How much cbd oil should i take for pmr

Cannabis and Cannabinoids in the Treatment of Rheumatic Diseases

This is an open-access article. All its content, except where otherwise noted, is distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chronic pain is a common complaint among patients, and rheumatic diseases are a common cause for chronic pain. Current pharmacological interventions for chronic pain are not always useful or safe enough for long-term use. Cannabis and cannabinoids are currently being studied due to their potential as analgesics. In this review we will discuss current literature regarding cannabinoids and cannabis as treatment for rheumatic diseases. Fibromyalgia is a prevalent rheumatic disease that causes diffuse pain, fatigue, and sleep disturbances. Treatment of this syndrome is symptomatic, and it has been suggested that cannabis and cannabinoids could potentially alleviate some of the symptoms associated with fibromyalgia. In this review we cite some of the evidence that supports this claim. However, data on long-term efficacy and safety of cannabinoid and cannabis use are still lacking. Cannabinoids and cannabis are commonly investigated as analgesic agents, but in recent years more evidence has accumulated on their potential immune-modulatory effect, supported by results in animal models of certain rheumatic diseases. While results that demonstrate the same effect in humans are still lacking, cannabinoids and cannabis remain potential drugs to alleviate the pain associated with rheumatic diseases, as they were shown to be safe and to cause limited adverse effects.


Chronic pain is commonly defined as pain that lasts for longer than three to six months and is a common complaint among many patients seeking medical attention. 1 The prevalence of chronic pain among the adult population in certain countries is estimated to be as high as 30%, 2 and rheumatic diseases are a leading cause for chronic pain. 3 Analgesia in rheumatic diseases is often an important part of treatment, especially since disease remission and response to therapy do not always entirely eliminate pain. In rheumatoid arthritis (RA) patients, it had been shown that pain can persist even with the achievement of clinical targets, and that pain was also the most common residual symptom associated with RA remission or low disease activity. 4 In this review, we will discuss the potential of using cannabis and cannabinoids in the treatment of rheumatic disease, based on the literature existing on this issue.

Management of chronic pain is difficult, and patients are often unsatisfied with the effect of treatment. 5 Drug options that are currently available may not be very safe for certain patient populations. Opioids are a problematic long-term solution for chronic pain, due to the risk they carry of significant adverse events, addiction, and overdose. 6 Opioid use was also found to be associated with more severe symptoms and unemployment in fibromyalgia. 7 Other drugs used to treat chronic pain, such as antidepressants (e.g. serotonin-norepinephrine reuptake inhibitors [SNRIs], tricyclic antidepressants [TCAs]), have been shown to be useful for this indication but have certain side effects (e.g. increased risk of cardiovascular events and falls with TCAs) that might limit their use in older patients. 8 One solution for long-term pain that has been studied in the context of pain relief in rheumatic diseases—but not thoroughly enough—is the use of cannabis or cannabinoids, which may potentially show therapeutic qualities as well. 9


It is assumed that the plant Cannabis sativa exerts its effects on human physiology through substances it contains, termed phytocannabinoids (over 100 of them have already been isolated so far). Those phytocannabinoids are thought to bind cannabinoid receptors throughout the human body, to which endocannabinoid (i.e. cannabinoids produced by human tissue) bind as well. Of the phytocannabinoids, tetrahydrocannabinol (THC) and cannabidiol (CBD) are the most well-studied and are used as medications. Tetrahydrocannabinol is considered to be the more psychoactive component in cannabis, while CBD is considered to be the major non-psychoactive component. Cannabinoid receptors are found in a variety of tissues throughout the body—from neurons in the frontal cortex, to the gastrointestinal tract and immune cells as well. 9 According to the “entourage theory,” the combination of THC and CBD creates a synergistic effect in which other phytocannabinoids possibly take part as well, suggesting that there could be a benefit in using cannabis rather than synthetic cannabinoids as analgesic or therapeutic agents. 10


Fibromyalgia is a common chronic pain syndrome causing diffuse pain, tenderness, fatigue, and sleep disturbances. Other complaints include cognitive symptoms, as well as headaches. 11 The prevalence of fibromyalgia is estimated at 2.7% globally. 12 Without a known pathophysiology and etiology, and therefore in the absence of disease-modifying or definitive treatment, analgesia is a significant part of fibromyalgia symptomatic treatment. Fibromyalgia patients may respond to certain pharmacological agents (e.g. antidepressants and anticonvulsants) or to other interventions such as aerobic exercise, physical therapy, and rehabilitation programs (non-pharmacological interventions were recommended as the first line of treatment in recent European League Against Rheumatism [EULAR] guidelines 13 ).

Fibromyalgia pain shares certain common characteristics with neuropathic pain, 14 and both are thought to involve a mechanism of central sensitization. 15 It should also be noted that current guidelines recommend treating it with similar agents to those used in neuropathic pain. 13

Ibuprofen, a non-steroidal anti-inflammatory drug (NSAID) usually used for the treatment of musculoskeletal pain, was not found to be an effective treatment option, 16 and a randomized double-blinded study that compared the addition of etoricoxib, a selective COX-2 inhibitor, to pre-existing medical therapy with the addition of placebo in female fibromyalgia patients found that etoricoxib did not improve patients’ pain, sleep, or disability parameters. 17 While tramadol (a weak opioid with mild SNRI activity) was found to be potentially effective in alleviating fibromyalgia pain, 13 opioids in general may cause an exacerbation of symptoms in this patient population. 7 Cannabis and cannabinoids were recommended for the treatment of neuropathic pain, 18 and, due to the similarities between neuropathic pain and fibromyalgia, as previously mentioned, it is not unreasonable to hypothesize that cannabis or cannabinoids might be effective for fibromyalgia-associated pain as well.

Data regarding the use of cannabinoids in the treatment of fibromyalgia consist of several studies investigating the use of nabilone—a synthetic analog of THC—and fewer in which cannabis was used. Two studies evaluating the use of nabilone in fibromyalgia were included in a Cochrane review that found that nabilone was not superior to placebo or amitriptyline (a TCA) in relieving fibromyalgia symptoms, 19 – 21 as neither study provided high/moderate-quality evidence for efficacy. However, one study included in this Cochrane review did show very low-quality evidence that nabilone compared with placebo led to a decrease in pain and anxiety as well as to an improvement in health-related quality of life. 21 In the other study included in this Cochrane review, very low-quality evidence that nabilone was superior to amitriptyline in improving sleep was found. 20 While cannabinoids were not suggested as treatment for fibromyalgia in the aforementioned Cochrane review, The National Academies of Science, Engineering, and Medicine suggested in their 2017 report that there was moderate evidence that cannabis or cannabinoids are effective for fibromyalgia. 22

In an observative study in which 28 fibromyalgia patients treated with cannabis were compared with 28 controls, significant pain relief, reduction of stiffness, and increase in relaxation and perception of well-being were all found, and were evaluated by visual analog scale (VAS) before and 2 hours after cannabis self-administration. 23 More compelling results emerge from a study that included fibromyalgia patients in Israel. In a recent publication by Sagy et al., 24 a prospective observational study was conducted, in which 367 fibromyalgia patients were treated with medical cannabis and followed up at six months. A total of 81.1% of patients achieved treatment response, and pain intensity decreased significantly from a median of 9 at baseline to 5 at six months (on a numeric rating scale of 0 to 10, with 0 being no pain, and 10 being worst pain imaginable). Dizziness, dry mouth, and gastrointestinal symptoms were among the most common side effects of the treatment. In a recent retrospective review, Habib and Artul 25 assessed 26 fibromyalgia patients treated with medical cannabis, using the Fibromyalgia Impact Questionnaire. The mean duration of cannabis treatment was 10.4 months, and the mean dose of cannabis was 26 g per month. Significant improvement was reported in every item of the questionnaire after cannabis treatment, and 50% of patients stopped using any other medical therapy for fibromyalgia. Adverse effects were mild and were reported by 30% of patients.

In another study, Habib and Avisar employed questionnaires on social media to reach out to Israeli fibromyalgia patients using cannabis 26 and found that, of 383 responders, 323 (84%) reported consuming cannabis; 142 (44%) of these were licensed to do so. The majority of patients reported pain relief (94%) and improved sleep quality (93%). Depression and anxiety were both also reported to improve under cannabis use by the patients. Most of the reported adverse effects were mild (e.g. eye or throat irritation); 12% reported experiencing adverse effects.

In another recent study that assessed the analgesic effect of inhaled cannabis with varying concentrations of THC and CBD, pressure and electrical pain thresholds, spontaneous pain scores, and drug high were measured before and after cannabis inhalation. The results showed that cannabis strains containing THC led to a significant increase in pressure pain threshold compared with placebo. However, no strain of cannabis was found to be superior to placebo’s effect on spontaneous or electrical pain responses. Drug high was assessed by the Bowdle questionnaire and was found to occur in 40%–80% of the subjects treated with inhaled cannabis, compared to 10% of the subjects in the placebo group. 27


Cannabis and cannabinoids were investigated as substances that can ameliorate chronic pain and other symptoms associated with rheumatic disease. However, it had also been suggested that cannabinoids have an inflammatory-modulating quality that could exert a therapeutic effect in such conditions, as cannabinoids were shown to have an overall anti-inflammatory effect on immune cells; these results were reinforced by studies in animal models of RA and systemic sclerosis (SSc). 9

In RA and osteoarthritis (OA), for example, the hypothesis that cannabinoids may have a disease-modifying quality is based on animal models, as well as in vitro studies that have shown that the synovia of RA and OA patients contained two endocannabinoids that the synovia of healthy controls did not. Results of the same study showed that, in fibroblast-like cells obtained from RA and OA patients, cellular receptors ERK-1 and ERK-2 underwent phosphorylation in response to cannabinoid stimulation, an effect which was attenuated by a cannabinoid receptor antagonist. 28

In another study, synovial tissue obtained from RA patients was shown to undergo attenuation and inhibition of cytokine production in response to a cannabinoid binding a cannabinoid receptor. 29 Animal models also suggest a possible therapeutic quality for cannabinoids in RA, with three studies using a murine model with collagen-induced arthritis showing a beneficial effect of the cannabinoids CBD, JWH-133, and HU-308. These substances were found to be associated with clinical improvement: CBD was associated with a decrease in cytokine release and production as well as a decrease in lymphocyte proliferation 30 ; JWH-133 was associated with a decrease in serum antibody levels, decreased cytokine production, and reduced bone destruction 31 ; and HU-308 was associated with less joint swelling and destruction, reduced synovial inflammation, along with a decrease in serum antibody levels. 32 Despite these promising results, clinical research focusing on cannabinoids’ disease-modifying qualities is still lacking.

The use of cannabinoids for the relief of pain associated with RA has been assessed by one study 33 which showed that, in comparison with placebo, the cannabis-based drug was associated with significant improvements in certain pain parameters and quality of sleep. With regard to drug safety, the study found no serious adverse effects in the active treatment group, with most adverse effects being mild or moderate.

In OA, a murine model with surgically induced OA showed that the severity of the disease was reduced in wild-type compared with mice that have undergone gene-deletion for a presumed relevant cannabinoid receptor. The same study also showed that treatment of wild-type mice with an agonist for the same cannabinoid receptor resulted in a partial protection against OA that did not occur in the gene-deletion group or in the wild-type placebo group. 34 In another study, the activity of an enzyme suspected of causing cartilage breakdown was reduced by the treatment of chondrocytes from OA patients with a cannabinoid. 35 Only one clinical trial assessed the use of an endocannabinoid modulator in OA for pain relief, and this was not found to be significantly more beneficial for OA-associated pain than placebo. 36 Other clinical trials assessing the use of cannabis and cannabinoids for OA are currently ongoing or are yet to be published. 37

Several studies have also shown that cannabinoids and cannabinoid receptors might play a role in SSc, as cannabinoid receptors have been shown to modulate SSc in murine models, 9 and were also found to be over-expressed in SSc fibroblasts. 38 A study on a murine model also found that treatment with cannabinoids prevented the development of cutaneous and pulmonary fibrosis and decreased the proliferation of fibroblasts and antibody development. 39 A clinical trial of a novel oral selective cannabinoid receptor agonist is currently in phase 3, after showing a statistically significant effect on skin fibrosis. 40

Research from recent years has shown some promising results regarding the potential of cannabinoids as disease-modifying therapeutics in rheumatic disease. To further investigate this theory, clinical trials should be conducted to evaluate the disease-modifying quality of cannabis in certain rheumatic diseases.

However, despite the evidence on the potential of cannabis and cannabinoids in the treatment of rheumatic disease and the pain associated with it, the literature regarding the use of cannabis as treatment for chronic pain in general contains conflicting reports. While The National Academies of Science, Engineering, and Medicine found in their 2017 report that there was substantial evidence that cannabis or cannabinoids effectively managed chronic pain in adults, 22 and in 2015 an updated review of randomized controlled trials suggested that cannabinoids are a reasonable treatment option for chronic non-cancer pain, being safe and “modestly effective,” 41 other reviews were less supportive of those claims.

An overview of systematic reviews on the efficacy and safety of cannabis-based medications for chronic pain concluded that there was insufficient information to recommend cannabinoids as treatment for chronic pain in rheumatic disease, 42 and a systematic review and meta-analysis from 2018 on the treatment of non-cancer chronic pain with cannabis and cannabinoids claimed that the number needed to treat to benefit was high and the number needed to treat to harm was low, and that the evidence for effectiveness of cannabinoids for chronic non-cancer pain was insufficient. 43 It should be emphasized that while the reviews cited in this paragraph evaluated studies and systematic reviews in which cannabis was used to treat chronic pain of many etiologies, in this article we wish to focus on the potential of cannabis as treatment for chronic pain caused by rheumatic diseases only. In a recent review of this topic, Sarzi-Puttini et al. 44 discussed the pros and cons of medical cannabis in the treatment of rheumatic diseases, claiming that, given the evidence currently available, cannabis should only be used as complementary treatment in rheumatic diseases at the moment, until high-quality evidence is found.


In conclusion, we believe that the use of cannabis and cannabinoids for pain relief in rheumatic diseases (and fibromyalgia in particular) shows great potential and may be a source of hope for those suffering from chronic pain associated with those conditions, and for the physicians treating them. More research into this question should be conducted, especially among larger cohorts of patients and for longer periods of time, to assess for long-term efficacy and adverse effects. 45 At this point, the data suggest that the use of cannabinoids and cannabis carries limited side effects in the treatment of rheumatic disease, 46 although drug interactions should always be kept in mind. 9 Research also suggests that cannabis and cannabinoids can improve some common and debilitating symptoms of rheumatic disease, thus making them an adequate potential treatment option in our opinion, when other treatment lines have been exhausted.

CBD oil to reduce prednisone

Has anyone tried taking CBD Hemp oil to reduce prednisone? I just started on 15mg capsules (2 days) and I feel relief. I’ve had PMR for 5 years and can’t seem to get below 8 mg of pred without a flare

1 like, 25 replies

25 Replies

Anhaga Nanduff

Posted 3 years ago

My suspicion is that some of these alternatives actually are working on pred withdrawal symptoms, which is in itself helpful. This is how aloe vera helped me last year, I think.

Mrs.Mac-Canada Nanduff

Posted 3 years ago

The short answer in my experience is yes, I believe it is helping me.

I just wrote you a long reply and it disappeared on me. I often have trouble using my iPad so could you PM me and we can exchange emails and do it that way. I can tell you more about it

Mrs.Mac-Canada Nanduff

Posted 3 years ago

Mrs_Hobbles Nanduff

Posted 3 years ago

I’ve used CBD successfully for Fibromylgia but not instead of pred, would be very interested to hear peoples thoughts on it though!

VickieS Nanduff

Posted 3 years ago

marla.090252 Nanduff

Posted 3 years ago

Hi Nanduff, I use CBD as well, and should remember to use it more often. . sigh. Pred brain. Yes, it works for me, but the high doses I need costs alot at the dispensary. I’m on the journey to reduce my Pred from original 15mg, to 12.5mg to 10mg, then using DSNS method I’m down to 7mg. Still have to reduce to 5mg before my hand surgeon will operate on a ruptured tendon in my finger. Even as slow as I’ve taken it, I’m flaring all the time. I get several days of being ok, then weather changes or my stress changes and I get walloped. When I vape the CBD, I’m good for about 2½ to 3 hours. But using it several times a day, I go thru my supply in short time, then back to the dispensary. I use the dried flower form of Hemp. I had to get a medical card, go to a Pain Specialist (more money) with my GP’s recommendation. Only these docs that could prescribe the use of medical marijuana or hemp.

Long story short, yes it works for me. Good luck on your journey!

Nanduff marla.090252

Posted 3 years ago

I started taking CBD Hemp THC. I’m taking 15 mg at night and it definitely seems to be helping. I’m on 7.5 mg of pred. I haven’t tried reducing yet but will in another week. My rheumi says to go down 1/2 mg every 2 weeks. I might try every 3 due to the numerous flares I’ve had over the years. Diagnosed in 2011 From what I’ve read from another member I might have to up the dose of CBD. I’ve never smoked and can’t get my head around vaping. My son in law has a prescription and vapes CBD with very low THC for his migraines and he sees a vast improvement. I live in the states and CBD Hemp oil can be purchased on line as well as in a health food store. It is a bit pricey .. but if I can off the pred..or at least under 5mg. I’ll pay th price.

Hope this helps!

Mrs.Mac-Canada marla.090252

Posted 3 years ago

i am using CBD oil to help me decrease my prednisone dose but not in lieu of taking enough prednisone to manage my inflammation. I think if you are having flares often you might try decreasing more slowly and never decrease before you are feeling well (as can be). After my last flare I made it back to 5mg and stayed there for 7 months then started to reduce very, very slowly. I have successfully made it to 3.5mg where I had flared twice before and I’m feeling good. I believe it is the CBD oil that has allowed me to do this especially since stress is my trigger and I have been going through some extremely difficult times with family.

I hope you are successful in getting down to the 5mg so you can have your surgery but go slowly so you avoid the seesaw with flares. They seem to get worse and harder to get back in control each time.

Anhaga Nanduff

Posted 3 years ago

At your dose level even three week intervals between tapers is probably too fast, especially as you describe having had “numerous flares”. Make it at least a month, each .5 reduction, and be aware of any increasing fatigue because that will mean your adrenals need a bit longer to catch up. I will be interested to learn if your taper proceeds uneventfully with the help of CBD.

Twopies Anhaga

Posted 3 years ago

So if you have fatigue, do you stay where you are until your adrenals catch up before reducing further or do you go back up a little for a while and then try to reduce again? Not trying to hack this post, just trying to figure things out. Thank you.

Anhaga Twopies

Posted 3 years ago

Nope, I think it would be counterproductive to use pred to deal with fatigue as it’s the pred which has caused it in the first place. I just go very slowly both so I don’t get a flare of PMR, which happened last year when I tried to go from 1.5 to 1, and also to make sure I don’t become ill from lack of cortisol. But that’s just me. I’m sure others have different ways, and I’m sure people have varying degrees of fatigue, and many maybe no problems at all! in my case I don’t have much stamina, but I don’t really get the deathly fatigue very often. It worries me that I get it at all by now, but there it is.

RD_Swede Anhaga

Posted 3 years ago

I stayed a year on 5 mg due to fatigue. It is a low dosage so I thought it was better to feel weell than continue down. After that year I tried to taper one day new dose and two days old dose for about a week. Then I reduced by 0.5 mg. Many others followed that regime and they called it the Ragnar method. Eileen et al later stretched out the tapering period and started the DSNS method which seems to work very well for many.

I am soon 81 and have been off pred for almost 10 years. Fortunately no flares. I used pred for 3 1/2 years including the year on 5 mg.

Good luck to all from Ragnar

Twopies Anhaga

Posted 3 years ago

Twopies RD_Swede

Posted 3 years ago

ill be at 3 years in September, no end in sight. Thank you for your thoughtful words. I’m thinking staying at 5 is the way to go.


Posted 3 years ago

whoops. Can’t count. 2 years! (Blame it on pred head!)

Anhaga RD_Swede

Posted 3 years ago

And we are all eternally grateful to you for figuring out how to taper successfully! Unfortunately on pred I developed increased ocular pressure, high blood sugar (controlled by a very strict diet which sadly has prevented my regaining lost weight), possibly bone thinning (corrected though diet and exercise) and a tendency to be easily injured, rotator cuff, that kind of thing. I think I would be worse off if I had stayed at 5 for a long time. At the moment I’m hanging around the 1.5 – 2 level.

mike42494 marla.090252

Posted 3 years ago

i have been on 10mg of prednisone for 3 years. i am tapering 1 mg every 3 weeks. I’m now at 7 mg daily. i started taking full spectrum cbd oil 6 weeks ago. i take 12.5 mg of cbd 3 x per day. it has really helped me. it takes a few weeks to feel any effect. i use LAZURUS full stength and since i am on disability the company gives a 60% DISCOUNT. A 6000mg bottle cost me $80.00 and will last 4 months.

marla.090252 mike42494

Posted 3 years ago

Hi Mike, (and all) It’s been a while since I’ve posted. Life has been an up and down journey for me recently. I’m currently back down to 6 ½ mg Pred having had PMR now for over 2 years. Since my last posting, I’ve had several flares due to the stress of my father-in-law’s heart attack, subsequent kidney failure, and eventual passing just before Christmas.

I finally got back in touch with hand surgeon #2 and got a song and pony show of different diagnosis and prognosis than the first visit. I found another hand surgeon, and now because there has been so much time since the tendon rupture he suggests not doing the surgery. My right arm ulna head has some osteoarthritis. The rough calcification severed one of the two tendons on my little finger, the small extensor tendon. This new surgeon doesn’t think I’d gain more extension (lifting my little finger, right hand, above horizontal) than I have (which is none). I agree with him, that flexion (gripping) is more important. So I will live with it. He will go in later to scrape the ulnar head so it doesn’t abraid the other tendons.

Using the new full spectrum CBD oil I purchased, (25 mg/0.5ml per day), is so horrible tasting, that I’m researching gel capsules for liquids to fill for dosing, instead of putting the drops on the back of my tongue. I also found that taking it with food helps with stomach reflux, and retasting the CBD oil. Once I finish with this bottle, I’m going back to vaping it. My Firefly 2 is an awesome vape (it heats, doesn’t burn the flower. You inhale vapor not smoke, I’ve never coughed using it). The CBD flower I get from the dispensary is grown for no THC. I get no after-effects from vaping CBD, like I do with the oil. Some folks don’t mind the flavor of the oil, but I basically gag on it, because of its high percentage (1,500 mg per 30ml bottle) of plant extracts.

Does it work? Yes, if you can build up your system to it (takes about 3 weeks, daily dosing). I just prefer to vape it instead. Hemp is Cannabis. It’s the plants’ Genus, split into a variety of Species. All strains and varieties of THC plants are mixed CBD, CBN, CBC, CBG and others in a low percentage. I found if I vape a mix of Hemp (CBD) to THC in a 60:40 ratio, I get NO high from it. This happens because of what is called the entourage effect, the brain associates with both cannabinoid sites, CB1 and CB2. These sites are also located thru-out the body. It’s the entourage effect that negates the high, as long as you calculate the percentages of each flower type and mix what works for you. Each person is different, just like with Prednisone, and how it’s assimilated in our bodies.

The science of this interaction is what I have been studying for the last 2 years while vaping Medical Cannabis (I have a medical card from my State Massachusetts, USA). The difference is medical cannabis undergoes testing for purity, potency, % of a few other cannabinoids (listed above). This makes medical cannabis more expensive, but safer than “street” Cannabis. There are actually over 85 different cannabinoids the Cannabis plant provides. It’s a huge topic, and far to complex to go into here. But suffice it to say, vaping mixed CBD:THC works better for me than straight CBD.