Quote (Balla @ Sep 19 2014 06:29am)
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.
Horyshet