There is massive evidence for cannabis being a legitimate example of a “panacea”


“In Greek mythology, Panacea (Greek Πανάκεια, Panakeia) was a goddess of universal remedy. … Panacea was said to have a poultice or potion with which she healed the sick. This brought about the concept of the panacea in medicine, a substance meant to cure all diseases.” – Wikipedia, “panacea”

The evidence that cannabis is not only one medicine but many medicines – a massive number of possible new medicines, rendering it the first true candidate for an actual “panacea” that has ever existed – has been accumulating in more and more places every year.

For one example, here is a collection of online peer reviewed studies both pro and con: 

60 Peer-Reviewed Studies on Medical Marijuana
Medical Studies Involving Cannabis and Cannabis Extracts (1990 – 2014)

Peer-reviewed studies on medical marijuana, listed by condition treated # of studies
Pro Con Not
Pro or
ALS 1 0 0
Bipolar Disorder 2 0 0
Cancer 5 1 1
General Use 2 0 0
Glaucoma 0 0 1
HIV/AIDS 5 1 2
Huntington’s Disease 0 0 1
IBD/Crohn’s 1 0 1
Multiple Sclerosis 11 3 5
Nausea 1 0 0
Pain 6 0 1
Parkinson’s Disease 2 0 1
PTSD 1 0 0
Psychosis / Schizophrenia 1 0 1
Rheumatoid Arthritis 1 0 0
Tourette’s Syndrome 2 0 0


Research into the applicability of cannabis as a preventive medicine for healthy people to use to stay healthy – as a relaxant and antidepressant – appears promising: 

A Brief History of the Use of Cannabis as an Anxiolytic, Hypnotic, Nervine, Relaxant, Sedative, and Soporific

By David Malmo-Levine and Rob Callaway, M.A., 2012

A Brief History of the Use of Cannabis as an Antidepressant and Stimulant

By David Malmo-Levine and Rob Callaway, M.A., 2012



Any modern well-written review of the evidence of cannabis’s efficacy in medicine will reveal a treasure trove of applications. This one from Ethan Russo from 2011 – an excerpt from a review of the medical applicability of the major cannabinoids and terpenes (of which there are hundreds) is particularly compelling: 


Over 100 phytocannabinoids have been identified (Brenneisen, 2007; Mehmedic et al., 2010), but many are artefacts of analysis or are produced in trace quantities that have not permitted thorough investigation. The pharmacology of the more accessible phytocannabinoids has received excellent recent reviews (Pertwee et al., 2007; Izzo et al., 2009; De Petrocellis and Di Marzo, 2010; De Petrocellis et al., 2011), and will be summarized here, with emphasis on activities with particular synergistic potential.

THC (Table 1) is the most common phytocannabinoid in cannabis drug chemotypes, and is produced in the plant via an allele co-dominant with CBD (de Meijer et al., 2003). THC is a partial agonist at CB1 and cannabinoid receptor 2 (CB2) analogous to AEA, and underlying many of its activities as a psychoactive agent, analgesic, muscle relaxant and antispasmodic (Pacher et al., 2006). Additionally, it is a bronchodilator (Williams et al., 1976), neuroprotective antioxidant (Hampson et al., 1998), antipruritic agent in cholestatic jaundice (Neff et al., 2002) and has 20 times the anti-inflammatory power of aspirin and twice that of hydrocortisone (Evans, 1991). THC is likely to avoid potential pitfalls of either COX-1 or COX-2 inhibition, as such activity is only noted at concentrations far above those attained therapeutically (Stott et al., 2005).

CBD is the most common phytocannabinoid in fibre (hemp) plants, and second most prevalent in some drug chemotypes. It has proven extremely versatile pharmacologically (Table 1) (Pertwee, 2004; Mechoulam et al., 2007), displaying the unusual ability to antagonize CB1 at a low nM level in the presence of THC, despite having little binding affinity (Thomas et al., 2007), and supporting its modulatory effect on THC-associated adverse events such as anxiety, tachycardia, hunger and sedation in rats and humans (Nicholson et al., 2004; Murillo-Rodriguez et al., 2006; Russo and Guy, 2006). CBD is an analgesic (Costa et al., 2007), is a neuroprotective antioxidant more potent than ascorbate or tocopherol (Hampson et al., 1998), without COX inhibition (Stott et al., 2005), acts as a TRPV1 agonist analogous to capsaicin but without noxious effect (Bisogno et al., 2001), while also inhibiting uptake of AEA and weakly inhibiting its hydrolysis. CBD is an antagonist on GPR55, and also on GPR18, possibly supporting a therapeutic role in disorders of cell migration, notably endometriosis (McHugh et al., 2010). CBD is anticonvulsant (Carlini and Cunha, 1981; Jones et al., 2010), anti-nausea (Parker et al., 2002), cytotoxic in breast cancer (Ligresti et al., 2006) and many other cell lines while being cyto-preservative for normal cells (Parolaro and Massi, 2008), antagonizes tumour necrosis factor-alpha (TNF-α) in a rodent model of rheumatoid arthritis (Malfait et al., 2000), enhances adenosine receptor A2A signalling via inhibition of an adenosine transporter (Carrier et al., 2006), and prevents prion accumulation and neuronal toxicity (Dirikoc et al., 2007). A CBD extract showed greater anti-hyperalgesia over pure compound in a rat model with decreased allodynia, improved thermal perception and nerve growth factor levels and decreased oxidative damage (Comelli et al., 2009). CBD also displayed powerful activity against methicillin-resistant Staphylococcus aureus (MRSA), with a minimum inhibitory concentration (MIC) of 0.5–2 µg·mL−1(Appendino et al., 2008). In 2005, it was demonstrated that CBD has agonistic activity at 5-hydroxytryptamine (5-HT)1A at 16 µM (Russo et al., 2005), and that despite the high concentration, may underlie its anti-anxiety activity (Resstel et al., 2009; Soares Vde et al., 2010), reduction of stroke risk (Mishima et al., 2005), anti-nausea effects (Rock et al., 2009) and ability to affect improvement in cognition in a mouse model of hepatic encephalopathy (Magen et al., 2009). A recent study has demonstrated that CBD 30 mg·kg−1 i.p. reduced immobility time in the forced swim test compared to imipramine (P < 0.01), an effect blocked by pre-treatment with the 5-HT1A antagonist WAY100635 (Zanelati et al., 2010), supporting a prospective role for CBD as an antidepressant. CBD also inhibits synthesis of lipids in sebocytes, and produces apoptosis at higher doses in a model of acne (vide infra). One example of CBD antagonism to THC would be the recent observation of lymphopenia in rats (CBD 5 mg·kg−1) mediated by possible CB2 inverse agonism (Ignatowska-Jankowska et al., 2009), an effect not reported in humans even at doses of pure CBD up to 800 mg (Crippa et al., 2010), possibly due to marked interspecies differences in CB2 sequences and signal transduction. CBD proved to be a critical factor in the ability of nabiximols oromucosal extract in successfully treating intractable cancer pain patients unresponsive to opioids (30% reduction in pain from baseline), as a high-THC extract devoid of CBD failed to distinguish from placebo (Johnson et al., 2010). This may represent true synergy if the THC–CBD combination were shown to provide a larger effect than a summation of those from the compounds separately (Berenbaum, 1989).

Br J Pharmacol. 2011 Aug; 163(7): 1344–1364.
PMCID: PMC3165946

Taming THC: potential cannabis synergy and phytocannabinoid-terpenoid entourage effects





. 2005 Dec; 146(7): 913–915.
Published online 2005 Oct 3. doi: 10.1038/sj.bjp.0706415
PMCID: PMC1751232
PMID: 16205721

Plant cannabinoids: a neglected pharmacological treasure trove

Many of the effects seen with anandamide, WIN and THC are not CB1-dependent (Howlett et al., 2002). As most of the plant cannabinoids do not bind to this receptor, it seems reasonable to evaluate these compounds for their activities in a wide array of assays. I sincerely believe that the plant cannabinoids are a neglected pharmacological treasure trove.

These are just a few of many, many examples of such evidence being compiled and evaluated on line. A comprehensive list or website on this topic does not exist due to the sheer massive volume of the evidence in question.