Best cbd oil for chemo induced neuropathy

Topical Cannabinoids for Treating Chemotherapy-Induced Neuropathy: A Case Series

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (



Chemotherapy-induced peripheral neuropathy is a common and often severe side effect from many chemotherapeutic agents, with limited treatment options. There is no literature on the use of topical cannabinoids for chemotherapy-induced neuropathy.

Case Presentations

The current manuscript presents a case series of patients presenting in oncology clinics at Sutter Health, CA and Mayo Clinic, Rochester, MN from April 2019 to December 2020 with chemotherapy-induced peripheral neuropathy who used topical creams containing the cannabinoids delta-nine-tetrahydrocannabinol (THC) and/or cannabidiol (CBD).


This case series suggests that topical cannabinoids may be helpful for patients with chemotherapy-induced peripheral neuropathy. This paper also discusses the potential mechanisms of action by which topical cannabinoids might alleviate established CIPN symptoms. A randomized placebo-controlled trial using a standardized product is planned to study the actual efficacy of such treatment.


Chemotherapy-induced peripheral neuropathy (CIPN) is a dose- and age-dependent side effect associated with 6 main antitumor agent drug classes: platinum-based drugs (eg, oxaliplatin), taxanes (eg, paclitaxel and docetaxel), vinca alkaloids (eg, vincristine), epothilones (eg, ixabepilone), proteasome inhibitors (eg, bortezomib), and immunomodulatory drugs (eg, thalidomide). 1 In a review of over 30 clinical studies, CIPN prevalence was reported to be approximately 68% when measured in the first month after finishing a variety of chemotherapy agents, most of which had been associated with CIPN; it was 60% at 3 months and 30% (6.4-53.5) at 6 months or more. 2

CIPN remains a challenge to treat, as most agents used in practice, such as tricyclic antidepressants, anticonvulsants (gabapentin and pregabalin), or serotonin-norepinephrine reuptake inhibitors (SNRI, primarily duloxetine) provide limited benefit to most patients and can have significant side effects. 3 -5

The mechanism of CIPN broadly includes the production of neuronal toxicity and inflammation. 6 The 6 main classes of antitumor agents, discussed above, cause damage to peripheral sensory, motor, and autonomic neurons, through such mechanisms as microtubule disruption, DNA damage, altered ion channel activity, myelin sheath damage, oxidative stress, and mitochondrial damage. 7 In addition, the cumulative damage leading to increased activation of the immune system ultimately promotes cell damage and death in peripheral neurons, leading to a sensitization to nociceptive responses. 6 The central nervous system may also play a role in CIPN by a number of mechanisms, including hyperactivity, reduced GABAergic inhibition, neuroinflammation, and overactivation of GPCR/MAPK pathways 8 -10

The cannabinoids delta-nine-tetrahydrocannabinol (THC) and cannabidiol (CBD) have shown some mild efficacy in the treatment of pain, 11,12 including neuropathic pain. 3,13 -20 However, not all studies have been positive; Lynch et al 21 reported in a small pilot RCT no overall benefit from nabiximol oral mucosal spray but noted that 5/18 patients were responders and concluded that a larger RCT is warranted.

Cannabinoids may exert their effects through peripheral and/or central mechanisms, as targets for action are present in both. THC interacts with the endocannabinoid system primarily through the activation of cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptors. 22 CBD does not interact efficiently to activate known cannabinoid (CB1 and CB2) receptors. 23 CBD, however, can antagonize the activity of CB1 and CB2 receptor agonists. 24 As a result of not activating CB1 receptors, CBD does not produce the psychoactivity that is typically associated with other cannabinoid agonists. Indeed, recent evidence suggests that CBD may reduce the untoward effects of psychoactive cannabinoids, including cognitive impairment, anxiety, and paranoia. 25

THC and additional CB1 and CB2 receptor agonists have been shown to be effective at reducing CIPN in multiple preclinical models. 6,26 THC and additional cannabinoids, through CB1 and/or CB2 receptors, have the potential to modulate pain through a variety of mechanisms, including inhibition of calcium channel activity, transient receptor potential (TRP) channels, serotonin, GABA and glutamate receptor signaling, and modulation of the immune system, leading to anti-inflammatory activity. 27 -29 Inhaled cannabis has also been reported to be effective for treating HIV-associated neuropathy, possibly via CB1 agonism. 15

CBD has been shown to be a molecule with pleotropic effects that ultimately leads to reduction in oxidative stress and inflammation. 30 Increasingly, preclinical evidence demonstrates that CBD has anti-neuropathic pain effects in multiple rodent models, including models of CIPN. 30 -34 Interestingly, there is significant overlap with mechanisms controlling pain when CBD and THC are compared. CBD has been shown to inhibit pain through modulation of calcium and TRP channels, serotonin receptors, glycine receptors, and modulation of the immune system 6 microglia and macrophage function, 35 leading to anti-inflammatory activity.

Cannabis is being used by at least 20% to 30% of cancer patients for pain, nausea, insomnia, and other cancer related issues. 36 -40 More research is desperately needed, noting that cannabis as an adjunct for supportive care is promising given the lack of serious adverse events and/or known interactions with chemotherapy. 36 Given that many patients do not have access to systemic Cannabis, and/or want to avoid the psychoactive effects of THC, a more local means of providing cannabinoids might be preferable. Cannabinoids happen to be lipophilic agents and, thus, can permeate skin. 41,42 Taking advantage of this delivery technique, a small pilot clinical trial evaluated a topical cannabinoid cream, reporting data that supported that it improved non-chemotherapy induced neuropathic pain. 43 The current report involves a case series of patient experiences using topical cannabis products for painful CIPN symptoms.


This is an informal case series obtained by interviewing patients in an oncology clinic who were using topical cannabis for CIPN symptoms from April 2019 to December 2020 at Sutter Medical Group, Sacramento CA and Mayo Clinic, Rochester, MN. Patients with CIPN were reporting that they were using topical cannabis for established painful CIPN. Due to this novel approach, patients with a history of painful CIPN seen in the oncology clinic were asked if they had tried topical cannabis for CIPN, and if so, what was their response. Patients were specifically asked by the authors about the type of product, duration of response, and any side effects. Charts were retrospectively reviewed to look at other prior treatments for neuropathy, prior chemotherapy, and type of cancer.

This case series was approved by the Sutter Health Expedited Review Committee, San Francisco, CA, May 14, 2020. Written consent for publication was obtained by the author from the patients with detailed case reports and is located in the patient medical record.


Patients were obtaining topical products from retail stores (containing hemp-derived CBD) or cannabis dispensaries (containing either CBD alone or CBD and THC). In some cases, creams containing only CBD were derived from hemp; in general, retail obtained hemp contains 0.3% or less of THC. 44 The creams used contained between 120-600 mg per unit (tube or jar) of CBD and 6-600 mg THC per unit. Some of the creams contain ingredients that are reported to increase skin absorption, such as essential oils or emu oils. 45,46 Some of these patients had tried other agents/acupuncture with little or no benefit but reported improvement in pain/burning or tingling sensations after starting topical cannabinoids. However, all patients that reported benefit had neuropathy symptoms return after several hours, suggesting that the benefit is transient. Only 1 patient reported side effects, specifically transient worsening of neuropathy that returned to baseline after discontinuing the topical. Table 1 describes patients that reported benefits from using topical cannabis, and Table 2 describes patients that did not have any benefit.

Table 1.

Patients Reporting Benefit From Topical Cannabis.

Pt Cancer type Chemotherapy Location of symptoms Treatments tried/failed Cannabis type
1 Myeloma RVD/transplant Feet Duloxetine, Gabapentin, pregabalin, acupuncture CBD
2 Breast AC-T Feet Gabapentin CBD/THC
3 Pancreatic FOLFOXIRI Hands/feet CBD/THC
4 Primary peritoneal Taxol/carbo Feet CBD
5 Breast Capecitabine/eribulin Feet THC/CBD
6 Lymphoma R-CVAD Hands/feet CBD
7 Breast AC-T Feet Gabapentin CBD
8 Breast AC-T Feet, legs CBD/THC
9 Ovarian Paclitaxel/carboplatin /bevacizumab Feet CBD
10 Breast AC-T Feet Acupuncture CBD
11 Uterine Paclitaxel Hands THC/CBD
12 Colorectal FOLFOX Hands/feet Gabapentin CBD/THC
13 Ovarian Paclitaxel/carboplatin Hands/feet Gabapentin CBD/THC
14 Pancreas FOLFOX Feet CBD
15 Pancreas FOLFOX Hands CBD/THC
16 Breast Paclitaxel/carboplatin Feet CBD/THC
17 Ovarian Paclitaxel/carboplatin Hands/feet Gabapentin CBD
18 Breast TC Hands CBD
19 Primary peritoneal cancer Paclitaxel/carboplatin Feet CBD
20 Breast AC-T Hands/feet Duloxetine, acupuncture, hydrotherapy CBD
21 Pancreatic FOLFOXIRI Feet CBD
22 Ovarian Taxol Hands/feet CBD/THC

Table 2.

Patients Who Tried Topical Cannabis Products and Did Not Report Any Benefit.

Pt Cancer type Chemotherapy Location of symptoms Treatments tried/failed Cannabis type
1 Bladder Carbo/Gem; cisplatin Feet CBD
2 Prostate Docetaxel Feet CBD
3 Breast AC-T Feet SSRI, gabapentin, acupuncture CBD/THC
4 Breast AC-T Hands/feet CBD

Abbreviations: RVD, lenalidomide/bortezomib/dexamethasone; AC-T, doxorubicin, cyclophosphamide/paclitaxel; TC, docetaxel and cyclophosphamide; FOLFOXIRI, 5-florouracil/leucovorin/oxaliplatin/irinotecan; FOLFOX, 5-florouracil/leucovorin/oxaliplatin

Sample Case Studies Demonstrating Responses to Treatments With a Topical Cream Containing CBD or CBD/THC

Case 1: 49-year-old male with myeloma, treated with chemotherapy in 2008 (lenalidomide, bortezomib, dexamethasone) followed by autologous bone marrow transplant. He developed severe neuropathy in his feet that limited his activities. He had tried gabapentin, pregabalin and duloxetine, without any benefit. He started acupuncture in 2019, which also was not beneficial. He had been using oral cannabis for years for arthritis pains/sleep, but it had no effect on his CIPN. He started using a CBD cream (250 mg/jar) 1 to 2 times per day and reported significant improvement in his neuropathic pain. This cream contains essential oils and ingredients that may enhance skin penetration. 48 He rated his baseline pain at 7 to 10 which diminished to 4-5/10 within 5 minutes of application; he noted that the effect lasted throughout the night. He noted a slight feeling on heat upon application but no pain or other adverse effects.

See also  What is green roads cbd oil used for

Case 2: 73-year-old female with breast cancer, treated with doxorubicin, cyclophosphamide, and paclitaxel (AC-T) for stage II breast cancer in 2017. She developed neuropathy in her feet that was bothersome at night. She had tried gabapentin, without benefit, and developed dizziness from it. She started a THC/CBD cream (unknown mg), obtained from local cannabis dispensary. This cream contains emu oil which has been shown to increase skin absorption . 49 Baseline neuropathy was rated at 8/10 which improved to 2-3/10, within minutes after application. She reported that the benefit lasted throughout the night with no adverse effects. She stopped gabapentin and continued to use the cannabis cream with ongoing benefit.

Case 3: 65-year-old male with pancreatic cancer who developed CIPN after oxaliplatin-based chemotherapy. His baseline neuropathy was rated as 6/10 in his feet and hands. He reported using an artisan cream containing approximately 600 mg CBD, 600 mg THC per jar. This cream also contained essential oils to aid in absorption . 48 His symptoms improved to 4/10 after application within a few days and benefits last most of the day. He continues to use the cream daily with no adverse effects.

Case 4: 71-year-old female with primary peritoneal cancer who developed painful CIPN after taxane-based chemotherapy, rated at 7/10. She reported using a CBD cream (250 mg/jar) that reduced pain to 3/10 within minutes and lasts about 12 hours. This cream contains essential oils and other ingredients to enhance skin absorption. She uses the cream daily with no side effects.

Case 5: 78-year-old female with advanced breast cancer who developed CIPN after capecitabine-eribulin chemotherapy. Baseline CIPN, rated at 6/10, reduced to 1/10 in feet after 15 minutes of applying a cream with CBD 180 mg/THC 6 mg per jar. She reports the benefit lasts 24 hours and she uses it daily with no reported side effects.

Case 6: 59-year-old male with lymphoma who developed severe CIPN in his feet and hands after receiving cyclophosphamide, vincristine, doxorubicin, and dexamethasone, rating his pain at 10/10 baseline. He uses a cream with 200 mg/jar CBD only and reports improvement to 5/10 after about 30 minutes. The effect lasts about 3 hours, without any side effects.

Case 7: 60-year-old female with breast cancer, who developed CIPN after AC-T chemotherapy, rated 8/10 at night in feet despite gabapentin. She uses a CBD cream (120 mg/jar) and notes improvement to 0/10 within 10 to 15 minutes, with the benefit lasting through the night. This cream contains essential oils to enhance absorption. She uses the cream nightly and reports no side effects.

Case 8: 55-year-old female who developed CIPN in her feet and legs after AC-T chemotherapy for breast cancer. Baseline CIPN rated at 6/10 which improved to 1/10 using a cream containing 477 mg THC and 158 mg CBD/jar. Noted improvement in 10 to 15 minutes and effect lasts 2 to 3 hours. She is using the cream a few times a week, mostly at night which helps with sleep with no side effects.

Case 9: 64-year-old female with recurrent ovarian cancer, developed painful CIPN after taxane-based chemotherapy. Baseline pain was rated at 6/10 in feet, improved to 4/10 after using CBD oil (250 mg/jar). She notes the oil starts to work in 10 minutes, with effect lasting through the night. She uses nightly, sometimes applies in the morning, as well, with no reported side effects.

Case 10: 62-year-old female with breast cancer who developed neuropathy due to AC-T chemotherapy in feet. She tried acupuncture without any benefit. Rated baseline neuropathy at 8/10 which improved to 5/10 after using CBD cream (unknown mg) after 10 minutes, with effect lasting about 3 hours. She is using the cream BID with no side effects.

The above 10 cases are summarized as the first ten cases in Table 1 , followed by 12 additional case summaries.


The positive results reported by patients in this case series are consistent with the current literature that cannabis products can decrease neuropathic pain in people, from a variety of conditions, including CIPN. Most of the patients reporting benefit described a partial decrease in painful CIPN symptoms with the onset of perceived benefit in about 10 to 15 minutes; this benefit generally lasted a few hours up to 24 hours. However, a minority of patients using topical products did not report any benefit. Only 1 patient reported a side effect, that being transient worsening of neuropathic pain: this patient discontinued use of the cream.

There are multiple preclinical models to suggest mechanisms by which cannabinoids may help alleviate CIPN. In rodent models of CIPN, a decrease of endocannabinoid levels has been observed, suggesting activation of the system may provide benefit. 47 -49 Indeed, THC and additional CB1 and CB2 receptor agonist, or modulators of the endocannabinoid system, have been shown to suppress neuropathic pain, by several different mechanisms, 29 including in models of CIPN. 26 Cannabinoid receptors, in particular CB1 receptors, can alter the activity of GABAergic and glutamatergic signaling in the brain and spinal cord. 50 In rats, a mixed CB1 and CB2 receptor agonist suppressed nociception via a CB1 specific mechanism 51 as well as vincristine associated neuropathy via CB1 and CB2 receptor activation. 52 In another rat model, a CB2 selective agonist attenuated painful neuropathy induced by paclitaxel. 53 The authors suggest that activation of CB2 suppresses nociception and central sensitization in a variety of tissue and nerve injury models of persistent pain. 54 Neuropathic pain may also involve abnormal hyper-excitability in skin afferent nerves. Skin cells express CB2 and endothelin receptors, and when activated, release B-endorphin, which can reduce hyperalgesia mediated by pro-inflammatory pathways. 55,56

An additional potential mechanism of CB1 and CB2 receptor activation leading to suppression of neuropathic pain is from modulation of immune system function. THC and the endocannabinoid system can inhibit the release of pro-inflammatory cytokines throughout the inflammatory response, by targeting T and B cells, and macrophage activity. 29

Similar to CB1 and CB2 receptors agonists, the neuroprotective and anti-inflammatory properties of CBD provide a potential mechanism for the protective effects of CBD in neuropathic pain, including CIPN. 57 For example, CBD has been shown to directly or indirectly modulate several receptors involved in modulating pain signaling, including 5-HT1A, 34 and transient receptors TRPV1 and TRPA1. 28,31 TRPV1 receptors are present in sensory peripheral nerves as well as keratinocytes and are activated by capsaicin, as well as by endogenous cannabinoids. 58 Capsaicin is a TRPV agonist that has been extensively studied in pain and has activity in treating neuropathic pain. It leads to overstimulation and desensitization of nociceptors and may lead to nerve regeneration and restoration. 59 A placebo-controlled, double-blinded, crossover trial of a capsaicin cream demonstrated that it substantially decreased chronic post-surgical scar pain and its benefit persisted after stopping the capsaicin. 60 CBD may also act as a neuroprotective agent as a result of direct antioxidant activity. 61 During secondary injury, CBD can reduce intracellular calcium levels and have neuroprotective effects. 62 CBD reduces mitochondrial damage during events of cellular stress, thereby diminishing generation of inflammatory and oxidative products. 63 CBD also inhibits microglial proliferation and pro-inflammatory cytokines and increases anti-inflammatory cytokine production in vivo. 31,32,64

Patients in this case report reporting benefit were using both topical CBD alone (n = 12) and a combination of CBD/THC topicals (n = 10). Given that CBD is a negative modulator of CB1, it would seem that topical THC working via a CB1 mechanism would not be involved in anti-nociception. The role of CBD and THC or the combination would need to be studied in a clinical trial to determine the contribution of each compound toward pain relief. Cannabis contains not only CBD and THC but many other cannabinoids and terpenoids which appear to play a role in its activity. The “entourage effect” describes the synergy of all of the compounds observed when using whole plant-based products which may be more effective than isolated compounds. 65 However, conducting research using THC and/or whole plant extracts is very difficult given federal regulations and extreme heterogeneity in types and concentrations of products.

This case series has limitations given the retrospective nature of the study, the lack of control groups, and wide heterogeneity of products used by patients. The placebo effect has also been demonstrated in a study in which an experimental product was shown to help symptoms regardless of whether subjects received cannabis or not. 66 However, experience in the clinic suggests that more patients surveyed responded to topical cannabis products than did not and provides the rationale for proceeding with a randomized placebo-controlled trial using a standardized product to determine the actual efficacy of such treatment.


This case series suggests that cannabinoids may be helpful for patients with chemotherapy-induced peripheral neuropathy. This paper also discusses the potential mechanisms of action by which topical cannabinoids might alleviate established CIPN symptoms. Noting that there is wide heterogeneity in the concentration and type of cannabis in topical creams available, a randomized placebo-controlled trial of a standardized product is needed to determine the actual utility of this approach for treating CIPN. Work is ongoing to develop such.


Authors Note: Stacy D’Andre now affilated to Mayo Clinic, Rochester, MN, USA.

Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.

See also  Cbd oil for cancer dosage

Ethics Approval and Consent to Participate/Publish: This case series was approved by the Sutter Health Expedited Review Committee, San Francisco, CA, May 14, 2020. Written consent for publication was obtained by the author from the patients with detailed case reports and is located in the patient medical record.

Availability of Supporting Data: All data collected are included in this published article.


1. Starobova H, Vetter I. Pathophysiology of chemotherapy-induced peripheral neuropathy . Front Mol Neurosci . 2017; 10 :174. doi: 10.3389/fnmol.2017.00174 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

2. Seretny M, Currie GL, Sena ES, et al. Incidence, prevalence, and predictors of chemotherapy-induced peripheral neuropathy: a systematic review and meta-analysis . Pain . 2014; 155 :2461-2470. doi: 10.1016/j.pain.2014.09.020 [PubMed] [CrossRef] [Google Scholar]

3. Lee G, Grovey B, Furnish T, Wallace M. Medical cannabis for neuropathic pain . Curr Pain Headache Rep . 2018; 22 :8. doi: 10.1007/s11916-018-0658-8 [PubMed] [CrossRef] [Google Scholar]

4. Gewandter JS, Dworkin RH, Finnerup NB, Mohile NA. Painful chemotherapy-induced peripheral neuropathy: lack of treatment efficacy or the wrong clinical trial methodology? Pain . 2017; 158 :30-33. doi: 10.1097/j.pain.0000000000000653 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

5. Flatters SJL, Dougherty PM, Colvin LA. Clinical and preclinical perspectives on chemotherapy-induced peripheral neuropathy (CIPN): a narrative review . Br J Anaesth . 2017; 119 :737-749. doi: 10.1093/bja/aex229 [PubMed] [CrossRef] [Google Scholar]

6. Blanton HL, Brelsfoard J, DeTurk N, et al. Cannabinoids: current and future options to treat chronic and chemotherapy-induced neuropathic pain . Drugs . 2019; 79 :969-995. doi: 10.1007/s40265-019-01132-x [PMC free article] [PubMed] [CrossRef] [Google Scholar]

7. Zajączkowska R, Kocot-Kępska M, Leppert W, Wrzosek A, Mika J, Wordliczek J. Mechanisms of chemotherapy-induced peripheral neuropathy . Int J Mol Sci . 2019; 20 :1451. doi: 10.3390/ijms20061451 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

8. Schmidt BL, Hamamoto DT, Simone DA, Wilcox GL. Mechanism of cancer pain . Mol Interv . 2010; 10 :164-178. doi: 10.1124/mi.10.3.7 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

9. Sherif MA, Cortes-Briones JA, Ranganathan M, Skosnik PD. Cannabinoid-glutamate interactions and neural oscillations: implications for psychosis . Eur J Neurosci . 2018; 48 :2890-2902. doi: 10.1111/ejn.13800 [PubMed] [CrossRef] [Google Scholar]

10. Omran M, Belcher EK, Mohile NA, et al. Review of the role of the brain in chemotherapy-induced peripheral neuropathy . Front Mol Biosci . 2021; 8 :693133. doi: 10.3389/fmolb.2021.693133 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

11. Johnson JR, Lossignol D, Burnell-Nugent M, Fallon MT. An open-label extension study to investigate the long-term safety and tolerability of THC/CBD oromucosal spray and oromucosal THC spray in patients with terminal cancer-related pain refractory to strong opioid analgesics . J Pain Symptom Manag . 2013; 46 :207-218. doi: 10.1016/j.jpainsymman.2012.07.014 [PubMed] [CrossRef] [Google Scholar]

12. Brown D, Watson M, Schloss J. Pharmacological evidence of medicinal cannabis in oncology: a systematic review . Support Care Cancer . 2019; 27 :3195-3207. doi: 10.1007/s00520-019-04774-5 [PubMed] [CrossRef] [Google Scholar]

13. Nugent SM, Morasco BJ, O’Neil ME, et al. The effects of cannabis among adults with chronic pain and an overview of general Harms . Ann Intern Med . 2017; 167 :319-331. doi: 10.7326/m17-0155 [PubMed] [CrossRef] [Google Scholar]

14. Wilsey B, Marcotte T, Tsodikov A, et al. A randomized, placebo-controlled, crossover trial of cannabis cigarettes in neuropathic pain . J Pain . 2008; 9 :506-521. doi: 10.1016/j.jpain.2007.12.010 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

15. Abrams DI, Jay CA, Shade SB, et al. Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial . Neurology . 2007; 68 :515-521. doi: 10.1212/01.wnl.0000253187.66183.9c [PubMed] [CrossRef] [Google Scholar]

16. Ellis RJ, Toperoff W, Vaida F, et al. Smoked medicinal cannabis for neuropathic pain in HIV: a randomized, crossover clinical trial . Neuropsychopharmacology . 2009; 34 :672-680. doi: 10.1038/npp.2008.120 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

17. Ware MA, Wang T, Shapiro S, et al. Smoked cannabis for chronic neuropathic pain: a randomized controlled trial . CMAJ . 2010; 182 :E694-E701. doi: 10.1503/cmaj.091414 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

18. Wilsey B, Marcotte T, Deutsch R, Gouaux B, Sakai S, Donaghe H. Low-dose vaporized cannabis significantly improves neuropathic pain . J Pain . 2013; 14 :136-148. doi: 10.1016/j.jpain.2012.10.009 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

19. Hoggart B, Ratcliffe S, Ehler E, et al. A multicentre, open-label, follow-on study to assess the long-term maintenance of effect, tolerance and safety of THC/CBD oromucosal spray in the management of neuropathic pain . J Neurol . 2015; 262 :27-40. doi: 10.1007/s00415-014-7502-9 [PubMed] [CrossRef] [Google Scholar]

20. Andreae MH, Carter GM, Shaparin N, et al. Inhaled cannabis for chronic neuropathic pain: a meta-analysis of individual patient data . J Pain . 2015; 16 :1221-1232. doi: 10.1016/j.jpain.2015.07.009 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

21. Lynch ME, Cesar-Rittenberg P, Hohmann AG. A double-blind, placebo-controlled, crossover pilot trial with extension using an oral mucosal cannabinoid extract for treatment of chemotherapy-induced neuropathic pain . J Pain Symptom Manag . 2014; 47 :166-173. doi: 10.1016/j.jpainsymman.2013.02.018 [PubMed] [CrossRef] [Google Scholar]

22. Pertwee RG. Cannabinoid pharmacology: the first 66 years . Br J Pharmacol . 2006; 147 :S163-S171. doi: 10.1038/sj.bjp.0706406 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

23. Showalter VM, Compton DR, Martin BR, Abood ME. Evaluation of binding in a transfected cell line expressing a peripheral cannabinoid receptor (CB2): identification of cannabinoid receptor subtype selective ligands . J Pharmacol Exp Ther . 1996; 278 :989-999. [PubMed] [Google Scholar]

24. Thomas A, Baillie GL, Phillips AM, Razdan RK, Ross RA, Pertwee RG. Cannabidiol displays unexpectedly high potency as an antagonist of CB1 and CB2 receptor agonists in vitro . Br J Pharmacol . 2007; 150 :613-623. doi: 10.1038/sj.bjp.0707133 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

25. Niesink RJ, van Laar MW. Does cannabidiol protect against adverse psychological effects of THC? Front Psychiatry . 2013; 4 :130. doi: 10.3389/fpsyt.2013.00130 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

26. Masocha W. Targeting the endocannabinoid system for prevention or treatment of chemotherapy-induced neuropathic pain: studies in animal models . Pain Res Manag . 2018; 2018 :5234943. doi: 10.1155/2018/5234943 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

27. Vučković S, Srebro D, Vujović KS, Vučetić Č, Prostran M. Cannabinoids and pain: new insights from old molecules . Front Pharmacol . 2018; 9 :1259. doi: 10.3389/fphar.2018.01259 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

28. Muller C, Morales P, Reggio PH. Cannabinoid ligands targeting TRP channels . Front Mol Neurosci . 2018; 11 :487. doi: 10.3389/fnmol.2018.00487 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

29. Donvito G, Nass SR, Wilkerson JL, et al. The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain . Neuropsychopharmacology . 2018; 43 :52-79. doi: 10.1038/npp.2017.204 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

30. Fernández-Ruiz J, Sagredo O, Pazos MR, et al. Cannabidiol for neurodegenerative disorders: important new clinical applications for this phytocannabinoid? Br J Clin Pharmacol . 2013; 75 :323-333. doi: 10.1111/j.1365-2125.2012.04341.x [PMC free article] [PubMed] [CrossRef] [Google Scholar]

31. Costa B, Trovato AE, Comelli F, Giagnoni G, Colleoni M. The non-psychoactive cannabis constituent cannabidiol is an orally effective therapeutic agent in rat chronic inflammatory and neuropathic pain . Eur J Pharmacol . 2007; 556 :75-83. doi: 10.1016/j.ejphar.2006.11.006 [PubMed] [CrossRef] [Google Scholar]

32. Toth CC, Jedrzejewski NM, Ellis CL, Frey WH, II. Cannabinoid-mediated modulation of neuropathic pain and microglial accumulation in a model of murine type I diabetic peripheral neuropathic pain . Mol Pain . 2010; 6 :16. doi: 10.1186/1744-8069-6-16 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

33. Xiong W, Cui T, Cheng K, et al. Cannabinoids suppress inflammatory and neuropathic pain by targeting α3 glycine receptors . J Exp Med . 2012; 209 :1121-1134. doi: 10.1084/jem.20120242 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

34. Ward SJ, McAllister SD, Kawamura R, Murase R, Neelakantan H, Walker EA. Cannabidiol inhibits paclitaxel-induced neuropathic pain through 5-HT(1A) receptors without diminishing nervous system function or chemotherapy efficacy . Br J Pharmacol . 2014; 171 :636-645. doi: 10.1111/bph.12439 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

35. Booz GW. Cannabidiol as an emergent therapeutic strategy for lessening the impact of inflammation on oxidative stress . Free Radic Biol Med . 2011; 51 :1054-1061. doi: 10.1016/j.freeradbiomed.2011.01.007 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

36. Kleckner AS, Kleckner IR, Kamen CS, et al. Opportunities for cannabis in supportive care in cancer . Ther Adv Med Oncol . 2019; 11 :1758835919866362. doi: 10.1177/1758835919866362 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

37. Behl D, D’Andre SD, Parise C. Patterns of use of medical cannabis in a community oncology clinic . J Clin Oncol . 2020; 38 :e24111-e24111. doi: 10.1200/JCO.2020.38.15_suppl.e24111 [CrossRef] [Google Scholar]

38. Pergam SA, Woodfield MC, Lee CM, et al. Cannabis use among patients at a comprehensive cancer center in a state with legalized medicinal and recreational use . Cancer . 2017; 123 :4488-4497. doi: 10.1002/cncr.30879 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

39. Martell K, Fairchild A, LeGerrier B, et al. Rates of cannabis use in patients with cancer . Curr Oncol . 2018; 25 :219-225. doi: 10.3747/co.25.3983 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

40. Donovan KA, Oberoi-Jassal R, Chang YD, et al. Cannabis use in young adult cancer patients . J Adolesc Young Adult Oncol . 2020; 9 :30-35. doi: 10.1089/jayao.2019.0039 [PubMed] [CrossRef] [Google Scholar]

41. Paudel KS, Hammell DC, Agu RU, Valiveti S, Stinchcomb AL. Cannabidiol bioavailability after nasal and transdermal application: effect of permeation enhancers . Drug Dev Ind Pharm . 2010; 36 :1088-1097. doi: 10.3109/03639041003657295 [PubMed] [CrossRef] [Google Scholar]

42. Stinchcomb AL, Valiveti S, Hammell DC, Ramsey DR. Human skin permeation of Delta8-tetrahydrocannabinol, cannabidiol and cannabinol . J Pharm Pharmacol . 2004; 56 :291-297. doi: 10.1211/0022357022791 [PubMed] [CrossRef] [Google Scholar]

43. Xu DH, Cullen BD, Tang M, Fang Y. The effectiveness of topical cannabidiol oil in symptomatic relief of peripheral neuropathy of the lower extremities . Curr Pharm Biotechnol . 2020; 21 :390-402. doi: 10.2174/1389201020666191202111534 [PubMed] [CrossRef] [Google Scholar]

44. Palmieri S, Mascini M, Ricci A, et al. Identification of Cannabis sativa L. (hemp) retailers by means of multivariate analysis of cannabinoids . Molecules . 2019; 24 :3602. doi: 10.3390/molecules24193602 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

45. Herman A, Herman AP. Essential oils and their constituents as skin penetration enhancer for transdermal drug delivery: a review . J Pharm Pharmacol . 2015; 67 :473-485. doi: 10.1111/jphp.12334 [PubMed] [CrossRef] [Google Scholar]

See also  Cbd oil for anxiety troy alabama

46. Mansour RSH, Sallam AA, Hamdan II, Khalil EA, Yousef I. Elucidation of penetration enhancement mechanism of Emu oil using FTIR microspectroscopy at EMIRA laboratory of SESAME synchrotron . Spectrochim Acta . 2017; 185 :1-10. doi: 10.1016/j.saa.2017.05.026 [PubMed] [CrossRef] [Google Scholar]

47. Guindon J, Lai Y, Takacs SM, Bradshaw HB, Hohmann AG. Alterations in endocannabinoid tone following chemotherapy-induced peripheral neuropathy: effects of endocannabinoid deactivation inhibitors targeting fatty-acid amide hydrolase and monoacylglycerol lipase in comparison to reference analgesics following cisplatin treatment . Pharmacol Res . 2013; 67 :94-109. doi: 10.1016/j.phrs.2012.10.013 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

48. Uhelski ML, Khasabova IA, Simone DA. Inhibition of anandamide hydrolysis attenuates nociceptor sensitization in a murine model of chemotherapy-induced peripheral neuropathy . J Neurophysiol . 2015; 113 :1501-1510. doi: 10.1152/jn.00692.2014 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

49. Khasabova IA, Khasabov S, Paz J, Harding-Rose C, Simone DA, Seybold VS. Cannabinoid type-1 receptor reduces pain and neurotoxicity produced by chemotherapy . J Neurosci . 2012; 32 :7091-7101. doi: 10.1523/JNEUROSCI.0403-12.2012 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

50. Spigelman I. Therapeutic targeting of peripheral cannabinoid receptors in inflammatory and neuropathic pain states . In: Kruger L, Light AR, eds. Translational Pain Research: From Mouse to Man . Chapter 5. CRC Press; 2010. [Google Scholar]

51. Pascual D, Goicoechea C, Suardíaz M, Martín MI. A cannabinoid agonist, WIN 55,212-2, reduces neuropathic nociception induced by paclitaxel in rats . Pain . 2005; 118 :23-34. doi: 10.1016/j.pain.2005.07.008 [PubMed] [CrossRef] [Google Scholar]

52. Rahn EJ, Makriyannis A, Hohmann AG. Activation of cannabinoid CB1 and CB2 receptors suppresses neuropathic nociception evoked by the chemotherapeutic agent vincristine in rats . Br J Pharmacol . 2007; 152 :765-777. doi: 10.1038/sj.bjp.0707333 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

53. Rahn EJ, Zvonok AM, Thakur GA, Khanolkar AD, Makriyannis A, Hohmann AG. Selective activation of cannabinoid CB2 receptors suppresses neuropathic nociception induced by treatment with the chemotherapeutic agent paclitaxel in rats . J Pharmacol Exp Ther . 2008; 327 :584-591. doi: 10.1124/jpet.108.141994 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

54. Rahn EJ, Hohmann AG. Cannabinoids as pharmacotherapies for neuropathic pain: from the bench to the bedside . Neurotherapeutics . 2009; 6 :713-737. doi: 10.1016/j.nurt.2009.08.002 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

55. Peppin JF, Albrecht PJ, Argoff C, et al. Skin matters: a review of topical treatments for chronic pain. Part one: skin physiology and delivery systems . Pain Ther . 2015; 4 :17-32. doi: 10.1007/s40122-015-0031-0 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

56. Yesilyurt O, Dogrul A, Gul H, et al. Topical cannabinoid enhances topical morphine antinociception . Pain . 2003; 105 : 303-308. doi: 10.1016/s0304-3959(03)00245-8 [PubMed] [CrossRef] [Google Scholar]

57. Zuardi AW. Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action . Rev Bras Psiquiatr . 2008; 30 :271-280. doi: 10.1590/s1516-44462008000300015 [PubMed] [CrossRef] [Google Scholar]

58. Caterina MJ. TRP channel cannabinoid receptors in skin sensation, homeostasis, and inflammation . ACS Chem Neurosci . 2014; 5 :1107-1116. doi: 10.1021/cn5000919 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

59. Anand P, Elsafa E, Privitera R, et al. Rational treatment of chemotherapy-induced peripheral neuropathy with capsaicin 8% patch: from pain relief towards disease modification . J Pain Res . 2019; 12 :2039-2052. doi: 10.2147/JPR.S213912 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

60. Ellison N, Loprinzi CL, Kugler J, et al. Phase III placebo-controlled trial of capsaicin cream in the management of surgical neuropathic pain in cancer patients . J Clin Oncol . 1997; 15 :2974-2980. doi: 10.1200/jco.1997.15.8.2974 [PubMed] [CrossRef] [Google Scholar]

61. Hampson AJ, Grimaldi M, Axelrod J, Wink D. Cannabidiol and (-)Delta9-tetrahydrocannabinol are neuroprotective antioxidants . Proc Natl Acad Sci USA . 1998; 95 :8268-8273. doi: 10.1073/pnas.95.14.8268 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

62. Ryan D, Drysdale AJ, Lafourcade C, Pertwee RG, Platt B. Cannabidiol targets mitochondria to regulate intracellular Ca 2+ levels . J Neurosci . 2009; 29 :2053-2063. doi: 10.1523/JNEUROSCI.4212-08.2009 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

63. Rajesh M, Mukhopadhyay P, Bátkai S, et al. Cannabidiol attenuates cardiac dysfunction, oxidative stress, fibrosis, and inflammatory and cell death signaling pathways in diabetic cardiomyopathy . J Am Coll Cardiol . 2010; 56 :2115-2125. doi: 10.1016/j.jacc.2010.07.033 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

64. Kozela E, Lev N, Kaushansky N, et al. Cannabidiol inhibits pathogenic T cells, decreases spinal microglial activation and ameliorates multiple sclerosis-like disease in C57BL/6 mice . Br J Pharmacol . 2011; 163 :1507-1519. doi: 10.1111/j.1476-5381.2011.01379.x [PMC free article] [PubMed] [CrossRef] [Google Scholar]

65. Russo EB. Taming THC: potential cannabis synergy and phytocannabinoid-terpenoid entourage effects . Br J Pharmacol . 2011; 163 :1344-1364. doi: 10.1111/j.1476-5381.2011.01238.x [PMC free article] [PubMed] [CrossRef] [Google Scholar]

66. De Vita MJ, Maisto SA, Gilmour CE, McGuire L, Tarvin E, Moskal D. The effects of cannabidiol and analgesic expectancies on experimental pain reactivity in healthy adults: a balanced placebo design trial . Exp Clin Psychopharmacol . 2021. Advance online publication. doi: 10.1037/pha0000465 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

CBD Oil During Chemotherapy?

I am undergoing chemotherapy for cancer, and a friend recommended I take CBD oil to help with the pain and nausea. Is it safe to do that, and does it work?

With medical cannabis now legal in 36 U.S. states, and cancer listed as a qualifying condition in many of them, it’s no wonder that more and more cancer patients are inquiring about using it, or its derivative cannabidiol (CBD). It’s also becoming more common for mainstream medical oncologists to consider recommending medical cannabis for their patients undergoing chemotherapy. Before you make any decisions about whether CBD or other forms of cannabis may be right for you, be sure to check with your doctor. Anything you take while undergoing chemotherapy could have unwanted or dangerous interactions with your chemo regimen, so don’t take CBD – or any other supplements or medications – without talking to your oncologist first.

Many patients have found that medical marijuana or its derivatives can help ease pain and nausea, especially those caused by chemotherapy, and the science supports that. In 2017, an ad hoc committee of the National Academies of Sciences, Engineering, and Medicine found strong evidence that cannabis or cannabinoids are effective for the treatment of chronic pain in adults and chemotherapy-induced nausea.

Cancer patients who use forms of medical marijuana for pain are often taking tetrahydrocannabinol (THC), which is the primary active ingredient that creates the psychoactive effects (the euphoria or “high”) that cannabis smokers experience. One recent study compared the effects of THC-dominant products against those based primarily on CBD and on products that have a mix of THC and CBD. Results showed CBD to be comparatively effective in relieving pain, without the psychoactive effects.

CBD is ubiquitous these days, and is available in oils, beauty products, capsules, and “edibles” like gummies. Even oromucosal CBD sprays have been tested and shown to be effective as an adjunctive treatment in chronic pain.

One of the most debilitating side effects of some chemotherapy regimens is peripheral neuropathy – pain in the arms and hands, legs and feet, caused by nerve damage. In a recent mouse study, researchers found evidence that CBD may be effective at staving off chemotherapy-induced peripheral neuropathy. As with many clinical trials investigating the benefits of cannabinoids, CBD was more effective when combined with very low doses of THC.

Please keep in mind that relying on CBD or cannabis alone as treatment for cancer may have serious health consequences, especially if using it delays the use of conventional medical care. While the studies so far have shown that cannabinoids can be safe in treating cancer and the effects of its treatments, they do not show that they help control or cure the disease.

Having said that, there have been some clinical trials of cannabinoids in treating cancer in humans that look promising, and more studies are planned. Although some of these investigations have concluded that THC and other cannabinoids such as CBD can help slow the growth or cause death in certain types of cancer cells, it would be premature to make changes in cancer protocols based on these results.

King KM, Myers AM, Soroka-Monzo AJ, Tuma RF, Tallarida RJ, Walker EA, Ward SJ. “Single and combined effects of Δ 9 -tetrahydrocannabinol and cannabidiol in a mouse model of chemotherapy-induced neuropathic pain.” Br J Pharmacol. 2017 Sep;174(17):2832-2841.

Shah SA, Gupta AS, Kumar P. “Emerging role of cannabinoids and synthetic cannabinoid receptor 1/cannabinoid receptor 2 receptor agonists in cancer treatment and chemotherapy-associated cancer management.” J Cancer Res Ther. 2021 Jan-Mar;17(1):1-9.

Petrovici AR, Simionescu N, Sandu AI, Paraschiv V, Silion M, Pinteala M. “New Insights on Hemp Oil Enriched in Cannabidiol: Decarboxylation, Antioxidant Properties and In Vitro Anticancer Effect.” Antioxidants (Basel). 2021;10(5):738. Published 2021 May 7.

Aviram J, Lewitus GM, Vysotski Y, Uribayev A, Procaccia S, Cohen I, Leibovici A, Abo-Amna M, Akria L, Goncharov D, Mativ N, Kauffman A, Shai A, Hazan O, Bar-Sela G, Meiri D. “Short-Term Medical Cannabis Treatment Regimens Produced Beneficial Effects among Palliative Cancer Patients.” Pharmaceuticals (Basel). 2020 Nov 30;13(12):435.

Mould RR, Botchway SW, Parkinson JRC, Thomas EL, Guy GW, Bell JD, Nunn AVW. “Cannabidiol Modulates Mitochondrial Redox and Dynamics in MCF7 Cancer Cells: A Study Using Fluorescence Lifetime Imaging Microscopy of NAD(P)H.” Front Mol Biosci. 2021 May 11;8:630107.

Ueberall MA, Essner U, Mueller-Schwefe GH. “Effectiveness and tolerability of THC:CBD oromucosal spray as add-on measure in patients with severe chronic pain: analysis of 12-week open-label real-world data provided by the German Pain e-Registry.” J Pain Res. 2019;12:1577-1604. Published 2019 May 20. ncsl/research/health/state-medical-marijuana-laws.aspx

National Academies of Sciences, Engineering, and Medicine. 2017. The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research. Washington, DC: The National Academies Press. nap/catalog/24625/the-health-effects-of-cannabis-and-cannabinoids-the-current-state, nap/resource/24625/Cannabis_committee_conclusions.pdf