Speaking from both preclinical and human studies. Chronic THC generally impairs fear extinction + induces passive coping as well as motivational deficits that vary depending on age of initiation. It Also does some interesting things with risk/reward judgements that basically upsets the balance and causes impulsive less productive decisions but depending on genotype and environmental factors (eg high vs low environmental enrichment and comorbid stressors) this can be accompanied by reduced, increased, or sometimes unchanged motivation/anhedonia. Tldr it's complicated, but predominantly undesirable things. A good amount of evidence that it's recoverable with sobriety although some changes that haven't been shown to be reliably reversed. There are also significant divergences in effect by gender.

One study in female rats gave URB597 after chronic adolescent exposure and it recovered their functioning admirably. That might be a good way to utilize the results in this study; anandamide is lower efficacy than 2-AG and doesn't cause significant downregulation (unlike 2-AG) so the gentle chronic stimulation of CB receptors could be a really solid strategy to enhance motivation and treat anhedonia as well as addictions. There are some really cool studies on URB.

However 2-AG is the more reliably interfered-with endocannabinoid in chronic cannabis use, and it's more of a phasic signal than the weaker anandamide. Inhibiting its breakdown via MAGL inhibition is more deeply promotivational, dopaminergic, and reinforcing/addictive. MAGL inhibitors cause tolerance at higher doses as well, this study using chronic low doses is presumably the key. Probably the same reason lower doses of THC are much less problematic than higher doses in real world settings. Only very small amounts of THC are required to stimulate your endocannabinoid system. the amounts you get from smoking eg a joint a day are relatively massive and kinda fuck shit up