Quote (Balla @ Sep 19 2014 08:29am)

Eh, there's some interesting effects but nothing worthy of concern in regards to metabolism & weight loss. Well, that's at least assuming you don't stay constantly high for most of the day.. then I could perhaps see deleterious effects.

In general, the biggest concern w/ cannabis use is simple hyperphagia (ravenous hunger) due to a robust rise in ghrelin levels + direct hypothalamic AMPK expression, both of which drive hunger. It does actually increase leptin, however, leptin isn't a judge of the acute satiety response, so paroxysmal hunger prevails. Ergo, by far the biggest cause of concern is simply consuming excessive calories consistently.

Other effects that MAY be deleterious to certain metabolic processes, include things like possible acute decrease in t3/t4 as a result of attenuated TSH production. It also may interact directly w/ mito CB1 receptors to repress mitochondrial complex 1 activity.. this may acutely and ephemerally decrease respiration rate. On the flip-side, it'll also decrease ROS prod, so it may be positive, depending (one of the reasons it's neuronally protective).
Interestingly, it inhibits neuronal NE release, yet induces sympathetic activation to very acutely augment metabolic rate & ventillation rate.. this may inhibit insulin secretion (apart from obvious direct CB1/CB2 direct transduction effects of decreasing intracellular Ca2+ induced exocytosis) . Seeing as how NPY will drive a strong CHO craving, this could cause some glucose intolerance, though I'm just surmising as to significance here. Logically flowing from SNS outflow, it also increases HR via impeding vagal tone, another aspect of a metabolic rate rise. Despite some of the potential noxious insulin perturbations, however, cannabis will inhibit 15-LOX, which has actually been shown to play an exorbitant role in obesity-induced beta cell destruction and diabetes development.

As far as direct adipocyte effects, it has potential to directly repress lipolysis via Gi coupled GPCR signaling which would decrease HSL, ATGL, and increase perilipin activation. It also may augment lipogenesis via SREBP induction, which then works through various lipogenic enzymes. However, I'm not sure if it's a direct activation or simply a reciprocal type of signaling (aka repression-activation & vice-versa).

Much of the effects seem to almost negate each other in terms of either increasing or decreasing metabolism via various mechanisms. This is much of the reason I'd say all in all - you're fine with pretty consistent use. I'd still advise against heavy use (ie multiple times per day, chronically) due to tentative deleterious ramifications and general neuronal issues that could occur over time (generally reversible but not worth the hassle). In either case, also given very robust homeostatic mechanisms employed by the body (much of the effects are likely simply a counterregulatory pathway), coupled with the highly ephemeral effects anyway, I'd say you're fine. It shouldn't have a bearing on weight loss apart from hyperphagia induced caloric excess.

Quote (Soad @ Sep 19 2014 01:56pm)

i smoke an oz a week.

Quote (FrozenWater @ Sep 19 2014 05:47am)

as far as neuronal issues.. what would be the difference between smoking multiple times a day, smoking once a day, smoking once a week, and smoking once every 2 weeks?

Quote (Balla @ Sep 19 2014 06:02pm)

Just general constant CB1/CB2 mediated transduction events. The problem w/ the constant activation is as it inhibits cAMP signaling events, it will generally inhibit CREB, which is integral for long-term memory and may induce LTD. It can also, via activating COX-2, cause AMPA receptor internalization, further opposing memory formation. Even use everyday SHOULD be fine (idiosyncrasies always govern, remember), assuming it's only some, say, once a night.. a bowl pack maybe. Then the effects cannot manifest so robustly. Further long term changes, though generally only seen with chronic & heavy use, would be shifts in PFC DA as well as alpha wave power, manifesting as quasi-ADHD symptoms while not under the influence.

As for the use at night, if you ARE going to use at night to sleep, make absolutely certain you use melatonin. It can inhibit the NE mediated melatonin synthesis in the pineal.. so supplementing melatonin helps ensure full REM.
I generally use every single night for quite some time now and I've suffered no hinderence, anecdotally. I think it may also help "unclog" my synapses via LTD induced synaptic pruning of the weakly formed synapses (ie memories I place no merit or salience on remembering are forgotten). I have actually noticed with some things such as names, I've gotten worse at recalling and I think that may be the cause. I truly do not care or place any salience on it, thus the synapses are weakly formed, and cannabis can come through and whipe it out, luckily. If done right, you should generally only notice true memory impairment while actually high, and that's mostly manifest in working memory and not full on long-term storage. That's because the CB1 receptors are located presynaptically, so it's a unique form of LTD, whereby it inhibits transmitter release (and decreases vesicular pool recycling), but given a robust enough stimulus & transmitter firing, LTP in the postsynaptic spine will still ensue just fine.
While on the subject, I wrote that previous post on the last page while high and heavily sleep deprived and hardly remember even writing it lolol. I'm surprised it was coherent at all.

Quote (ViviLOL @ Sep 19 2014 10:11pm)

when u gon get blunted wiff me?

Quote (Balla @ Sep 19 2014 06:15pm)

Shit bruh, tbh if we lived close, I'm sure we'd smoke all the time and just chat about medical stuff

Quote (Balla @ Sep 19 2014 02:29am)

Eh, there's some interesting effects but nothing worthy of concern in regards to metabolism & weight loss. Well, that's at least assuming you don't stay constantly high for most of the day.. then I could perhaps see deleterious effects.

In general, the biggest concern w/ cannabis use is simple hyperphagia (ravenous hunger) due to a robust rise in ghrelin levels + direct hypothalamic AMPK expression, both of which drive hunger. It does actually increase leptin, however, leptin isn't a judge of the acute satiety response, so paroxysmal hunger prevails. Ergo, by far the biggest cause of concern is simply consuming excessive calories consistently.

Other effects that MAY be deleterious to certain metabolic processes, include things like possible acute decrease in t3/t4 as a result of attenuated TSH production. It also may interact directly w/ mito CB1 receptors to repress mitochondrial complex 1 activity.. this may acutely and ephemerally decrease respiration rate. On the flip-side, it'll also decrease ROS prod, so it may be positive, depending (one of the reasons it's neuronally protective).
Interestingly, it inhibits neuronal NE release, yet induces sympathetic activation to very acutely augment metabolic rate & ventillation rate.. this may inhibit insulin secretion (apart from obvious direct CB1/CB2 direct transduction effects of decreasing intracellular Ca2+ induced exocytosis) . Seeing as how NPY will drive a strong CHO craving, this could cause some glucose intolerance, though I'm just surmising as to significance here. Logically flowing from SNS outflow, it also increases HR via impeding vagal tone, another aspect of a metabolic rate rise. Despite some of the potential noxious insulin perturbations, however, cannabis will inhibit 15-LOX, which has actually been shown to play an exorbitant role in obesity-induced beta cell destruction and diabetes development.

As far as direct adipocyte effects, it has potential to directly repress lipolysis via Gi coupled GPCR signaling which would decrease HSL, ATGL, and increase perilipin activation. It also may augment lipogenesis via SREBP induction, which then works through various lipogenic enzymes. However, I'm not sure if it's a direct activation or simply a reciprocal type of signaling (aka repression-activation & vice-versa).

Much of the effects seem to almost negate each other in terms of either increasing or decreasing metabolism via various mechanisms. This is much of the reason I'd say all in all - you're fine with pretty consistent use. I'd still advise against heavy use (ie multiple times per day, chronically) due to tentative deleterious ramifications and general neuronal issues that could occur over time (generally reversible but not worth the hassle). In either case, also given very robust homeostatic mechanisms employed by the body (much of the effects are likely simply a counterregulatory pathway), coupled with the highly ephemeral effects anyway, I'd say you're fine. It shouldn't have a bearing on weight loss apart from hyperphagia induced caloric excess.