All Activity

I am likely to be among the first in any given crowd to support drug-positive perspectives. Over 130 different psychoactive compounds have passed through my brain over the years, and Cannabis has been of incredible use to my ability to function & participate in life (I am currently a daily user). I am also a neuroscience major pursuing a PhD in psychopharmacology. Spreading more accurate, less biased information about psychoactive drugs is my life’s purpose. But within this purpose, it’s also necessary for me to distribute accurate information about their drawbacks as well. I feel a calling to this mission akin to that which a priest might feel to their religion. In certain communities, Cannabis is regarded as sacred medicine. Many hesitate to call it a drug, and many hesitate to claim it has any side effects at all. This neglect poses a significant threat to many people; the Cannabis of today is far different than what humans have been using for thousands of years, and treating it as harmless is neither fully informed nor constructive for the vast majority of people. To explain exactly what a high-THC low-CBD “Cannabis diet” does to your brain, I’ll need to get into the muck & grime of neurotransmission, so you’ll probably see some crazy chemical names and stuff in this article that look really daunting, but I promise anyone can understand this stuff if they take a deep breath and keep track of the terms. I’ll also simplify it as much as I can and make it at least somewhat entertaining? Hopefully? Your Nervous System and its Cannabinoids The nervous system is classified into two parts: the central nervous system (CNS) and the peripheral nervous system (PNS). The CNS is the brain and spinal cord; it’s where all your complex cognition and perception takes place. The PNS is the set of nerve tendrils your brain reaches through your body so you can actually feel stuff and control your movement. There’s a lot of communication between the CNS and PNS, and the PNS can actually do some stuff that influences your perception and cognition. But for the sake of this article, I’m going to be focusing on the CNS, particularly the brain. Your brain is made up of brain cells; the predominant cells are called neurons, and these are responsible for the vast majority of what your brain does. Your brain has 86 billion neurons (on average), and each of those neurons shares an average of 10,000 connections, or synapses, with other neurons. For a neuron to fire, the intracellular voltage (the electrical charge on the inside of the neuron) must reach a certain level higher than the extracellular voltage (charge outside the neuron). To change the balance of charges, the neuron opens and closes ion channels, which are proteins on the cell membrane that let specific ions through. Ions are positively or negatively charged molecules; usually singular atoms such as Ca2+ (Calcium missing 2 electrons). The balance of charges between the inside and outside of the neuron is called the membrane potential; when this reaches the neuron’s threshold potential, it becomes an action potential, at which point an electrical signal travels down the neuron’s axon to its axon terminal. This terminal is the presynaptic terminal; it’s primarily on the giving end of the synapse, where the next neuron’s dendrites will pick up what it’s putting down. What it’s putting down is a short burst of chemical release: various ions, things like dopamine and serotonin; basically just a dump of various chemical compounds that will influence the next neuron(s) in line. These chemical compounds will bind to receptors on the next neuron and alter its own membrane potential, which will adjust how close it is to firing. Receptors are more-or-less chemical robots; they’re highly specialized proteins that, upon receiving a ligand (a chemical key; a neurotransmitter or a drug in most cases), will accomplish certain tasks for the cells present. In nervous systems, they’re usually divided into two groups: ionotropic and metabotropic. Ionotropic receptors include things like ion channels; they directly influence membrane potentials by allowing the exchange of ions across cell membranes. They’re typically the endpoint of any signalling cascade (basically a chain reaction of communication). But metabotropic receptors are just as important; they can significantly modulate the activity of ionotropic receptors and neurons as a whole, it’s simply an indirect way they go about doing so. This includes things like dopamine receptors (D1 through D5), serotonin receptors (except 5ht3), and some glutamate receptors (MGluR1 through MGluR8), among many others. Receptors are also classified as excitatory or inhibitory. Excitatory means their activation leads to a higher membrane potential, and inhibitory means the opposite. This gets a little complicated when talking about metabotropic receptors, because they can often activate different signalling pathways that have excitatory AND inhibitory effects, but in most cases, a receptor is considered either primarily excitatory or primarily inhibitory. Dopamine and glutamate receptors are largely excitatory, while serotonin and GABA receptors are largely inhibitory. The Endocannabinoid System (ECS) is a system of transmission found within mammalian nervous systems that has gained sharply increased interest in the past 40 years. It has a hand in regulating everything from blood pressure to sensory input to cognitive abilities, and modulates the activity of other major neurotransmitters like serotonin, dopamine, and acetylcholine. The transmission of the ECS in the CNS is primarily mediated by two endocannabinoids (portmanteau of endogenous, meaning “from within,” and cannabinoid, which is a compound that acts on cannabinoid receptors). These compounds are anandamide and 2-arachydonoylglycerol (2-AG). Anandamide is pretty insignificant; it’s released in very small amounts and metabolized quickly. 2-AG is far more present in your CNS and thought to play a much bigger role in mediating sensory and emotional perception. Both of these compounds are, at best, about 1/10 the potency of THC by weight. They are both metabolized (broken down) in the brain primarily by an enzyme called FAAH (Fatty Acid Amide Hydrolase). There are two main cannabinoid receptors: CB1 and CB2. CB2 isn’t heavily present in the CNS, at least not remotely to the extent of the role it plays in the PNS. CB1 is what’s mainly responsible for creating an altered headspace. THC is an agonist at CB1 (activates the receptor), while CBD is a negative allosteric modulator (NAM; decreases the ligand’s influence on the CB1 receptor). Brain Debriefing The big squiggly lump on top is called your cerebral cortex (might be shortened to just ‘cortex’). It’s where the vast majority of your memories are stored, including emotional, logical, and sensory information. Your cortex does a bit of the work on its own, but it also outsources a good bit of the work to the lower portion. It’s not really an unhealthy professional dynamic though; they get along pretty well, communicate about each other’s needs, and are generally good at reaching fair compromises. But the thing to know is that the cortex primarily functions as an information warehouse, which includes some management in organization, routing, and distribution. The cortex includes the frontal lobe, which is what the rest of your brain uses mostly for storing logical processes and higher-order cognition, including complex emotion. The structural integrity of the frontal lobe is incredibly important for functioning on a competent level: assessing nuance, comprehending abstract concepts, being able to integrate and apply previous information in new situations. Dysfunction in this region is widely seen in depression, schizophrenia, and personality disorders. The lower part of your brain is divided into the subcortex and brainstem. Your brainstem holds the midbrain, which is responsible for a lot of sensory processing; basically routing hastily-assembled sensory input to the hippocampus, which gets other subcortical regions involved. The other regions all do their own stuff with the information, basically putting little markers on it to tell the hippocampus where in the cortex they should send it. This information gets sent to the cortex, and the cortex basically adds bits of other memories to fill in the gaps and errors, then commits this information to its memory by systematically adding and deleting synapses in the proper order if it’s important enough. The midbrain contains the Tegmentum, which has a bunch of different incredibly complex roles that aren’t important for me to explain in this article. But the Tegmentum houses the Ventral Tegmental Area (VTA), which serves as a starting point for the mesolimbic pathway. The mesolimbic pathway is the region most closely involved in the processing of reward, motivation, and euphoria. To put it simply, the VTA receives both complete and incomplete stimuli, assesses the positive+negative effects of them (with the help of some other regions like the Lateral Habenula), and then sends them to the mesolimbic pathway. The mesolimbic pathway allows this reward transmission to affect acute (short-term) perception, and sends this reward signal to the Nucleus Accumbens (NAc) to be committed to the cerebral cortex as a rewarding stimulus. The NAc sends the signal back to the VTA to be re-assessed, and this circuit continues until it is acted upon or fades away due to other signals that outweigh it. The Amygdala essentially does the same thing, but instead evaluates information for whether it causes noxious stimuli. This means that it detects things you experience that cause fear, anxiety, paranoia, danger, aversion. It’s closely linked with the mesolimbic pathway and NAc, as well as the Lateral Habenula (LHb, a “limiter” on reward transmission). All of these regions are heavily involved in influencing cognitive patterns and perception of both environmental & abstract dynamics. Hyperactivity in these regions is often linked to symptoms of psychosis, anxiety, OCD, and bipolar. What Your Receptors Can Do for You! Your brain has many different ways it maintains homeostasis (chemical balance). It largely does this at the receptor level. When a ligand (molecule such as a drug or neurotransmitter) binds to a receptor, it attaches itself to a certain site on the receptor. A binding site is an area of the receptor where a ligand can attach itself, thus changing the chemical composition of the receptor which modifies its behavior. When a ligand activates a receptor, this is called agonism. For example, THC is an agonist at the CB1 receptor. There are also molecules that can block, or antagonize, a receptor. This means it can knock a previous ligand from a receptor’s binding site, bind to it, and then prevent other ligands from further activating or deactivating it. An inverse agonist is a ligand that both antagonizes and deactivates a receptor, reducing it to its resting state. Anticholinergics like benadryl and scopolamine are good examples of this; they fully deactivate acetylcholine receptors. In order to maintain homeostasis, receptors may deactivate long-term, or downregulate. Downregulation can happen in several ways, but the two I want to focus on are internalization and heteromerization. When a receptor has experienced a certain level of stimulation for a long enough time, it undergoes a process called internalization. This is when the receptor leaves the cell membrane and retreats into the neuron. Here, it can either be metabolized and used to build other receptors (or excreted), or it can be recycled where it’s stored in the cytoplasm until it can be of future use. Heteromerization is a bit more complex; when a receptor heteromerizes, it forms a bond with another receptor. This usually shuts off the transmission of both receptors, and creates a new type of transmission that generally has an effect counterintuitive to the normal behavior of the receptors. It rarely has the exact opposite effect, which means that some irregular stuff can pop up when enough receptors heteromerize. The binding affinity of a molecule is how strongly it’s attracted to the binding site of a receptor. If a molecule has a high binding affinity, it’s strongly attracted to the receptor and is much more likely to occupy the binding site. This is measured as a Ki value, with lower value generally meaning the molecule binds more strongly to the receptor. Ki value does not indicate whether it is an agonist or antagonist, and it does not indicate how strong the effect is on the receptor. Potency is typically measured by EC50, or the concentration at which 50% of the drug’s ceiling effect is reached. A drug’s ceiling is the level at which its primary target receptors are fully occupied by the drug. EC50 is generally measured by mol/L, or moles of the drug per liter of blood. It’s worth mentioning that for many drugs, the dose-response curve (graphed line of the dose with the level of effects it induced) is not linear, so EC50 is not a 100% reliable measure of potency either. The Evolutionary Footprint of Cannabis A ton of people know the basics of how THC works. They know it releases dopamine and serotonin in the reward system. They know CBD makes it less potent. They might even know about cannabinoid receptors. But, as brains often do, they are reaching conclusions about it based on incomplete information. First of all, to set the record straight: the fact that we have cannabinoid receptors does not imply that we are meant to consume Cannabis. These receptors evolved with entirely different molecules in mind: the previously-mentioned anandamide and 2-AG. We named the receptors after the plant, because we discovered the plant’s effects on them before we discovered the ECS. Same reason opioid receptors are called that, despite evolving for the purpose of endorphin transmission (fun fact: endorphin is a portmanteau between ‘endogenous’ and ‘morphine!’). That being said, mammals have likely been consuming Cannabis for millions of years. Many species of mammals are observed eating Cannabis in nature, and Cannabis itself is at least 48 million years old. Our distant ancestors likely consumed this stuff. It’s reasonably safe to say our neurocognition has evolved alongside this plant’s cannabinoids for millions of years. People often know about how the compound largely present in Cannabis is THCa (tetrahydrocannabinolic acid), an inactive variant of THC. To make it psychoactive, it must be decarboxylated (often via heating), which knocks a carbon and oxygen atom off the structure and turns it into THC. This THC can then be consumed orally. Smoking reproduces this process very rapidly, but absorbing into your bloodstream directly from your lungs, instead of drawing out the absorption with a time-consuming liver filtration. The thing is, for the previous 10 million years before cooked meals and handpipes, mammals have been consuming their cannabinoids raw. Not only this, but they’ve been consuming landrace plant matter that contains about 1% THCa and 2-3% CBD. The vast majority of this THCa is metabolized and excreted before ever decarboxylating or hitting your brain. So, for the past 10 million years (minus the past 5 thousand, give or take), the mammalian brain has been adjusting and getting real comfy in this zone of maybe 0.5mg THC / 3mg CBD / 1mg CBG in a healthy hemp meal, absorbed over the course of 3-5 hours by the GI tract. Now, imagine if we suddenly learned how to get the absorption time to under 10 minutes by putting it in our lungs. Imagine if we suppressed the plant’s production of all the cannabinoids except THC (which we elevated 2000%) in the course of 100 years; a time frame 0.00001% that within which we have been co-evolving with it. Imagine if we started extracting that THC to 90% purity and just smoking it like that. You can see how that might go a little poorly perhaps? Why High THC Kinda Really Sucks, and How Cannabinoids Help Each Other Out There are over 140 cannabinoids known to occur within Cannabis, all with slightly varying effects. The ones I’m primarily going to focus on are THC (Δ9-tetrahydrocannabinol), CBD (cannabidiol), and CBG (cannabigerol). THC is an incredibly potent drug, and it has properties similar to those of a lot of different drugs as well. Most of these are exerted downstream from the CB1 agonism. But too much CB1 agonism, or CB1 overstimulation, can result in a whole bunch of really nasty neurocognitive anomalies that can make you real stupid and real crazy. For one, it’ll cause CB1 downregulation, which causes tolerance. In addition to this, THC causes a heteromerization between CB1 and 5ht2a receptors. 5ht2a is a type of serotonin receptor involved heavily in perception, thought, and creativity. This is the receptor psychedelics like psilocybin and LSD agonize to exert their effects. Causing a heterodimer between CB1 and 5ht2a ‘changes the channel’ on the signalling pathway for 5ht2a, thereby deactivating its previous effects. Typically, 5ht2a begins its intracellular signalling pathway by coupling with a protein called Gq, modulating its alpha subunit, and then sending it on its merry way to excite the neuron and induce neuroplasticity. When it’s heteromerized with CB1, it switches to a protein called Gi instead of Gq. Gi also excites neurons, but in a different and creepier way; primarily via cAMP, which is one of the ways dopamine excites neurons. And this would be all well and dandy, except for the fact that 5ht2a and CB1 receptors are expressed really densely in the prefrontal cortex (which can induce obsessive-compulsive characteristics), as well as the basal ganglia (which, over time, can potentially cause GABA interneuron downregulation or even apoptosis in this region; one of the mechanisms by which methamphetamine induces schizophrenia). But this isn’t the only time THC and 5ht2a tango. The CB1-5ht2a induced Gi protein signalling also triggers a signalling pathway called Akt/mTOR via the subunit βγ. This causes remaining standalone 5ht2a receptors to potentiate their own signalling of Gi proteins, but instead activating the inhibitory subunits on these Gi proteins. This causes a potentiation of the pro-hallucinogenic subunits on their usual Gq proteins, which can lead to further symptoms of psychosis. It’s worth mentioning that by ‘symptoms of psychosis,’ I don’t necessarily mean overt delusions and hallucinations, but things like paranoia, intrusive thoughts, avolition (loss of ability to do daily tasks), and disorganized thinking as well. Individuals with cannabis-induced psychotic disorders often present with irregular symptomology, so things like delusions and hallucinations are less frequently present. Causing this rift between different 5ht2a receptors, such a fundamental receptor for neuroplasticity, can also cause fairly scattered and erratic patterns of neuroplasticity across your brain, meaning memories and lessons learned won’t last as long as they should. This can be a fantastic thing until you have to navigate daily life, re-learning the same things again and again. Additionally, THC causes heteromerizations between D1 and D2 dopamine receptors. This inhibits both of their activities and changes the channel to Gq. When a D1-D2 mediated Gq protein goes off to do its business in NAc neurons, it causes a downstream release of dynorphin, an endorphin that’s selective for κ-opioid receptors. This isn’t as fun as it sounds; when κ-opioid receptors are stimulated without accompaniment by μ-opioid stimulation in the NAc, they cause aversion, dysphoria, dread, and derealization causing a downstream uptick of activity in the amygdala. The amygdala gets together with the NAc and stimulates the LHb, which in turn deactivates the mesolimbic pathway and potentiates amygdala transmission. This system of receptors is thought to be heavily involved in panic disorder, PTSD, anhedonia, and dissociative disorders. The most similar drug you might’ve heard of is Salvia divinorum, known for its traumatic, reality-breaking experiences. D1-D2 heteromers are seen at highly elevated levels in schizophrenic subjects. Furthermore, consuming THC alongside tobacco has been shown to potentially increase the activity of FAAH in your cerebral cortex. If you recall, your two major endocannabinoids are metabolized by this enzyme, and raising its activity leads to a faster metabolism of these endogenous pleasure molecules, leading to further dependence on THC. All of that is where CBD comes in. CBD is a negative allosteric modulator (NAM) of CB1 receptors. It has a balancing effect on individual receptors, preventing overstimulation. It has been shown to prevent downregulation of CB1 receptors, and reverse the neurocognitive deficits induced by D1-D2 heteromers. It’s also a NAM of 5ht2a receptors, which reduces the pro-psychotic effects mediated by these receptors, and eventually should (hypothetically) reverse CB1-5ht2a heterodimers. It has also been shown to prevent D1 dopamine receptor internalization. On top of all this, it’s an inhibitor of the FAAH enzyme, which allows endocannabinoids to populate your cortex at long last. This all shows up on the psychological side too; CBD significantly reduces cognitive impairment and psychogenic effects of THC in multiple studies. THC has shown its peak therapeutic potential in clinical trials at a ratio of about 1:1 with CBD. But CBD isn’t entirely without side effects either, unfortunately. Chronic CBD use has been shown to potentially have a sensitizing effect involving norepinephrine. Sensitizing norepinephrine increases symptoms of anxiety, potentially even leading to eventual cardiotoxicity. But that’s where CBG comes in. CBG doesn’t significantly act on cannabinoid receptors at all, as a matter of fact; it’s only called a cannabinoid due to its origins in the Cannabis plant and structural similarity to other cannabinoids. CBG acts as an agonist of α-2a adrenergic autoreceptors. These receptors occur on the presynaptic terminal, acting as a braking function on natural norepinephrine release. This isn’t a pharmacologically perfect fix, as it doesn’t fix the sensitization to norepinephrine, but it does dampen the level of norepinephrine transmission that occurs. Where do Genes Factor In? You’ve likely heard that only those genetically predisposed to mental illness end up developing psychological disorders from cannabis use. This is 100% true, but it’s a loaded statement: a substantial chunk of people are predisposed in some way to a psychotic disorder, even without any family history. Let’s take one gene, HTR2A. This gene encodes the 5ht2a receptor, whose altered activity by THC is thought to be largely responsible for Cannabis-induced psychotic disorders. Hypermethylation of the HTR2A gene is widely seen in schizophrenia patients. THC programs 5ht2a to genetically potentiate itself through the Akt/mTOR pathway, which results in HTR2A methylation. Over 40% of a randomly selected population tested positive for a high-activity HTR2A gene variant called rs6311. This variant is associated with increased risk of schizophrenia, bipolar, OCD, and autism. That’s over 40% of the population that could have increased susceptibility to THC-induced psychological disorders. And that’s 1 of over 200 gene variants & mutations associated with psychotic disorders. It’s entirely true that different people carry different levels of susceptibility to these disorders that can be induced. But there’s a very good chance that the majority of people are susceptible to some degree, regardless of family history, even without showing any symptoms previously. What Now? This article covers only a sliver of what we know about cannabinoid pharmacology, and there is even more we don’t know about THC. But what we do know is that it carries both creative and destructive potential, learning how to minimize its destructive potential is a necessity when it’s being introduced to society en masse. The great thing about pure cannabinoids is, if you’re in the US, they’re extremely cheap. I personally get a 50 gram jar of pure CBD online for about forty dollars, and it lasts me about 2 years at 150-200mg/day. If you’re smoking cannabis flower daily, incorporate at least 100mg of CBD daily into your Weed Diet. If you start to develop some symptoms of anxiety and restlessness after a while, look into CBG. Unless you’re treating chronic illness like migraine or autoinflammatory disorders, you shouldn’t need any cannabinoids beyond the Big Three. If you’re using extracts like dabs/carts/dispos, look into switching to flower. Seriously. Gets you higher in a far more neurologically sustainable way. If you refuse to lose the juice, get on seriously high levels of CBD; I’m talking 200mg+ a day. That shit rots your brain, and that’s an informed opinion, trust. I never even mentioned the fact that most illicit carts & dispos contain THCp, which has all the side effects of THC at about 5x the potency, and 0% CBD, which means all those precious receptors of yours are getting overstimulated as hell. Best of luck on your cognitive odyssey, and have a beautiful night! By Somnesque, click for original post and comments. Sources THC induces d1-d2 heteromerization https://pmc.ncbi.nlm.nih.gov/articles/PMC6971351/ D1-D2 heteromer releases dynorphin in the NAc https://pmc.ncbi.nlm.nih.gov/articles/PMC2978591/ Cannabis use causes elevated expression of CB1-5ht2a heteromers https://pubmed.ncbi.nlm.nih.gov/29294249/ Cannabis tobacco co-use elevates FAAH activity https://pmc.ncbi.nlm.nih.gov/articles/PMC12341708/ CBD reduces D1-D2 heteromer neuroadaptations https://pubmed.ncbi.nlm.nih.gov/31972514/ CBD prevents CB1 downregulation https://www.nature.com/articles/s41386-025-02213-0 CBD inhibits FAAH https://pmc.ncbi.nlm.nih.gov/articles/PMC119890 CBD reduces THC-induced cognitive impairment https://pmc.ncbi.nlm.nih.gov/articles/PMC6820200/ Around 40% of people have rs6311 gene variant https://pmc.ncbi.nlm.nih.gov/articles/PMC4134733/

Not sure if there is a meme topic, but here goes, lets post a meme, welcome to share anything good.

Hi @trichomechaser Welcome back, glad to see you been hard at work. Amazing varities you have and working with amadeadly, top stuff. So your seeds are available through your new site? Sad chapter in cannabis history seeing BnB shut doors as of yesterday, but I believe they will be back with something new.

Hey guys - I know it's quiet around forums these days, but I just wanted to share some of the recent work/hunts I've been doing. Almost 2 years ago I seeded up my mother library with a Headbanger male (Karma Genetics). I had selected him months earlier for his awesome branching and strong stem rub. In the tent were female Rest in Peace (CSI:Humboldt), Le Mans (Swamp Boys), Race Fuel (Archive Seeds), Crazy Hazy (Archive Seeds), Headbanger (Karma), Grease Monkey (Exotic Genetix), Chem 4 x Chem D (CSI:Humboldt), GG4 x Chem D (CSI:Humboldt), and a few others. The goal was just preservation, as I needed to clear my mother room. I hadn't planned to sell any of them. However, after running through the progeny of a few of the crosses I've actually had a few people reach out to grab some and so some are already on the their across the world (pretty awesome). The standout cross I've tested so far was the Rest in Peace x Headbanger (now named Slayer). Slayer is a combination of OG Kush (Ghost OG cut), Chem 91 (SkunkVA cut) and Sour Diesel lineage. I ran through an initial batch and then immediately popped more after flowering them out. Phenotypes range from sour grapefruit and creamy citrus to fuel-forward danker types. Here are some of the finds: I also tested out a few others, but the other other stand out was the GG4 x Chem D (also known as G4D) crossed to the Headbanger. The resulting strain was dubbed GHB, which started out as just a label on my pot, but when smoking her - it also fits the effects. There are some really funky old school chemmy phenotypes in this one. Finally, I also tested some of my Strawberry Fuel. A cross between my Strawberries & Cream cut (currently being run in production by Bushman Jay through Amadeadly/Creme) and Race Fuel (a primarily OG Kush strain by Archive Seeds). I found some real killer stuff in here. I've kept a few cuts around to work with some more. I kept the #3 which was nothing but frosty dank fuel (thanks Race Fuel) and then a sweet fruity variety that turns the terps in Strawberries & Cream up 200%. A few of these are currently available on Biltong and Budz, but with B&B shutting down at the end of this month - I've been setting up Seed Stash for sales to start soon.

Holy bumps... I saw this pop up now and just wanted to share some thoughts because I actually encountered the same exact problem a couple of years ago and I was losing my mind over it. I chatted quite extensively with Bushman Jay about it and got some tips to clean up the mother library but I was never able to get them clean. Eventually, I tossed my entire mother library (years of collecting) and started from scratch - but that resolved all my problems. I haven't had the problem again since, so I do believe it is a pathogen. It seems closest to fussarium, if not fussarium itself. And the process tended to follow: -> Take Clone Off Visibly Healthy Mother -> Cut looks good in the dome until day 3 or 4 -> Stems start to rot and tops begin to brown -> Clones become mushy and collapse A similar effect can occur when there isn't enough light in the cloning area, and then the plant starts to brown and die from the top. But the aggressive symptoms in the OP's post makes me pretty confident the issue lay with the mother stock.

I started with a 70cm tent, a 150W LED, and an inline fan just like Naughty.Psychonaut suggested. For finishing touches like a quality glass piece or a small water pipe, I personally use SmokeDay.com for fast and discreet shipping. Keeping gear simple and solid, not the cheapest, saved me headaches and money.

Hi @Psychotic_Cheez, welcome to 420sa. Another good ingredient to add to aloe vera, is cinnamon. Good as anti fungal and anti bacterial.

I have to ask,are you mistaken end of stem root rot for callouses?Both look the same but with end of stem root rot,the end is soft and mushy,as oppose to callouses,which is also brown but firm.2) I use Aloe vera gel,instead of a powder.In one instance,I used a humidity dome for the first 7 days,then the internet told me to open the vents slightly.When i did,all my clones fell over flat.So I don't open the vents anymore.

This is a social media post, getting a bit of attention, I think the narrative needs to change, with inclusivity, and small thank you to the future thinking growers/breeders who saved something that is hardly found in South Africa. Quiet sad to see us South Africans looking at Durban Poison stolen from our shores, almost 50 years after the fact. I think we need to thank these breeders for coming here and saving, preserving our genetics. If it was not for them turning it into a cup winning house hold brand name, who would have done that. I am sure that these breeders paid a small fortune for the seeds they purchased from farmers, seeded weed, being foreigners. Nothing was stolen, and yes if you dont do something with your strains, business will take it over. Whats your take? I do think that some how from heritage, South Africans should have a right to the name Durban poison.

A friend of mine called me this morning saying that they found a joint in their daughters school bag, and they asked my advice. A difficult topic to discuss, since I am not a parent and the legality of cannabis. The child did explain to the parent that they are using cannabis for their anxiety they face, and not using it for recreational use, and they feel cannabis is far better than the prescription drugs they have been given by a doctor. i am not to sure what the answer is, but wondering if any other parents have experienced this type of situation and what the outcome was.

Volkswagen is looking to industrial hemp as a sustainable alternative to leather and petroleum-based synthetic materials, potentially putting hemp-based interiors into production vehicles from 2028. The automotive industry is undergoing a major transformation. Electric vehicles, renewable energy and recyclable components are changing the way cars are designed and manufactured. Now, one of the world's biggest automotive manufacturers is looking at an unlikely material to help reshape the car interior: industrial hemp. Volkswagen has partnered with German start-up Revoltech GmbH to develop a new hemp-based surface material that could be used in Volkswagen vehicles from 2028. The development represents an important step in the growing use of hemp as an industrial material, moving the plant far beyond its traditional associations with textiles, food and cannabis. From leather to hemp Volkswagen's project is focused on developing an alternative to imitation leather rather than simply replacing traditional animal leather with another synthetic material. The material, called LOVR™, stands for Leather-free, Oil-free, Vegan and Residue-based. It is being developed using industrial hemp fibres and a fully bio-based adhesive. Volkswagen says the material is made from residues generated by the regional hemp industry, including hemp cultivated for the food industry. That approach is particularly interesting because the hemp being used is industrial hemp, not high-THC cannabis. Industrial hemp varieties can be cultivated for fibre, seeds, food and other industrial applications. The hemp fibres are processed into a single-layer surface material designed specifically for automotive applications. The result is intended to provide the appearance and functionality required for vehicle interiors while reducing dependence on conventional petroleum-based materials. Why is Volkswagen interested in hemp? Modern vehicle interiors contain a surprising amount of synthetic material. Seats, door panels, dashboards, headliners and other surfaces can involve plastics, synthetic leather, foams, adhesives and composite materials. Finding alternatives is therefore an important part of reducing the environmental footprint of vehicle manufacturing. Hemp has several characteristics that make it attractive for industrial applications. The plant produces strong fibres and can be used to create a wide range of materials. In the Volkswagen-Revoltech project, the emphasis is particularly interesting because the raw material can come from hemp-processing residues that might otherwise have limited value. Rather than growing a crop specifically to manufacture car seats, the concept aims to make use of material already generated by the hemp industry. Volkswagen says the material can also be manufactured using existing industrial production facilities, potentially allowing it to be scaled without building an entirely new manufacturing infrastructure. A material designed for the circular economy Perhaps the most exciting aspect of the project is what happens to the material at the end of a vehicle's life. According to Volkswagen, the hemp-based material is designed to be recyclable or compostable once it reaches the end of its useful life in an automobile. This is significant because the automotive industry is increasingly looking beyond simply reducing emissions during vehicle operation. Manufacturers are also examining the environmental impact of raw materials, manufacturing, vehicle use and disposal. A material that can potentially return to a biological cycle rather than becoming another difficult-to-recycle composite could therefore have advantages beyond its initial production. Volkswagen is not simply replacing animal leather It would be easy to describe the project as "Volkswagen replacing leather with hemp", but that is not quite what the company has announced. Volkswagen's current development is specifically positioned as a substitute for imitation leather, while the company describes the hemp material as a leather alternative for future interiors. That distinction matters. Synthetic leather, often called vegan leather or leatherette, can be made from petroleum-derived plastics such as polyurethane or PVC. While these materials avoid animal products, they do not necessarily solve all of the environmental problems associated with conventional synthetic materials. LOVR is intended to offer another pathway: a bio-based, vegan and potentially circular material derived from industrial hemp. Could hemp become a major automotive material? Volkswagen's announcement could have implications well beyond Volkswagen itself. The global automotive industry is constantly looking for materials that are lighter, more sustainable, cost-effective and scalable. If hemp-based materials can meet automotive requirements for durability, abrasion resistance, appearance, safety, temperature stability and long-term performance, manufacturers could potentially use them in everything from seating surfaces to door panels and other interior components. Volkswagen says the material has already received positive feedback in customer surveys and that potential vehicle applications are being investigated with its development teams. The company has identified 2028 as a potential starting point for use in vehicle projects. However, this does not mean every Volkswagen vehicle will have hemp interiors in 2028. The company's announcement describes 2028 as a potential introduction point for the technology rather than a commitment to eliminate conventional materials across its entire vehicle range. Hemp's automotive history is already established Interestingly, hemp is not completely new to the automotive industry. Hemp fibre has been used in automotive composite materials for years, particularly in Europe. Natural fibres can be incorporated into panels and other components because they can offer useful strength-to-weight characteristics while reducing reliance on conventional petroleum-derived materials. What makes the Volkswagen-Revoltech project different is its focus on creating a visible surface material that can serve as an alternative to leather or synthetic leather. That brings hemp directly into one of the most noticeable areas of a vehicle: the interior. Imagine opening the door of a future Volkswagen and sitting on a material that looks and feels similar to premium leather, but is made primarily from agricultural hemp residues. That is the possibility Volkswagen is now investigating. The bigger opportunity for industrial hemp The Volkswagen project also demonstrates why the future of hemp may extend far beyond CBD, food and traditional textiles. Industrial hemp can potentially supply raw materials for construction, packaging, insulation, textiles, bioplastics, composites and automotive components. The automotive sector is particularly important because it operates at enormous scale. If a material is adopted by a major global manufacturer, demand for its raw materials could increase dramatically. That could create new opportunities for farmers, processors and manufacturers involved in the industrial hemp supply chain. It also demonstrates the potential value of hemp waste and by-products. Instead of viewing agricultural residues as waste, companies can increasingly treat them as valuable feedstocks for new products. What happens next? Volkswagen and Revoltech still have development work to complete before the material becomes a mainstream automotive product. Automotive materials must satisfy demanding requirements. They need to withstand years of use, temperature changes, sunlight, friction and repeated cleaning. They also need to meet strict safety and manufacturing requirements. The fact that Volkswagen is investigating the material for potential vehicle projects from 2028 nevertheless represents a significant milestone. The company says the material can be produced using existing industrial plants, which could help with scalability if testing and development are successful. The road to 2028 The move towards hemp-based vehicle interiors is part of a much larger transformation taking place in manufacturing. For decades, the automobile industry has relied heavily on petroleum-derived plastics, synthetic fabrics and animal-based materials. Today, manufacturers are looking for alternatives that can reduce environmental impacts without compromising quality. Hemp offers an intriguing combination of properties: it is renewable, produces useful fibres, can generate valuable agricultural by-products and can potentially be incorporated into recyclable or compostable materials. Volkswagen's collaboration with Revoltech demonstrates that industrial hemp is increasingly being considered not simply as an agricultural crop, but as a high-value industrial feedstock. By 2028, Volkswagen could potentially be putting hemp-based surface materials into some of its vehicles. That does not mean the end of leather or synthetic materials overnight. But it could mark the beginning of a much bigger shift. The next time you sit inside a Volkswagen, the material covering the seat or door panel could have started life not in a leather tannery or petrochemical plant, but in a field of industrial hemp. And that could be one of the most interesting developments yet in the modern hemp revolution.

Shot Cuzzy, It’s great to be back in the game. The level of info & tech now is just crazy. Digging the site… still miss weed.co.za. Legge

Hey @Woz Just firing off a welcome note to you, its been over 15 years and good to see you getting back into cannabis growing. Welcome to 420sa.co.za, its a lekker site with a growing future.

Hi, I live in Durban KZN, I am looking to swap 2x 600w ballasts with Reflectors and 600w HPS globes for atleast a 150cm x 150cm grow tent and possibly 2x extractors, inlet + outlet. You can connect with me via WhatsApp 072 638 0384 Thanks Brandon

Great selection of product and delivered within 24 hours. Many thanks.

That’s a solid point. A lot of people still only look at THC and CBD, but the cannabinoid profile really changes the experience and therapeutic potential. THC-P definitely opened some eyes because of how strongly it interacts with CB1 receptors, although the potency also means people need to be careful with dosage and tolerance. I also think one of the most overlooked things is how cannabis works as a whole-plant medicine rather than just isolated cannabinoids. The entourage effect between cannabinoids, terpenes, flavonoids, and minor compounds seems to make a huge difference for pain, inflammation, anxiety, sleep, and even mood regulation. Sometimes a balanced flower with THC, CBD, CBG, and the right terpene profile works better than blasting high THC alone. CBD is probably still the best entry point for most people because of the safety profile and research backing it, but there’s growing interest in cannabinoids like CBN for sleep, CBG for inflammation and gut health, and THCV for appetite and focus. The science is finally catching up to what a lot of patients and growers have been saying for years. Do you think the future of medical cannabis is going to move more toward personalized cannabinoid + terpene combinations instead of just “high THC” products? And have you noticed certain terpene profiles working better for chronic pain compared to others?