Cannabis: Pro Or Anti-metabolic?

charlie

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Another short update: Almost all the water weight I dropped since quitting weed has returned, minus about two or three pounds. I was undereating for a while so the difference was tissue loss. I don't feel any better or worse though I will say my sleep quality was better with cannabis. Maybe cannabis only becomes harmful when used throughout the day while using it just once at night has little effect on the metabolism?

Why isn't this guy banned already? He's obviously a bot.
Well now I'm embarrassed, having replied to a bot. Hopefully it found its way over to the other Ray Peat message board where it belongs. Anyway, you said you find cannabis pro-metabolic. How often do you use it?
 
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Thought I'd update this thread after having labs done while using cannabis multiple times a week. My testosterone came back at 823ng/dl. The reference range has the upper boundary at 850ng/dl which seems lower than the reference ranges I've seen in the past. Total estrogen levels were 107pg, well within the normal range of 60pg to 190pg. I could lower my estrogen further but every time I've tried exemestane I felt lifeless.

The last time I had labs drawn was at the age of 24. Back then my testosterone was at ~700 at 190lbs (86kg) height 6ft 1in (185cm). I was 145lbs at the most recent blood drawing and coming off a couple of months of severe carb/calorie restriction which I thought would have surely tanked my test levels.

The only thing that was messed up was my shbg, double the top end of the range, which was likely due to the carb and calorie restriction.

I'm willing to conclude that cannabis has little impact on hormonal levels with prolonged usage. Of course, what I've written is anecdotal, but it's in line with a recent European study that I read that showed frequent cannabis users had significantly higher test levels than nonusers. I'm making decent progress rebuilding my lost muscle tissue too. It surely isn't hurting my workout recovery as I sleep incredibly well with it and wake up energized, ready to take on the day.
 

Jing

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The stoners I knew in the past were all of very slight build too. Perhaps heavy use can promote muscle loss? Not sure how this would tie in to its effect on the metabolism though.
I don't think it promotes muscle loss it's just heavy stoners are less likely to use their muscles and they don't really eat that much.
 
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I don't think it promotes muscle loss it's just heavy stoners are less likely to use their muscles and they don't really eat that much.
You're most likely correct. I can't see heavy stoners working up the motivation to lift weights, or do much of anything for that matter. I am convinced that there are no real negative effects, hormonal or otherwise, with moderate use. Heavy use or being stoned all day every day is another matter entirely.

And in case anyone was wondering, no I did not lose around 40 pounds (mostly muscle) as a result of cannabis use as I wasn't using it during that time. It's a long story which I don't have time to relay now but I will later if y'all are interested.
 

pro marker

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i smoked once when i was 17 and i got severe derealization that i havent recovered from 6 years later. life is unlivable and everything feels like a dream. just putting this out there incase anybody is considering trying it. please do not it is not worth the risk. there are thousands of people just like me that got it from trying it once. dont do it. check out the many forums dedicated to dpdr.
 
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i smoked once when i was 17 and i got severe derealization that i havent recovered from 6 years later. life is unlivable and everything feels like a dream. just putting this out there incase anybody is considering trying it. please do not it is not worth the risk. there are thousands of people just like me that got it from trying it once. dont do it. check out the many forums dedicated to dpdr.
Dang, I'm sorry to hear that. I experienced derealization a few times but it was from clenbuterol. Only lasted a few minutes but it was disturbing. I can't imagine living with that sensation.

If you haven't already, you ought to create a thread on the topic to see if anyone here has dealt with and recovered from dpdr. Surely it can be overcome. Best of luck to you.
 

Goat-e

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Thought I'd update this thread after having labs done while using cannabis multiple times a week. My testosterone came back at 823ng/dl. The reference range has the upper boundary at 850ng/dl which seems lower than the reference ranges I've seen in the past. Total estrogen levels were 107pg, well within the normal range of 60pg to 190pg. I could lower my estrogen further but every time I've tried exemestane I felt lifeless.

The last time I had labs drawn was at the age of 24. Back then my testosterone was at ~700 at 190lbs (86kg) height 6ft 1in (185cm). I was 145lbs at the most recent blood drawing and coming off a couple of months of severe carb/calorie restriction which I thought would have surely tanked my test levels.

The only thing that was messed up was my shbg, double the top end of the range, which was likely due to the carb and calorie restriction.

I'm willing to conclude that cannabis has little impact on hormonal levels with prolonged usage. Of course, what I've written is anecdotal, but it's in line with a recent European study that I read that showed frequent cannabis users had significantly higher test levels than nonusers. I'm making decent progress rebuilding my lost muscle tissue too. It surely isn't hurting my workout recovery as I sleep incredibly well with it and wake up energized, ready to take on the day.

Very interesting and correlates with my experience as well. I only started using cannabis several years into my Peat journey and it helped fix some long term stomach inflammation which NOTHING over twenty years (including four of 'Peating') were able to resolve. I read about people using cannabis for Chron's etc and after much debate decided to try it. Very glad I did, I also discovered it got rid of three-day migraines which again nothing else could touch. I vape a small amount at night and it helps promote sleep and feels like a stabilising substance to me. I've more muscle mass than I've ever had in my life so it's not hurting that either.

Where did you find the study you mentioned, I'd like to read it if possible?
 
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managing

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i smoked once when i was 17 and i got severe derealization that i havent recovered from 6 years later. life is unlivable and everything feels like a dream. just putting this out there incase anybody is considering trying it. please do not it is not worth the risk. there are thousands of people just like me that got it from trying it once. dont do it. check out the many forums dedicated to dpdr.
A couple of things here. First off, this is a great argument for legalization. Not sure whether your's was legally obtained or not but in the illicit trade people alter it with all kinds of things to make "customers" feel like they are getting some kind of special high.

Next, purely by chance and circumstance, I was 23 when I tried it the first time. I am glad, because since then much research has established that the still developing brain is affected and changed by cannabis. Nobody has proven that this change is bad--or that it is not. So I think the most prudent course of action is to not use cannabis until 21 or older.

I agree with @Randle Cyclist that you should create a thread asking for others thoughts and feedback.
 

pro marker

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A couple of things here. First off, this is a great argument for legalization. Not sure whether your's was legally obtained or not but in the illicit trade people alter it with all kinds of things to make "customers" feel like they are getting some kind of special high.

Next, purely by chance and circumstance, I was 23 when I tried it the first time. I am glad, because since then much research has established that the still developing brain is affected and changed by cannabis. Nobody has proven that this change is bad--or that it is not. So I think the most prudent course of action is to not use cannabis until 21 or older.

I agree with @Randle Cyclist that you should create a thread asking for others thoughts and feedback.

it was bought on the street. i remember it having weird orange balls in it. the two other people who smoked it were fine and didnt feel weird at all they said.
 
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Where did you find the study you mentioned, I'd like to read it if possible?
I read it a few months ago but unfortunately I did not bookmark it as I wasn't really planning on updating this thread until I had hard data. I believe this is the one:

The effect of tetrahydrocannabinol on testosterone among men in the United States: results from the National Health and Nutrition Examination Survey

The following two studies also reach the same conclusion but the authors of the Danish one were reluctant to attribute the slightly higher test levels solely to cannabis as they weren't able to exclude cigarette smokers:

Association Between Use of Marijuana and Male Reproductive Hormones and Semen Quality: A Study Among 1,215 Healthy Young Men

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Cloudhands

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Thought I'd update this thread after having labs done while using cannabis multiple times a week. My testosterone came back at 823ng/dl. The reference range has the upper boundary at 850ng/dl which seems lower than the reference ranges I've seen in the past. Total estrogen levels were 107pg, well within the normal range of 60pg to 190pg. I could lower my estrogen further but every time I've tried exemestane I felt lifeless.

The last time I had labs drawn was at the age of 24. Back then my testosterone was at ~700 at 190lbs (86kg) height 6ft 1in (185cm). I was 145lbs at the most recent blood drawing and coming off a couple of months of severe carb/calorie restriction which I thought would have surely tanked my test levels.

The only thing that was messed up was my shbg, double the top end of the range, which was likely due to the carb and calorie restriction.

I'm willing to conclude that cannabis has little impact on hormonal levels with prolonged usage. Of course, what I've written is anecdotal, but it's in line with a recent European study that I read that showed frequent cannabis users had significantly higher test levels than nonusers. I'm making decent progress rebuilding my lost muscle tissue too. It surely isn't hurting my workout recovery as I sleep incredibly well with it and wake up energized, ready to take on the day.
Yoo have you thought about this or changed your mind at all? Im currently trying to convince myself that weed either is or isnt dangerous and would love some feedback
 
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Nope, I haven't given it much thought though I did take a break for few weeks earlier this year without any noticeable benefits. I will continue to use it at night for pain relief as long as I have sciatica flare ups. What I have noticed is that there seems to be some kind of reverse tolerance at play. I'm requiring less and less to achieve the desired effects. Just one small hit from my vaporizer every night and I'm golden. It no longer lowers my body temperature either. I'm as lean as ever so it's not harming my body composition. I ought to have my T levels checked again this year but I feel that they're probably within the same range as last year.

It's become a bit cliche but I believe that the dose indeed makes the poison. I doubt the amounts I use are harmful. I just measured out what I vaporize every evening and it comes out to be just under 40mg of bud which means I am consuming under 8mg of THC every night assuming its potency is around 20%. However, I am curious as to why I have a reverse tolerance when most people experience just the opposite.
 

boris

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Yoo have you thought about this or changed your mind at all? Im currently trying to convince myself that weed either is or isnt dangerous and would love some feedback

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.



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


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.

.....
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.




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.
 
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cjm

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You can counter the pounding/racing heart with a few milligrams of lidocaine. (It's a "peaty" substance and accompanies cannabis very well.)

This is a really good suggestion -- I can confirm it works for this exact stated purpose. I've been sipping on an 8 ounce bottle of 200 mg total lidocaine over the course of the day the past couple days. Just a sip (~20 mg) works for weed/smoking-induced anxiety (it works for nicotine vaping as well). I've also noticed it numbs the throat slightly and prevents irritation from the hot smoke.
 

Cloudhands

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This is a really good suggestion -- I can confirm it works for this exact stated purpose. I've been sipping on an 8 ounce bottle of 200 mg total lidocaine over the course of the day the past couple days. Just a sip (~20 mg) works for weed/smoking-induced anxiety (it works for nicotine vaping as well). I've also noticed it numbs the throat slightly and prevents irritation from the hot smoke.
i smoke cannabis a LOT and heres what i think about doing it in a prometabolic fashion.

1)concentrates are better than flower because they contain less plant material
2) dont smoke strains that have any amount of catpiss smell. this is ammonia and will increase no2 production a lot.
3) lots of vitamin E, vitamin C and all other antioxidants should be consumed often if smoking
4) research alternate cannabanoids (cbg, cbd, cbda, thca, cbn). cannabis has been selectively bread for high thc content but needs to be balanced by other cannabanoids to maximize its therapeutic effect. CBG and CBN abolish anxiety.
5) know your source. theres so much remediated, unwashed, moldy, terribly fertilized, pesticized, and synthetically enhanced weed out there thats very bad for you.
6) dont just get high and stare at your phone. Being stoned is supposed to enhance whatever activity youre doing, not be the activity
 
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