The term kief refers to the sticky, bulbous crystalline formations on the tip of a gland called a “trichome.” Trichomes are external resin glands packed with the chemicals that give marijuana its flavors and smells, called “terpenes.” They also contain high concentrations of cannabinoids. These chemicals which interact with our body to produce marijuana’s signature effects.
Until recently, medical science knew very little about the endocannabinoid system and how CBD and THC attach themselves to brain receptors to carry out their effects in the body. There are at least two receptors that interact with cannabis compounds to generate the effects we’ve gotten used to. THC attaches to CB1 receptors to generate the euphoric feeling that marijuana is known for, and CBD, which contains no psychoactive ingredient, attaches to CB2 receptors, and among other things, it counteracts the effects of CB1 receptors and assists the body in managing pain.
These states are Idaho, Kansas, Nebraska and South Dakota. Now, even though marijuana-derived CBD is legal in these states, the laws are still unclear, so there are still businesses selling CBD, and patients using CBD in these states. We totally believe in the benefits CBD offers and support the CBD movement, but if you are in one of these states, be cautious and careful when considering using CBD products.
Some users may experience an episode of acute psychosis, which usually abates after six hours, but in rare instances, heavy users may find the symptoms continuing for many days. A reduced quality of life is associated with heavy cannabis use, although the relationship is inconsistent and weaker than for tobacco and other substances. It is unclear, however, if the relationship is cause and effect.
The endocannabinoid system is tonically active in control of pain, as demonstrated by the ability of SR141716A (rimonabant), a CB1 antagonist, to produce hyperalgesia upon administration to mice (Richardson et al 1997). As mentioned above, the ECS is active throughout the neuraxis, including integrative functions in the periacqueductal gray (Walker et al 1999a; Walker et al 1999b), and in the ventroposterolateral nucleus of the thalamus, in which cannabinoids proved to be 10-fold more potent than morphine in wide dynamic range neurons mediating pain (Martin et al 1996). The ECS also mediates central stress-induced analgesia (Hohmann et al 2005), and is active in nociceptive spinal areas (Hohmann et al 1995; Richardson et al 1998a) including mechanisms of wind-up (Strangman and Walker 1999) and N-methyl-D-aspartate (NMDA) receptors (Richardson et al 1998b). It was recently demonstrated that cannabinoid agonists suppress the maintenance of vincristine-induced allodynia through activation of CB1 and CB2 receptors in the spinal cord (Rahn et al 2007). The ECS is also active peripherally (Richardson et al 1998c) where CB1 stimulation reduces pain, inflammation and hyperalgesia. These mechanisms were also proven to include mediation of contact dermatitis via CB1 and CB2 with benefits of THC noted systemically and locally on inflammation and itch (Karsak et al 2007). Recent experiments in mice have even suggested the paramount importance of peripheral over central CB1 receptors in nociception of pain (Agarwal et al 2007)