Posted on

ldn and cbd oil

The Medicine Center Pharmacy is hosting an informational seminar for patients currently taking Low-Dose Naltrexone (LDN) and CBD oil products, or who are interested in learning more about its uses in the treatment of autoimmune disease and chronic pain.

We will review the state of the current research on its effectiveness for various conditions. Both CBD oil products and LDN have prompted many questions at our pharmacy and we are happy to share experiences and feedback with you. We will provide accurate information regarding the potential benefits of LDN and CBD oil from the experiences of our own patients, as well as to provide a forum to connect with others dealing with the difficulties of autoimmune and chronic pain disorders.

This seminar will examine the specific chronic pain conditions for which LDN has been shown to be an effective, non-opioid, treatment option for patients experiencing moderate to severe pain, inclusive of Complex Regional Pain Syndrome (CRPS), Fibromyalgia, Neuropathies, back pain and autoimmune disease. In addition, LDN’s unique ability to control pain in opioid-dependent patients, and assist in the tapering and elimination of opioids, will be reviewed. A comprehensive review of current literature will be discussed, its mechanism of action, as well as the clinical experience gained from the treatment of thousands of LDN patients, to form the clinical indication specific dosing guidance and titration protocols which are essential to achieving therapeutic success for your patients.

Ldn and cbd oil

Gene expression studies of (A) TH in the VTA, (B) μ receptor (Oprm1) in the NAc and (C) 5‐HT1A receptor in the DR of C57BL/6J mice treated with naltrexone (NTX; 0.7 mg·kg −1 , p.o.), CBD [a single administration of a microparticle formulation providing CBD continuous controlled release (20 mg·kg −1 ·day −1 , s.c.)] or their combination. The columns represent the means and vertical lines ± the SEM. & Represents the values from the groups that are significantly different (P < 0.05) from VEH + VEH and VEH + NTX groups. # Represents the values from the groups that are significantly different (P < 0.005) from CBD + VEH, VEH + NTX and VEH + VEH groups (n = 11 for each group).

Statistical analyses were performed using two‐way ANOVA with repeated measures followed by the Student–Newman–Keuls test to compare the treatment and control groups at different time points on the OEA paradigms; post hoc tests were only applied when ANOVA (F value) indicated significance. The data obtained from the gene expression studies and PR phase in OEA were statistically analysed using the two‐way ANOVA test. Statistical analyses were performed with SigmaPlot v11.0 (Systat Software Inc., Chicago, IL, USA) software. Differences were considered significant if the probability of error was less than 5%. The data and statistical analysis comply with the recommendations on experimental design and analysis in pharmacology (Curtis et al., 2018).

Saccharin substitution (9 days): The saccharin (Sac) concentration was gradually faded out as the ethanol concentration was gradually increased (Grant and Samson, 1986). Each solution combination was fixed to three consecutive sessions per combination (0.15% Sac–2.5% EtOH, 0.10% Sac–5% EtOH, 0.05% Sac–8% EtOH).

Materials

5‐HT1A receptor gene expression was reduced in the DR of CBD + VEH (−22%) and CBD + NTX (−27%) groups compared with their corresponding control group VEH + VEH (P < 0.05, two‐way ANOVA followed by Student–Newman–Keuls test). The administration of naltrexone failed to induce any modification (Figure  3 C).

Considering the role of the 5‐HT1A receptor in alcohol consumption and the allosteric effects of CBD on these receptors, it is possible that the effects of the association of CBD plus naltrexone may be mediated, at least in part, by 5‐HT1A receptors. To further investigate the relative specificity of the 5‐HT1A receptor in the mechanism underlying the effects of CBD and naltrexone, mice were pretreated with the 5‐HT1A antagonist WAY 100635 before receiving naltrexone and/or CBD in the OEA paradigm. Interestingly, pretreatment with WAY 100635 blocked the effects (reduction of ethanol intake and motivation) induced by CBD and naltrexone without having any effect by itself. Despite this finding, further studies are needed to clarify this mechanism, these results support the involvement of 5‐HT1A receptors in the effects of CBD plus naltrexone.

The effects of low doses of naltrexone (0.7 mg·kg −1 , p.o.) and/or CBD (20 mg·kg −1 ·day −1 , s.c.) on ethanol consumption and motivation to drink were evaluated in the oral‐ethanol self‐administration paradigm in C57BL/6 mice. Gene expression analyses of the opioid μ receptor (Oprm1) in the nucleus accumbens (NAc), tyrosine hydroxylase (TH) in the ventral tegmental area (VTA) and the 5‐HT1A receptor in the dorsal raphe nucleus (DR) were carried out by real‐time PCR. The role of 5‐HT1A receptors in the ethanol reduction induced by the administration of CBD + naltrexone was analysed by using the 5‐HT1A receptor antagonist WAY100635 (0.3 mg·kg −1 , i.p.).

Experiment 1: to evaluate the effects of the combination of CBD plus naltrexone on ethanol consumption and motivation to drink

For the oral self‐administration procedure, absolute ethanol (Merck, Spain) and saccharin sodium salt were dissolved in tap water [8% (v . v ‐1 ) ethanol solution (EtOH)].

Interestingly, recent evidence revealed that CBD reduces http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=9082 craving and relapse (Ren et al., 2009) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2286 intake (Weiss et al., 2016). Furthermore, our group has demonstrated that CBD also decreases http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2299 intake and ethanol preference in the two‐bottle choice paradigm in mice. In addition, a single administration of a controlled release formulation of CBD (30 mg·kg −1 ·day −1 , s.c.) that lasted for up to 2 weeks significantly decreased motivation to drink and ethanol consumption in the oral ethanol self‐administration (OEA) paradigm. CBD also reduced ethanol‐induced relapse but had no effect over non‐reinforcing substances, such as water. These behavioural effects were associated with alterations in key targets and brain regions closely related with alcohol consumption, such as http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=1243 in the ventral tegmental area (VTA), the opioid http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=319 (Oprm1) and cannabinoid receptors (http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=56, http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=57, http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=109) in the nucleus accumbens (NAc), both critical regions for reward, goal‐directed behaviour and habit formation (Viudez‐Martinez et al., 2018). Altogether, these results supported the potential therapeutic use of CBD in the treatment of AUD.