Cannabis: Pro Or Anti-metabolic?

[Jessie]

I've become more anti-cannabis since the last time I posted on this thread. Personally, I don't think it would be wise for anyone with hypothyroidism to use this product. If you're dealing with any sort of hyperventilation or low CO2 problems, then using cannabis will just make the situation worse.

If you're healthy, then perhaps it won't cause you harm. I do still think cannabis in it's raw state is probably anti-inflammatory, but it's not psychoactive. And thus probably useless for the vast majority of people interested in cannabis, lol.

Also, even raw cannabis may have goitrogens or other anti-thyroid properties in it, we don't really know. But raw greens usually have stuff like that in them.

 

[MadnessofMemory]

There was a time when I vaped small amounts of cannabis most nights for around a year.

It was prometabolic for me. I became significantly leaner, more vascular, and retained muscle mass, all while eating more. Marijuana can increase insulin sensitivity and blunt the stress response.

My favorite aspect of using was the total elimination of post-workout stress and decreased social anxiety. Since I only vaped small amounts at night, the next day after using, when it wore off, was when I felt these beneficial effects.

But, I still don’t recommend it. After a year of consistent use, my libido gradually vanished and my mood was consistently flat and dull. I also became slightly paranoid over small things. Even when I wasn’t under the influence, life felt like a dream. All symptoms of low dopamine.

It’s very difficult (probably impossible) to not run into dopamine issues with frequent marijuana use. I think just about anyone will run into mental issues if they consistently use it long enough.

 

[Cloudhands]

There was a time when I vaped small amounts of cannabis most nights for around a year.

It was prometabolic for me. I became significantly leaner, more vascular, and retained muscle mass, all while eating more. Marijuana can increase insulin sensitivity and blunt the stress response.

My favorite aspect of using was the total elimination of post-workout stress and decreased social anxiety. Since I only vaped small amounts at night, the next day after using, when it wore off, was when I felt these beneficial effects.

But, I still don’t recommend it. After a year of consistent use, my libido gradually vanished and my mood was consistently flat and dull. I also became slightly paranoid over small things. Even when I wasn’t under the influence, life felt like a dream. All symptoms of low dopamine.

It’s very difficult (probably impossible) to not run into dopamine issues with frequent marijuana use. I think just about anyone will run into mental issues if they consistently use it long enough.

well ive been smoking almost daily for the past 10 years give or take a few breaks here or there and i dont have any issues

 

[Warrior]

Its an odd herb, for sure but there are a lot of variables at play when it comes to your own system as well as type and methods of consumption.

it calms the mind but stresses the body because if you have good embodied awareness you'll notice how it activates your kidneys/adrenals when it kicks in. This is also the reason why lifelong smokers suddenly toke one day and find themselves a paranoid wreck and can't smoke again as they've damaged their endocrine system by overstimulation.

Metaphysically it pulls down your dreamworld energy to Earth which is what accounts for the altered sleep cycle and increased creativity with a commensurate release of physical tension. It also induces Alpha brainwaves which are focused on the present and thus healing. Same as being in the zone when exercising and thus can be used as a springboard for higher states of awareness by using it to marshal your perception as this was its role originally when mixed with various other herbs for the adepts to create relaxed focus.

CBD on the other hand is the good twin and well worth looking into as it won't provide a high, per se, but its health benefits are immense. I do suspect a lot of the issues I've outlined in terms of weed are due to the CBD levels being bred out of it as the natural ratios/terpenes are out of whack these days. That and the lack of sunlight means the plant doesn't get the correct information spectrum during development which is all interlinked as well as the chemicals they dump in along with improper flushing.

 

[Cloudhands]

Its an odd herb, for sure but there are a lot of variables at play when it comes to your own system as well as type and methods of consumption.

it calms the mind but stresses the body because if you have good embodied awareness you'll notice how it activates your kidneys/adrenals when it kicks in. This is also the reason why lifelong smokers suddenly toke one day and find themselves a paranoid wreck and can't smoke again as they've damaged their endocrine system by overstimulation.

Metaphysically it pulls down your dreamworld energy to Earth which is what accounts for the altered sleep cycle and increased creativity with a commensurate release of physical tension. It also induces Alpha brainwaves which are focused on the present and thus healing. Same as being in the zone when exercising and thus can be used as a springboard for higher states of awareness by using it to marshal your perception as this was its role originally when mixed with various other herbs for the adepts to create relaxed focus.

CBD on the other hand is the good twin and well worth looking into as it won't provide a high, per se, but its health benefits are immense. I do suspect a lot of the issues I've outlined in terms of weed are due to the CBD levels being bred out of it as the natural ratios/terpenes are out of whack these days. That and the lack of sunlight means the plant doesn't get the correct information spectrum during development which is all interlinked as well as the chemicals they dump in along with improper flushing.

i agree with a lot of this. Part of why i love weed is because it makes me more sensitive to exercising and other activities.
Some people can handle being high, others cant. Its like if a mouse walked up to you. Some people scream, others find it cute, so wether or not something elicits a "stress response" (adrenal, cortisol, etc) is partially dependant on the perception/personality of the user. Same with all psychotropic substances. Lsd can be both lifechanging in a positive or negative way. For me im so used to being stoned no one can ever tell. I was even majoring in mathematics for a while prepandemic while smoking the most i ever have. Maybe im a freak of nature tho, in general i experience low anxiety, and smoking cannabis just helps me remain a wizard amongst sheep

 

[MadnessofMemory]

well ive been smoking almost daily for the past 10 years give or take a few breaks here or there and i dont have any issues

I hear this so often from smokers it might as well be a cliche.

 

[Sapien]

A single use can help you get out of a rut, think out of the box, solve problems, motivate you etc. (like once a year for example). Long term continuos use will harm the brain and can bring your dopamine out of whack and can cause demotivation and apathy.

THC is neurotoxic, it releases PUFA in the brain, elevates prostaglandins, and calcifies braincells. Vitamin E and Aspirin can help block some of the damage if you decide to consume it.

(PDF) Effects of Cannabis Use on Human Behavior, Including Cognition, Motivation, and Psychosis: A Review

PDF | With a political debate about the potential risks and benefits of cannabis use as a backdrop, the wave of legalization and liberalization... | Find, read and cite all the research you need on ResearchGate

www.researchgate.net

There is both preclinical and clinical evidence supporting the view that cannabis use is associated with an amotivational state. In rhesus monkeys, heavy chronic cannabis use or administration has been found to dampen motivation, as measured on progressive ratioand conditioned position responding operant tests.36 There is preliminary laboratory evidence supporting an association between reduced motivation for reward-related behavior in cannabis users compared with control individuals.37 Because these findings appear to be related to repeated doses of THC, it is likely that reduced motivation is one pathway to impaired learning, as THC can disrupt reward-based learning.38 In support of this theory, cannabis users exhibit reduced striatal dopamine synthesis capacity,39 with an inverse relationship to amotivation. Inasmuch as dopamine signaling sustains motivation,40 impaired dopamine synthesis could underlie the amotivational state in cannabis users. Similarly, imaging investigations documented decreased reactivity to dopamine stimulation in cannabis users that was associated with negative emotionality and that would also contribute to reduce engagement in non–drug-related activities.41

Hippocampal Neurotoxicity of Δ9-Tetrahydrocannabinol

Marijuana consumption elicits diverse physiological and psychological effects in humans, including memory loss. Here we report that Δ9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, is toxic for hippocampal neurons. Treatment of cultured neurons or hippocampal slices...

www.jneurosci.org

THC is toxic for cultured hippocampal neurons​

To determine whether THC is neurotoxic and to elucidate mechanisms for toxicity, we examined its effect on the viability of cultured primary hippocampal neurons from neonatal rats (Fig.1). Survival of hippocampal neurons was monitored as a function of THC concentration and time after treatment using the MTT tetrazolium salt [3,(4,5-dimethylthiazol-2-yl)2,5-diphenyl-tetrazolium bromide] assay as a measure of cell viability (Hansen et al., 1989). Concentrations of THC as low as 0.5 μm were toxic to hippocampal neurons, and the rate of neuron death increased with THC concentration (Fig. 1A,B). For example, 50% of the neurons were killed within 3 hr of treatment with 10 μm THC or 6 d after exposure to 1.0 μm THC. The lower doses used are comparable to THC concentrations measured in human plasma after consumption of a single marijuana cigarette (Chiang and Barnett, 1984). THC concentrations in the brain may be even higher after smoking marijuana, because THC is lipophilic (Thomas et al., 1990) and readily crosses the blood–brain barrier. Blood levels of THC reach a maximum shortly after smoking marijuana and decline rapidly thereafter. However, even a 15 min exposure to THC was toxic for cultured hippocampal neurons (Fig.1C). Cultured cortical neurons were much less sensitive to THC than hippocampal neurons (data not shown). Because THC is lipophilic, some of its effects may be attributable to interactions with membrane lipids rather than receptor activation. However, SR141716A, an antagonist of CB1 receptors (Rinaldi-Carmona et al., 1994), completely inhibited THC-induced neuron death (Fig.2). These data indicate that THC toxicity is mediated through CB1 receptors and not caused by nonspecific interactions with the membrane lipid phase.

THC increases intracellular Ca2+ in hippocampal neurons​

Intracellular free Ca2+([Ca2+]i) is modulated by activation of cannabinoid receptors (Mackie and Hille, 1992; Mackie et al., 1993; Shen et al., 1996; Sugiura et al., 1996) and prolonged increases in [Ca2+]i are generally toxic (Trump and Berezesky, 1995; McConkey and Orrenius, 1996). Consequently, the effects of THC on [Ca2+]i were analyzed by fluorescent imaging using the Ca2+ fluorophore fura-2 AM (Fig.4). Addition of 10 μm THC to hippocampal neurons caused a delayed increase in [Ca2+]i that reached a maximum at 90 min (Fig. 4A). Treatment of neurons with 2 μm THC also increased [Ca2+]i but with slower kinetics (data not shown). When cells were treated with THC without extracellular Ca2+ and in the presence of EGTA, there was no significant increase in [Ca2+]i (Fig.4A). Addition of extracellular Ca2+ at the end of this incubation led to an instantaneous rise in [Ca2+]i, suggesting that a plasma membrane channel is activated by THC. Lanthanum, a potent blocker of Ca2+ channels, completely inhibited this rise in [Ca2+]i (Fig. 4B). THC-induced Ca2+ increases were also inhibited by the cannabinoid receptor antagonist SR141716A (Fig. 4C). Because stimulation of CB1 receptors increased [Ca2+]i, we examined the effect of chelating Ca2+ on THC neurotoxicity. Chelation of extracellular Ca2+ with EGTA did not rescue hippocampal neurons from THC toxicity (Fig.5). This suggests that THC neurotoxicity is not dependent on increases in intracellular Ca2+, because THC-stimulated increases in [Ca2+]i required extracellular Ca2+. This distinguishes THC neurotoxicity from other forms of toxicity that are triggered by increased [Ca2+]i.
...

THC neurotoxicity is abrogated by vitamin E as well as inhibitors of phospholipase A2 and cyclooxygenase​

Activation of cannabinoid receptors can stimulate phospholipase A2 (PLA2), which catalyzes release of arachidonic acid (Reichman et al., 1988; Audette et al., 1991;Shivachar et al., 1996), the substrate for several major pathways. One branch, catalyzed by cyclooxygenases (COX), generates prostanoids, prostaglandins, and thromboxanes. Another pathway catalyzed by lipoxygenases produces leukotrienes. Both pathways generate free radicals (Wei et al., 1981; Pourcyrous et al., 1990; Yamamoto, 1991;Lafon-Cazal et al., 1993) that can lead to lipid peroxidation and cell death. Preincubation with quinacrine, an inhibitor of PLA2, partially protected neurons from THC-induced cell death (Fig. 5). Neurons were also protected by dexamethasone (data not shown), which induces the expression of annexin I (Flowers, 1988). Annexin I inhibits PLA2 (Croxtall et al., 1995) and the expression of COX (Fu et al., 1990). Indomethacin and aspirin, inhibitors of COX, completely protected neurons from THC, whereas NDGA, a lipoxygenase inhibitor, was not protective (Fig. 5). Because COX generates reactive oxygen species (ROS), which can cause cell death by stimulating the oxidation of lipids, proteins, and nucleic acid (Yamamoto, 1991; Troy and Shelanski, 1994; Greenlund et al., 1995;Simonian and Coyle, 1996), we examined the effect of antioxidants on THC-induced neuron death. Vitamin E completely protected neurons from THC (Fig. 5). These data suggest that THC may kill neurons by stimulation of the cyclooxygenase pathway with generation of ROS.
...

THC stimulates the release of arachidonic acid from primary hippocampal neurons​

If THC neurotoxicity is attributable to activation of the PLA2–COX pathway in neurons, THC should stimulate arachidonic acid release. Treatment of cultured hippocampal neurons with THC induced the release of arachidonic acid from cultured hippocampal neurons, which was completely blocked by SR141716A, the CB1 receptor antagonist (Fig. 6). The kinetics for arachidonic acid release were dependent on THC concentration. For example, the rate of arachidonic acid release was three times faster in the presence of 10 μm THC (Fig.6B) compared with 3.5 μm THC (Fig.6A). Interestingly, pertussis toxin did not affect THC-induced increases in arachidonic acid release, suggesting that the enhancement of arachidonic acid release by THC is not mediated through Gi coupling. To determine whether exogenously added arachidonic acid affects neuron viability, primary hippocampal neurons were treated with increasing concentrations of arachidonic acid and monitored for cell viability. Exogenous arachidonic acid at 10 μm killed 100% of the cultured hippocampal neurons 24 hr after exposure (data not shown). However, it is unlikely that free arachidonic acid added to the outside surface of a cell is comparable to arachidonic acid release by activation of PLA2 caused by receptor stimulation.
...

THC induces cell body shrinkage, nuclear condensation, and genomic DNA strand breakage in cultured hippocampal neurons​

To determine whether THC induces morphological changes in cultured hippocampal neurons, we examined its effects on cell morphology and genomic DNA integrity using TUNEL for in situ DNA labeling (Gavrieli et al., 1992). Neuron cell bodies were lightly counterstained (Fig. 7A), whereas DNA strand breaks were detectable as small dark bodies in culture (Fig.7B,C). THC increased DNA strand breaks that were evident within days after treatment with 2 μm THC (Fig. 7B) or within 6 hr after treatment with 10 μm THC (Fig. 7C). In addition, THC caused a marked decrease in cell body size relative to control cells.

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On the basis of the data presented in this study, we conclude that binding of THC to cannabinoid CB1 receptors in hippocampal neurons leads to neuronal death. THC is neurotoxic at concentrations as low as 0.5–1.0 μm, which are comparable to THC levels measured in human plasma after consumption of marijuana cigarettes. Although THC neurotoxicity was unaffected by Ca2+ chelators and activators of adenylyl cyclase, it was abated by inhibitors of PLA2 and completely blocked by aspirin and indomethacin, inhibitors of COX. This suggests that activation of PLA2 by THC may contribute to increases in arachidonic acid. Because protection by quinacrine was only partial, other mechanisms may contribute to the arachidonic acid release. For example, THC may also increase intracellular arachidonic acid by inhibition of arachidonic acid acylation (Reichman et al., 1991). We hypothesize that THC-induced neuron death is triggered by a signal transduction cascade that increases arachidonic acid and activates COX with the formation of ROS (Fig. 9). THC enhancement of arachidonic acid release from cultured neurons and protection of neurons from THC by vitamin E supports this hypothesis.

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Personally I don't think it's worth it anymore. I don't remember the last time I smoked, but when I am really content and have good nutrition and good digestion I can reach a similar state of creativity, I rather focus on that.

great post thank you so much for taking the time. Tremendous value to me in my research on cannabis