IL-6 by 68% and 72%, respectively). Furthermore, CBG downregulated inflammatory signal transduction, such as P38-MAPK, ERK1/2 and Akt phosphorylationpost neutrophil activation by 41%, 54% and 78%, respectively. Importantly, 60% of the CBG downregulation of IL-6 was consistent with the CB2 receptor axis in a selective way. In addition, CBG attenuated neutrophil migration toward IL-8 by 67%. To further evaluate CBG therapeutic capacity, we used CAIA as an in vivo model. CBG treatment resulted in improving mice arthritis clinical scores and body weight in comparison to RA-diseased mice. Moreover, CBG reduced leukocyte recruitment to the inflamed joints by 48%, primarily through the inhibition of neutrophil and monocyte cells to 27% and 49%, respectively. Additionally, CBG showed its anti-inflammatory effect by decreasing inflammatory cytokines like IL-6 and IL-1β by 98% and 60% in the blood. Also, CBG reduced MCP-1 and IL-1β cytokines in the joints by 22% and 38%, respectively. Conclusions: These results show that CBG has anti-inflammatory capacity and therapeutic potential in regulating neutrophil-mediated immunity in RA. These findings are preclinical and require further validation before therapeutic positioning.
. . .
Cannabinoids produce more than 100 naturally occurring chemicals, the most abundant of which are Δ-9-tetrahydrocannabinol (THC), cannabidiol (CBD), terpenes and flavonoids. THC and CBD bind with cannabinoid receptors (CB1 and CB2), which are present in the brain, immune system and many organs [20]. THC and CBD help to manage conditions ranging from chronic pain persistent inflammation, cancer, inflammatory bowel disease, and neurological disorders to even viral diseases such as Human Immunodeficiency virus (HIV) and SARS-CoV-2 [21]. Both THC and CBD exhibit promising therapeutic properties; however, impairments and the increased incidence of mental health diseases are associated with acute and chronic THC use, respectively, and significant side effects are associated with the chronic use of high-dose CBD [22]. Preclinical in vitro and in vivo studies show promising results regarding the anti-arthritic properties of cannabinoids, psychoactive and non-psychoactive alike [23]. Our previous studies demonstrated that a high-CBD extract (CBD-X) significantly reduced pro-inflammatory cytokine secretion in human-derived PBMCs, neutrophils and T cells [24]. More recent findings further show that CBD-X exerts anti-inflammatory effects in rheumatoid arthritis by inhibiting pro-inflammatory cytokine secretion, limiting immune-cell recruitment and attenuating inflammatory signal transduction [25]. However, CBD-X is an extract that has 37% CBD, 1.7% THC, 0.3% CBG and other unknown terpenes and flavonoids [25]. Therefore, we decided to focus our research on purified cannabinoids.
Cannabigerol (CBG) serves as the precursor molecule for the most abundant cannabinoids. While THC and CBD have been more widely studied than CBG, it has had increased attention due to the wide range of potential health benefits [26]. Studies indicate that CBG may have therapeutic potential in treating neurologic disorders (e.g., Huntington disease, Parkinson disease and multiple sclerosis) and inflammatory bowel disease, as well as having antibacterial activity [27]. Moreover, there are anti-inflammatory effects of CBG in rheumatoid arthritis synovial fibroblasts and peripheral blood mononuclear cell cultures [28]. Furthermore, research showed CBG has potential anti-inflammatory properties, including the diabetic kidney disease progression of rats subjected to a high-fat, high-sucrose diet [29].
CBG is a multi-target player that interacts with the endocannabinoid system and other key signaling pathways, such as CB1, CB2, transient receptor potential (TRP) channels and α2-adrenoceptor, potentially influencing inflammation, pain, neurodegeneration and other ailments. CB1 and CB2 are the two main types of cannabinoid receptors. Unlike THC and CBD, CBG does not bind directly to the CB1 receptors in the brain, which are responsible for the psychoactive effects of cannabis. CBG weakly agonizes the action of CB1 and partially acts as an agonist on CB2 receptor agonists [26]. Cannabinoid receptor 2 deficiency exacerbates inflammation and neutrophil recruitment [30]. The expression of the CB2 mRNA can be detected in neutrophils [31]. The CB2 receptor is primarily expressed only when there is active inflammation. Accordingly, CBG’s interaction with CB2 downregulates the inflammation [32]. Furthermore, CBG interacts with TRP channels, which play a crucial role in regulating the cytoplasmic calcium concentration from the extracellular sources as well as the calcium stored within the endoplasmic reticulum (ER). CBG serves as a strong agonist of TRPA1 and a weaker agonist of TRPV1, TRPV2 and TRPV4 while antagonizing TRPM8 (TRP melastatin type 8) [26]. CBG acts as a potent agonist of Peroxisome proliferator-activated receptor gamma (PPARγ), a transcription factor that suppresses NFκB or MAP kinases [33]. In addition, CBG is a potent serotonin 1A receptor (5-HT1A) antagonist, which is known to reduce the activity of NF-κB and the phosphorylation of its inhibitor α (IκB- α), resulting in a decrease in cytokine secretion [29].
Recent computational modeling indicates that CBG possesses a unique 3D conformational flexibility, characterized by ‘coiled’ and ‘stapled’ poses that are sterically distinct from the rigid bicyclic structure of CBD [34]. In addition, CBG exhibits affinity and activity characteristics between Δ9-THC and CBD at the cannabinoid receptors but appears to be unique in its interactions with the α-2 adrenoceptors, PPARγ and 5-HT1A [27].
However, CBG shows anti-inflammatory effects, but due to the lack of research, it is not widely used. Its physicochemical properties lead to considerable challenges, such as poor intestinal absorption, extensive first-pass metabolism, low bioavailability and variable brain penetration, all of which limit its effective application in clinical settings [35]. In addition, the regulatory status of cannabis, sources for cannabis and funding to support studies are difficult barriers to navigate [36].
There is growing interest in CBG and its promising therapeutic potential in treating immune-related diseases. Our aim in this study is to examine the regulatory effect of CBG in mitigating inflammatory RA disease severity through regulating neutrophil activity. We hypothesized that CBG through CB2 receptor mediation directly suppresses neutrophil activation and recruitment, thereby attenuating RA severity.
One of the world's biggest seedbanks, NASC, has a series of interview Q/A with the breeders they carry. One thing that stood out to me was how many breeders were talking about how they moved to Maine for the better laws. They didn't explain in the videos what they meant so I had to look it up myself.
Level I
| Application Fee | $20,000 |
|---|---|
| Initial Fee (Certificate of Operation) | $180,000 |
| Annual License Renewal Fee | $200,000 |
Level II
| Application Fee | $2,000 |
|---|---|
| Initial Fee (Certificate of Operation) | $18,000 |
| Annual License Renewal Fee | $20,000Level I Application Fee $20,000Initial Fee (Certificate of Operation) $180,000Annual License Renewal Fee $200,000Level IIApplication Fee $2,000Initial Fee (Certificate of Operation) $18,000Annual License Renewal Fee $20,000 |
https://mainecannabis.org/licensing/cultivation
A Tier 1 cultivation facility license comprises two subcategories: plant-count-based Tier 1 cultivation facility license and plant-canopy-based Tier 1 cultivation facility license. The plant-count-based Tier 1 cultivation facility license permits the licensee to cultivate a specified number (up to 30) of mature marijuana plants and an unlimited number of immature marijuana plants and seedlings. The plant-canopy-based Tier 1 cultivation facility license allows the cultivation of not more than 500 square feet of plant canopy area of mature marijuana plants.
A Tier 2 cultivation facility license authorizes the licensee to cultivate up to 2,000 square feet of plant canopy of mature plants. A Tier 3 cultivation facility licensee can cultivate up to 7,000 square feet of plant canopy of mature plants, while a Tier 4 cultivation facility licensee is permitted to cultivate no more than 20,000 square feet of plant canopy of mature plants, unless allowed to do so by the DAFS (Department of Administrative and Financial Services) under 28-B MRS §304. A nursery cultivation facility license authorizes the licensee to cultivate up to a 1,000-square foot plant canopy area, subject to the provisions and limitations of 28-B MRS §501(3).
| License Type | Annual License Fee (Outdoor Only) | Annual License Fee (Indoor/both) | Application Fee |
|---|---|---|---|
| Tier 1 Cultivation Facility (Plant-Count-Based) | $9 per mature plant | $17 per mature plant | $100 |
| Tier 1 Cultivation Facility (Plant-Canopy-Based) | $250 | $500 | $100 |
| Tier 2 Cultivation Facility | $1,500 | $3,000 | $500 |
| Tier 3 Cultivation Facility | $5,000 | $10,000 | $500 |
| Tier 4 Cultivation Facility (for each increase in canopy size) | $15,000 (+$5,000) | $30,000 (+$10,000) | $500 |
| Nursery Cultivation Facility | $350 | $350 | $60License Type Annual License Fee (Outdoor Only) Annual License Fee (Indoor/both) Application FeeTier 1 Cultivation Facility (Plant-Count-Based) $9 per mature plant $17 per mature plant $100Tier 1 Cultivation Facility (Plant-Canopy-Based) $250 $500 $100Tier 2 Cultivation Facility $1,500 $3,000 $500Tier 3 Cultivation Facility $5,000 $10,000 $500Tier 4 Cultivation Facility (for each increase in canopy size) $15,000 (+$5,000) $30,000 (+$10,000) $500Nursery Cultivation Facility $350 $350 $60 |
So you see a massive gulf between the states like ours and Maine in their layout of cultivation tiers. Maine offers two lightweight tiers at the bottom that are quite affordable for a breeder or hobbyist to grow for the purpose of the seed/clone market. The way these breeders work is they do they primary work with a small license like this, and then send bulk seed off to friends in California or other places to do larger phenotype hunts and dial down the genetics.
If there is literally a pattern of one type of business saying we moved to X state because the laws there are better, doesn't it warrant other states looking at their own laws? We already had a Tier III Cultivation License available in Ohio that was smaller than what we have now... And they removed it to focus on only the big players with more money. Who's idea was it to make Ohio less business friendly? Is that the kind of decision politicians are too full of ego to ever unmake when they realize it was a mistake?
https://marijuana.school/minnesotas-new-2026-cannabis-omnibus-bill/
The newly minted Ratio Hemp-Infused Cannabis Product category explicitly allows businesses holding low-potency licenses to cross over and sell significantly stronger formulations—provided they balance the intoxicating THC content with therapeutic, non-intoxicating secondary cannabinoids like CBD, CBG, CBN, or CBC.
The Golden Rule for Higher Potency: To unlock the expanded milligram allowances, products must maintain a structured ratio. Manufacturers are permitted to include up to 100 mg of secondary cannabinoids per serving alongside the increased THC counts.
This is for people age 40+ without Parkinsons, or 30+ with a diagnosis.
Michael J. Fox has been advertising this on Instagram as part of his Parkinsons research. After signing up and answering basic questions about yourself you will get a package in the mail. This has a pencil and 4 booklets each with 10 scratch and sniff multiple choice questions. You log back into the website and enter the data as you scratch and sniff each page. Trust me when I say many of these questions are very pertinent to whether or not you are identifying the same smells as other cannabis breeders.
I don't want to give away any of the choices because that would influence other people. Let's just say a broad range is covered and you would do yourself some good to see how you interpret them. Worst case scenario you spent some time and helped medical research only to realize you get confused by certain scents. The test only took me thirty minutes.
https://en.wikipedia.org/wiki/HU-345
I'm curious if anyone else thinks it is perhaps unwise to experiment with such high ratios of CBN in vaporization devices until we know exactly what happens when we do that. Currently only one of the possible byproducts has a chemical name, and we know almost nothing about how it effects humans. I see people making their own mixes with large amounts of CBN, just like the industry is. For edibles and tinctures, fine, since you aren't heating it again to further degrade it.
What concerns me is starting off with an amount of CBN that is many times above what is naturally possible in the plant were it sun dried like people did decades ago (or perhaps in some cultures still) and then heating it again. I feel like products whether professional or homemade should start off mimicking what the plant would produce unless they know it is safe otherwise to go outside those bounds.
For reference CBD degrades to CBE. If you are smoking a type 3/2 a tiny portion will degrade every time. I've experimented some with it, as GVB BioPharma produced a Crystal Resistant Distillate high in CBE and other minors which I've used on rare occasions. I haven't noticed any weird effect from that so far. When I first tried it, I definitely noticed it felt different, and more "whole" than any commercial cartridge I had ever purchased. Obviously I haven't used grams and grams of it, so I can't state for certain it's safe or not, just that I don't notice side effects.
CBC degrades into CBL, some naturally before you've even smoked/vaped it. Again, CBL is a known cannabinoid that was first isolated in the 1960's and you can buy in pure form today if you want to experiment with it. It is suspected to have health benefits, but like many of the relatively unknown minors, nobody seems to be researching it yet.
Now when it comes to CBN, itself already being a degradation of THC, I just don't want to jump to the assumption before we have any actual evidence that whatever it turns into is a useful or positive drug. Wikipedia lists HU-345 as a "non-classical cannabinoid", whatever that means. If any of you have used these products feel free to share your experiences with them. Do you think going above like 2-5% CBN in a vaporizer adds any benefit to the user? How is it different? Have you also tried products that were closer to natural ratios of CBN to THC?
https://www.frontiersin.org/journals/chemistry/articles/10.3389/fchem.2022.1038729/full