Safety Warning: This product has not been evaluated by the US FDA and is not intended to diagnose, treat, cure, or prevent any disease. This product contains <0.3% THC, compliant with the Federal Farm Bill.
2 oz. jar (1000mg CBD), 2 oz. stick (1000mg CBD), 0.35 oz. jar (200mg CBD), 0.5 oz. stick (250mg CBD)
Disclaimer: Keep out of reach of children. Not to be used during pregnancy or lactation. Please consult a physician before taking if you have a medical condition or are currently taking other medications.
Storage: Store in a cool, dry place, away from light. Do not use if safety seal is broken.
This is our Salve for topical use. It contains 1000 mg CBD (per 2 oz container) from Full Spectrum Hemp Extract Oil and camphor, eucalyptus, peppermint, and lavender botanical extracts. PHARM CBD full spectrum oil contains all the cannabinoids and terpenes that are grown in our hemp plants, including THC, but at low concentrations (<0.3%). Apply this topical for muscle and joint recovery.
Directions for Use: Apply as needed to affected areas 2-3 times daily. Massage into skin until fully absorbed.
CBD Content: 18-20 mg CBD per gram of salve.
In addition to its good safety profile and the lack of psychoactive effects, CBD presents also a wide range of therapeutic effects . Possibly for these reasons, CBD is currently one of the most studied cannabinoids . Several experimental in vitro and in vivo studies have shown that CBD has a broad range of therapeutic applications, displaying anti-inflammatory and immunomodulatory properties , anti-psychotic , analgesic  and anti-epileptic  effects, among others. Compared to Δ9-THC, CBD shows low affinity for cannabinoid receptor type 1 (CB1) and type 2 (CB2) . CB1 receptors are mainly found in the terminals of central and peripheral neurons and CB2 receptors mainly in immune cells . Several in vitro studies have shown that CBD, at low concentrations, has weak CB1 and CB2 antagonistic effect . It has also been reported that it behaves as a negative allosteric modulator of CB1, meaning that CBD does not activate the receptor directly but alter the potency and efficacy of orthosteric ligands of this receptor: Δ9-THC and 2-arachidonoylglycerol (2-AG) . These preliminary results need further validation, but may explain the ability of CBD to antagonize some of the effects of Δ9-THC reported in in vitro, in vivo and clinical human studies . It has also been suggested that the role of CBD as an allosteric modulator of CB1 can explain its therapeutic role in the treatment of central and peripheral nervous system disorders . CBD has also shown to have a strong inhibition effect of neutrophil chemotaxis and proliferation. In addition, it may induce stimulation of arachidonic acid release, reducing prostaglandin E2 (PGE2), and nitric oxide (NO) production. Furthermore, CBD reduces the expression of specific interleukins (IL-12 while increasing that of IL-10) by macrophages, and decreases the production and release of pro-inflammatory cytokines, such as IL-1, IL-6 and interferon gamma (IFNγ) from lipopolysaccharide (LPS)-activated microglial cells . The role of CBD as an inverse agonist of CB2 receptor may explain its known anti-inflammatory effects but this needs further investigation. There is also evidence of an antagonistic effect of CBD at the novel cannabinoid receptor G protein-coupled receptor 55 (GPR55), emerging from in vitro and in vivo studies. GPR55 has a role in bone physiology via regulating osteoclast function, formation and ultimately bone mass. CBD may affect the endocannabinoid system also indirectly, for example CBD can affect the endocannabinoid tone by increasing availability of anandamide; one possible mechanism is by inhibition of fatty acid amide hydrolase (FAAH), the enzyme that hydrolyzes the endocannabinoid anandamide .
Four randomized parallel-group trials (196 participants) assessed the role of CBD on cognitive impairment and psychotic symptoms in patients with psychotic disorders (schizophrenia) [28-31]. One study was judged as being at high risk of bias and three at uncertain risk of bias. Studies included patients with a confirmed diagnosis of schizophrenia. CBD was administered orally, in the form of oral gelatin capsules with doses ranging from 600 to 1,000 mg/day and the effects were compared to a placebo and active control. Boggs et al (2018) assessed the effects of CBD (600 mg/day for 6 weeks) as an adjunctive treatment in chronic schizophrenia patients, for a period of 6 weeks. No significant difference was observed between placebo and CBD group on cognitive function and psychotic symptoms . Leweke et al (2012) included a small group of acute schizophrenia patients who were administered 200 up to 800 mg/day for 4 weeks or amisulpride, a potent antipsychotic. CBD was as effective as amisulpride in improving psychotic symptoms and associated with marked tolerability and safety, when compared with amisulpride . McGurie et al (2019) administered 1,000 mg/day for 6 weeks to a group of schizophrenia patients as an adjunct to current antipsychotic treatment and found a significant improvement on positive psychotic symptoms and clinicians’ impressions of illness improvement. Despite improvement on cognitive function and overall level of functioning, no significant difference was found compared to placebo . Hallak et al (2010) included a small group of heterogeneous schizophrenia patients and administered a single dose of CBD (300 or 600 mg). They found no effect of CBD on selective attention, measured by Stroop color and word test .
PRISMA flow diagram of literature search and selection process. PRISMA: Preferred Reporting Items for Systematic Reviews and Meta-Analyses.
a Active-controlled trial, amisulpride. b Concomitant treatment. c CBD-rich botanical extracts capsules contained other compound (up to 4.7% THC). IR: individually randomized; NR: non-randomized; CR: cluster randomized; CBD: cannabidiol; HDL: high-density lipoprotein.
a Cortex Technologies, Hadsund, Denmark. b Delfin Technologies, Kuopio, Finland. c Concomitant treatment for the condition with anti-oxidant and pain killer. d Concomitant treatment with anti-seizure drugs. N/A: non-available; HPV: human papillomavirus; ADR: adverse drug reaction.