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Cbd oil for dogs can you treat cruciate ligament

How I Treated Our Dog’s Partial Cruciate Tear

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A few years ago I received an email from a fellow dog lover whose dog was diagnosed with a partial cruciate tear and I realized that I never updated my blog about Sydney’s condition.

Before you read further, please know that a partial cruciate tear is very serious and if you suspect that your dog has a tear, please contact your vet immediately.

What’s a Cruciate Tear?

“Cranial cruciate rupture is the tearing of the cranial cruciate ligament; it is the most common cause of rear-leg lameness in dogs and a major cause of degenerative joint disease (progressive and permanent deterioration of joint cartilage) in the stifle joint; rupture may be partial or complete.” Source:

How Sydney’s Partial Cruciate Tear was Diagnosed?

Sydney had been limping pretty badly and didn’t want to put weight on her rear, left leg. Our veterinarian did a physical exam with Sydney standing up (she wouldn’t lie down) where she tested her motion, watched her walk, and felt her knee area for movement.

Sydney was prescribed pain pills for a little under a month along with rest.

Because it wasn’t a full cruciate tear, surgery wasn’t recommended.

Diet and Exercise to Help Repair a Cruciate Tear in Dogs

We limited Sydney’s exercise, curbing her zoomies around the yard. I walked with her (mommy and me time) while J played with Rodrigo, Scout, and Zoey. This was the easy part because Sydney is like me, she’s a couch potato.

The diet part was harder and this is where I made one crucial mistake. I did reduce the amount of food she was eating, but I did it by sight. She was still eating too much for her decreased activity level and she gained 10 pounds over the year – that’s a lot for a dog.

J purchased a new digital scale that’s more accurate than the one I was using and I weigh all of our dogs’ meals. This and light exercise is helping Sydney finally losing weight, however, she didn’t keep it off. My girl’s sedentary ways kept bringing the weight back and I had to find a right balance of food to help her lose – I learned a lot about calories, fat, and fasting, which I will discuss below.

Supplements for a Partial Cruciate Tear in Dogs

The following supplements were added to Sydney’s diet per discussions with our nutritionist and they work to boost joint and bone health.

  • a quality joint supplement – I recommend Cosequin DS Plus with MSM
  • a natural pain relief supplement – I recommend DGP for Pets
  • a quality CBD oil – I recommend IrieCBD for Pets (use KTW15 to save 15% off your order)
  • a teaspoon of golden paste per meal – CLICK HERE for the recipe

Diet and Exercise to Help with Weight Loss in Dogs

Ronny LeJeune, a professional dog trainer in Louisiana, helped her dog, Loki, heal from a cruciate tear and her dog is in amazing shape. I mention Ronny because she’s a good person to follow on social media to learn about dog training and canine body awareness.

I learned a lot from Ronny about helping my dogs stay in shape and to specifically help Sydney get back into shape. Today, I follow the following regimen for Sydney:

Exercise Regimen for My Dog

WALKING: Sydney and I walk twice a day at least 5 days a week allowing rest days for her muscles to repair and build. I walk her for a short time in the morning and for longer (or two short walks) in the evening.

EXERCISE: To keep Sydney’s knee flexible, I do an indoor exercise to get her to put weight on both of her back legs. She loves to be brushed and will use her back legs to scratch her sides. Through grooming, I get her to do three sets of scratching on each side (hope that makes sense).

STRETCHING: Sydney doesn’t always stretch on her own so I stretch her legs, moving them in their normal range of motion, for a few minutes after a long walk.

Diet for My Dogs

DECREASE THE FAT: I made the mistake of switching Sydney to an all tripe diet; at the time, I didn’t realize how high in fat tripe is and she gained weight. Sydney still enjoys tripe, but it’s part of a meal instead of an entire meal. I also feed more lean proteins like rabbit and beef.

DECREASE THE SERVING AMOUNT: I decreased Sydney’s meals by 40%. I was worried about hunger pukes, but that hasn’t been a problem because I make up half of the difference with fermented vegetables or thawed green beans.

INTRODUCE FASTING: I now fast all of my dogs once a week. On Friday night, they get a big meal, a few ounces more than I usually feed them, and they don’t eat again until Saturday afternoon. If my dogs are begging for food, which has happened once, so far, I give them a small meal of goats milk mixed with turkey broth from Answers Pet Food.

How Sydney is Doing Today

Sydney is doing great. There was a time when she was more active and playful, and she was walking up to 2-3 miles, and she’s walking on all of her legs. She had a setback, which sucked, so we’re working our way back. Today, she’s back to her happy and playful self and she’s walking up to 1 mile a day.

There was a time when she had regular appointments for chiropractic care and acupuncture, but that has decreased to quarterly and we’ve introduced Bowan therapy, a holistic technique that involves moving the muscles in a specific way, working on the soft connective tissue of the body. Bowen therapy treats musculoskeletal, sports injuries, and chronic conditions.

Sydney isn’t a fan of going to the vet, but she loves how she feels after she leaves and when we get home, she sleeps for hours and then she’s ready to take on the world.

I’m not a veterinarian so I can’t tell you that what I did will work for your dog. This is what worked for me and I don’t believe that it’s a happy coincidence, but I have no scientific proof to offer either. I do know that better nutrition leads to healthier dogs and natural supplements are better tolerated by dogs and humans.

Pharmacokinetics, Safety, and Clinical Efficacy of Cannabidiol Treatment in Osteoarthritic Dogs

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.


Objectives: The objectives of this study were to determine basic oral pharmacokinetics, and assess safety and analgesic efficacy of a cannabidiol (CBD) based oil in dogs with osteoarthritis (OA).

Methods: Single-dose pharmacokinetics was performed using two different doses of CBD enriched (2 and 8 mg/kg) oil. Thereafter, a randomized placebo-controlled, veterinarian, and owner blinded, cross-over study was conducted. Dogs received each of two treatments: CBD oil (2 mg/kg) or placebo oil every 12 h. Each treatment lasted for 4 weeks with a 2-week washout period. Baseline veterinary assessment and owner questionnaires were completed before initiating each treatment and at weeks 2 and 4. Hematology, serum chemistry and physical examinations were performed at each visit. A mixed model analysis, analyzing the change from enrollment baseline for all other time points was utilized for all variables of interest, with a p ≤ 0.05 defined as significant.

Results: Pharmacokinetics revealed an elimination half-life of 4.2 h at both doses and no observable side effects. Clinically, canine brief pain inventory and Hudson activity scores showed a significant decrease in pain and increase in activity (p < 0.01) with CBD oil. Veterinary assessment showed decreased pain during CBD treatment (p < 0.02). No side effects were reported by owners, however, serum chemistry showed an increase in alkaline phosphatase during CBD treatment (p < 0.01).

Clinical significance: This pharmacokinetic and clinical study suggests that 2 mg/kg of CBD twice daily can help increase comfort and activity in dogs with OA.


Routine nonsteroidal anti-inflammatory drug (NSAID) treatments, though efficacious, may not provide adequate relief of pain due to osteoarthritis (OA) and might have potential side effects that preclude its use, particularly in geriatric patients with certain comorbidities, such as kidney or gastrointestinal pathologies (1–4). In a systematic review of 35 canine models of OA and 29 clinical trials in dogs, treatment with NSAIDs caused adverse effects in 35 of the 64 (55%) studies, most commonly being gastro-intestinal signs (3). Although other pharmacological agents are advocated, such as gabapentin or amantadine, there is little evidence regarding their efficacy in dogs with chronic or neuropathic pain related to OA. Recent medical interest in alternative therapies and modalities for pain relief has led many pet owners to seek hemp related products rich in cannabinoids.

The endocannabinoid receptor system is known to play a role in pain modulation and attenuation of inflammation (5–7). Cannabinoid receptors (CB1 and CB2) are widely distributed throughout the central and peripheral nervous system (8–10) and are also present in the synovium (11). However, the psychotropic effects of certain cannabinoids prevent extensive research into their use as single agents for pain relief (5, 12). The cannabinoids are a group of as many as 60 different compounds that may or may not act at CB receptors. One class of cannabinoids, cannabidiol (CBD), may actually be an allosteric non-competitive antagonist of CB receptors (13). In lower vertebrates, CBD is also reported to have immunomodulatory (14), anti-hyperalgesic (15, 16), antinociceptive (17, 18), and anti-inflammatory actions (5, 19), making it an attractive therapeutic option in dogs with OA. Currently there are several companies distributing nutraceutical derivatives of industrial hemp, rich in cannabinoids for pets, yet little scientific evidence regarding safe and effective oral dosing exists.

The objectives of this study were to determine: (1) single-dose oral pharmacokinetics, (2) short-term safety, and (3) efficacy of this novel CBD-rich extract, as compared to placebo, in alleviating pain in dogs with OA. Our underlying hypotheses were that appropriate dosing of CBD-rich oil would safely diminish perceived pain and increase activity in dogs with OA.

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Materials and methods

CBD oil and protocols approval

The industrial hemp used in this study was a proprietary hemp strain utilizing ethanol and heat extraction with the final desiccated product reconstituted into an olive oil base containing ~10 mg/mL of CBD as an equal mix of CBD and carboxylic acid of CBD (CBDa), 0.24 mg/mL tetrahydrocannabinol (THC), 0.27 mg/mL cannabichromene (CBC), and 0.11 mg/mL cannabigerol (CBG); all other cannabinoids were less than 0.01 mg/mL. Analysis of five different production runs using a commercial analytical laboratory (MCR Laboratories, Framingham, MA) show less than a 9% difference across batches for each of the detected cannabinoids listed above. The study was performed after the Cornell University institutional animal care and use committee (IACUC) approved the study following the guidelines for animal use according to the IACUC. Client owned dogs were enrolled after informed consent in accordance with the Declaration of Helsinki.


An initial investigation into single-dose oral pharmacokinetics was performed with 4 beagles (3.5–7 years, male castrated, 10.7–11.9 kg). Each dog received a 2 mg/kg and an 8 mg/kg oral dosage of CBD oil, with a 2-week washout period between each experiment. The dogs were fed 2 h after dosing. Physical examination was performed at 0, 4, 8, and 24 h after dosing. Attitude, behavior, proprioception, and gait were subjectively evaluated at each time point during free running/walking and navigation around standard traffic cones (weaving). Five milliliters of blood was collected at time 0, 0.5, 1, 2, 4, 8, 12, and 24 h after oil administration. Blood samples were obtained via jugular venipuncture and transferred to a coagulation tube for 20 min. Samples were centrifuged with a clinical centrifuge at 3,600 × g for 10 min; serum was removed and stored at −80°C until analysis using liquid chromatography-mass spectrometry (LC-MS) at Colorado State University Core Mass Spectrometry facility.

Extraction of CBD from canine serum and mass spectrometry analysis

CBD was extracted from canine serum using a combination of protein precipitation and liquid-liquid extraction using n-hexane as previously described (20), with minor modifications for microflow ultra-high pressure liquid chromatography (UHPLC). Briefly, 0.05 mL of canine serum was subjected to protein precipitation in the presence of ice-cold acetonitrile (80% final concentration), spiked with deuterated CBD as the internal standard (0.06 mg/mL, CDB-d3 Cerilliant, Round Rock, TX, USA). 0.2 mL of water was added to each sample prior to the addition of 1.0 mL of hexane to enhance liquid-liquid phase separation. Hexane extract was removed and concentrated to dryness under laboratory nitrogen. Prior to LC-MS analysis, samples were resuspended in 0.06 mL of 100% acetonitrile. A standard curve using the CBD analytical standard was prepared in canine serum non-exposed to CBD and extracted as above. Cannabidiol concentration in serum was quantified using a chromatographically coupled triple-quadropole mass spectrometer (UHPLC-QQQ-MS) using similar methods as previously described (21).

CDB serum concentration data analysis

From the UHPLC-QQQ-MS data, peak areas were extracted for CBD detected in biological samples and normalized to the peak area of the internal standard CBD-d3, in each sample using Skyline (22) as well as an in-house R Script ( CBD concentrations were calculated to nanograms per mL of serum as determined by the line of regression of the standard curve (r 2 = 0.9994, 0–1,000 ng/mL). For this assay, the limits of detection (LOD) and limits of quantification (LOQ) represent the lower limits of detection and quantification for each compound in the matrix of this study (23, 24). Pharmacokinetic variables were estimated by means of non-compartmental analysis, utilizing a pharmacokinetic software package (PK Solution, version 2.0, Montrose, CO, USA).

Inclusion and exclusion criteria for the clinical trial

The study population consisted of client-owned dogs presenting to Cornell University Hospital for Animals for evaluation and treatment of a lameness due to OA. Dogs were considered for inclusion in the study if they had radiographic evidence of OA, signs of pain according to assessment by their owners, detectable lameness on visual gait assessment and painful joint(s) on palpation. Each dog had an initial complete blood count ([CBC] Bayer Advia 120, Siemens Corp., New York, NY, USA) and serum chemistry analysis (Hitachi 911, Roche Diagnostics, Indianapolis, IN, USA) performed to rule out any underlying disease that might preclude enrolment. Elevations in alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were allowed if prior hepatic ultrasound was deemed within normal limits except for potential non-progressive nodules (possible hepatic nodular hyperplasia). All owners completed a brief questionnaire to define the affected limb(s), duration of lameness, and duration of analgesic or other medications taken. All dogs underwent radiographic examination of affected joints and a radiologist confirmed the presence or absence of OA, and excluded the presence of concomitant disease that might preclude them from enrolment (i.e., lytic lesions).

During the trial, dogs were only allowed to receive NSAIDs, fish oil, and/or glucosamine/chondroitin sulfate without any change in these medications for 4 weeks prior to or during the 10-week study period as standard of care for the disease process. Other analgesic medications used, such as gabapentin and tramadol, were discontinued at least 2 weeks prior to enrolment. Dogs were excluded if they had evidence of renal, uncontrolled endocrine, neurologic, or neoplastic disease, or were undergoing physical therapy. Every dog was fed its regular diet with no change allowed during the trial.

Clinical trial

The study was a randomized, placebo-controlled, owner and veterinarian double-blind, cross-over trial. Dogs received each of two treatments in random order (Randomizer iPhone Application): CBD, 2 mg/kg every 12 h, or placebo (an equivalent volume of olive oil with 10 parts per thousands of anise oil and 5 parts per thousands of peppermint oil to provide a similar herbal smell) every 12 h. Each treatment was administered for 4 weeks with a 2-week washout period in between treatments. Blood was collected to repeat complete blood counts and chemistry analysis at weeks 2 and 4 for each treatment.

At each visit, each dog was evaluated by a veterinarian based on a scoring system previously reported (25) as well as by its owner (canine brief pain inventory [CBPI], Hudson activity scale) before treatment initiation and at weeks 2 and 4 thereafter (26–28).

Statistical analysis

Initial power analysis was performed to assess number of dogs needed for this study as a cross over design with a power set 0.80 and alpha of 0.05 using prior data suggesting a baseline CBPI or Hudson score change of ~15 points (two tailed) with a standard deviation of 20. When calculated it was assumed that 14 dogs would be necessary to find differences in outcomes of interest (29).

Statistical analysis was performed with a commercially available software package (JMP 12.0, Cary, NC, USA). All continuous data were assessed utilizing a Shapiro–Wilk test for normality. Considering a majority of our blood, serum and scoring data were normally distributed a mixed model analysis was used to analyze these outcomes, including the fixed effects of treatment, time, sequence of treatment assignment, gender, age, NSAID usage, treatment × time; as well as random effects of observation period, period nested within dog, time point nested within period nested within dog to account for the hierarchical nature of data in a cross-over design as well as repeated measurements for each dog. For ordinal veterinary scoring data a similar linear mixed model was used, but differences from baseline were first calculated to approximate a normal distribution to meet assumptions for a mixed model analysis. Residual diagnostics of all final models showed that residuals were normally distributed and fulfilled the assumption of homoscedasticity, and assumptions where therefore met. This statistical modeling approach allowed for adequate control of hierarchical data structure necessary in a cross-over design, as well as for the performance of easily interpretable time × treatment Tukey post-hoc comparisons that were our main interest, as compared to an ordinal logistical regression (30, 31). To control for baseline differences and therefore the possible difference in relative change in CBPI pain, and activity interference assessments and Hudson scoring across dogs, the initial CPBI or Hudson Scores were included for these analyses as a covariate. Pairwise comparisons between all-time points of both groups were corrected for multiple comparisons with Tukey’s post-hoc tests to examine the interaction of time and treatment variables, and to assess differences between change from baseline at any time point as they related to treatment. A p-value of less than 0.05 was defined as the significance cut-off.



Pharmacokinetics demonstrated that CBD half-life of elimination median was 4.2 h (3.8–6.8 h) for the 2 mg/kg dose, and 4.2 h (3.8–4.8 h) for the 8 mg/kg dose (Table ​ (Table1). 1 ). Median maximal concentration of CBD oil was 102.3 ng/mL (60.7–132.0 ng/mL; 180 nM) and 590.8 ng/mL (389.5–904.5 ng/mL; 1.2 uM) and was reached after 1.5 and 2 h, respectively, for 2 and 8 mg/kg doses. No obvious psychoactive properties were observed on evaluation at any time point during the 2 and 8 mg/kg doses over 24 h. These results led to dosing during the clinical trial at 2 mg/kg body weight every 12 h, due the cost prohibitive nature of 8 mg/kg dosing for most larger patients, the impractical nature of more frequent dosing, the volume of oil necessary and anecdotal reports surrounding 0.5-2 mg/kg dosing recommended by other vendors.

Table 1

Serum pharmacokinetic of single oral dosing (2 mg and 8 mg/kg) of CBD oil in dogs.

Cmax (ng/mL) Tmax (h) T1/2 elim (h) AUC 0-t (ng-hr/mL) MRT (h)
DOSE (2 mg/kg)
Dog 1 61 1 4.4 183 6.0
Dog 2 132 1 3.9 351 4.2
Dog 3 102 2 3.8 382 5.1
Dog 4 101 2 6.8 437 9.1
Median (Range) 102 (61–132.0) 1.5 (1.0–2.0) 4.2 (3.8–6.8) 367 (183–437) 5.6 (4.2–9.1)
DOSE (8 mg/kg)
Dog 1 499 2 3.8 2,928 5.7
Dog 2 389 1 4.8 1,753 7.0
Dog 3 905 2 4.2 3,048 5.1
Dog 4 682 2 4.1 2,389 5.2
Median (Range) 591 (389–905) 2.0 (1.0–2.0) 4.2 (3.8–4.8) 2,658 (1,753–3,048) 5.6 (5.1–7.0)

Cmax, maximum concentration; Tmax, time of maximum concentration; T1/2 el, half-life of elimination; AUC 0-t, area under the curve (time 0–24 h); MRT, median residence time.

Dogs included in the clinical trial

Twenty-two client-owned dogs with clinically and radiographically confirmed evidence of osteoarthritis were recruited. Sixteen of these dogs completed the trial and were included in the analyses; their breed, weight, age, sex, worse affected limb, radiographic findings, use of NSAIDs and sequence of treatments are summarized in Table ​ Table2. 2 . Dogs were removed due to osteosarcoma at the time of enrolment, gastric torsion (placebo oil), prior aggression issues (CBD oil), pyelonephritis/kidney insufficiency (CBD oil), recurrent pododermatitis (placebo oil), and diarrhea (placebo oil).

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Table 2

Characteristics of dogs enrolled in a placebo-controlled study investigating the effects of CBD on osteoarthritis.

Breed Weight (kg) Age (years) Sex Radiographic findings and OA localization NSAID
Rottweiler 35.3 10 FS – Moderate, intracapsular swelling with moderate osteophytosis, left stifle Carprofen (2.1 mg/kg BID)
Mix 30.6 13 MC – Moderate-to-severe, right-shoulder osteoarthrosis; mild, left-shoulder osteoarthrosis
– Moderate-to-severe, bilateral hip osteoarthrosis
Mix 27.2 9 FS – Moderate medial coronoid remodeling (with fragmentation on the right) and bilateral elbow osteoarthrosis None
Mix 30.5 14 MC – Moderate enthesiopathies on right carpus; mild, left-antebrachiocarpal osteoarthrosis
– Bilateral moderate coxofemoral osteoarthrosis
Mix 23.5 10 FS – Moderate bilateral stifle osteoarthrosis and moderate intracapsular swelling Carprofen (2.2 mg/kg)
Mix 28.1 10 FS – Moderate bilateral elbow osteoarthrosis
– Moderate left-stifle osteoarthrosis with intracapsular swelling
Metacam (0.1 mg/kg
English Bulldog 25.2 8 MC – Severe osteoarthrosis, left elbow
– Moderate intracapsular swelling and mild osteoarthrosis, right stifle
Carprofen (2 mg/kg BID)
German Shorthaired Pointer 21.5 14 FS – Moderate bilateral elbow osteoarthrosis Carprofen (2.4 mg/kg BID)
Labrador Retriever 26.1 13 FS – Bilateral severe stifle osteoarthrosis due to cranial cruciate ligament disease Meloxicam (0.1 mg/kg SID)
Mix 18.2 13 FS – Bilateral moderate elbow osteoarthrosis and medial epicondylitis Meloxicam (0.1 mg/kg SID)
Mix 22 9 FS – Moderate, stifle osteoarthrosis with moderate intracapsular swelling None
Bernese Mountain Dog 50 3 M – Bilateral severe elbow osteoarthritis, medial coronoid disease, and medial epicondylitis Carprofen (2 mg/kg SID)
Belgian Malinois 25.1 9 FS – Severe bilateral elbow osteoarthrosis
– Bilateral moderate hip osteoarthrosis
Carprofen (2 mg/kg BID)
Mix 28.6 13 FS – Severe bilateral elbow osteoarthritis
– Severe bilateral hip osteoarthritis
Border Collie 22 14 MC – Severe thoracolumbosacral osteophytosis
– Multifocal carpal enthesiophytes
Beagle 17.6 5 MC – Mild left elbow osteoarthrosis, with possible medial coronoid disease
– Moderate-to-severe bilateral stifle osteoarthrosis

FS, female spayed; MC, male castrated; Mix, mixed breed; SID, once daily; BID, twice daily.

Clinical trial

CBPI and Hudson change from baseline scores showed a significant decrease in pain and increase in activity (p < 0.01) at week 2 and 4 during CBD treatment when compared to baseline week 0, while no other statistical significances were observed across treatment in this cross-over design (Table ​ (Table3). 3 ). Lameness as assessed by veterinarians showed an increase from baseline in lameness with age (p < 0.01), whereas NSAID use (p = 0.03) reduced lameness scores. Veterinary pain scores showed a decrease from baseline in dogs on NSAIDs (p < 0.01). CBD oil resulted in a decrease in pain scores when compared to baseline on evaluation at both week 2 and week 4 (p < 0.01 and p = 0.02, respectively), and week 2 CBD oil treatment was lower than baseline placebo treatment (p = 0.02) and week 4 placebo treatment (p = 0.02). No other veterinary pain comparisons were statistically significant. No changes were observed in weight-bearing capacity when evaluated utilizing the veterinary lameness and pain scoring system (Table ​ (Table3 3 ).

Table 3

Canine Brief Pain Inventory (Pain and Activity questions) and Hudson Scale mean and standard deviation; lameness, weight-bearing and pain scores median and ranges at each time for cannabidiol (CBD) and placebo oils.

CBD oil Placebo oil
Week 0 Week 2 Week 4 Week 0 Week 2 Week 4
CBPI Pain (0–40) 21 ± 8 14 ± 6 * 14 ± 8 * 17 ± 7 19 ± 9 19 ± 9
CBPI activity interference (0–60) 35 ± 15 25 ± 15 * 26 ± 14 * 27 ± 15 29 ± 15 31 ± 16
Hudson (0–110) 54 ± 13 67 ± 15 * 67 ± 10 * 65 ± 14 64 ± 16 60 ± 19
Veterinary lameness§ 3 (1–4) 3 (1–4) 3 (1–4) 3 (2–4) 3 (2–4) 3 (1–4)
Veterinary pain ∫ 3 (3–4) 3 (2–4) * 3 (1–4) * 3 (2–4) ** 3 (2–4) 3 (2–4) **
Veterinary weight-bearing = 2 (1–3) 2 (1–3) 2 (1–3) 2 (1–3) 2 (1–3) 2 (1–3)

** Represents significant differences (p < 0.05) from week 2 of CBD oil treatment. §Lameness was scored as follows: 1 = no lameness observed/walks normally, 2 = slightly lame when walking, 3 = moderately lame when walking, 4 = severely lame when walking, 5 = reluctant to rise and will not walk more than 5 paces. ∫Pain on palpation was scored as follows: 1 = none, 2 = mild signs, dog turns head in recognition, 3 = moderate signs, dog pulls limb away, 4 = severe signs, dog vocalizes or becomes aggressive, 5 = dog will not allow palpation. = Weight-bearing was scored as follows: 1 = equal on all limbs standing and walking, 2 = normal standing, favors affected limb when walking, 3 = partial weight-bearing standing and walking, 4 = partial weight-bearing standing, non-weight-bearing walking, 5 = non-weight-bearing standing and walking.

Table 4

Serum chemistry values of dogs receiving CBD or placebo oils.

Reference CBD oil Placebo oil
Week 0 Week 2 Week 4 Week 0 Week 2 Week 4
Sodium 145–153 mEq/L 149 ± 3 149 ± 2 149 ± 1 149 ± 1 149 ± 2 149 ± 2
Potassium 4.1–5.6 mEq/L 4.9 ± 0.3 4.9 ± 0.5 4.9 ± 0.3 4.8 ± 0.4 4.9 ± 0.4 4.9 ± 0.3
Chloride 105–116 mEq/L 110 ± 3 109 ± 3 109 ± 2 110 ± 2 110 ± 2 110 ± 2
SUN 10–32 mg/dL 20 ± 9 20 ± 7 20 ± 6 19 ± 6 21 ± 7 19 ± 6
Creatinine 0.6–1.4 mg/dL 1.0 ± 0.3 1.1 ± 0.3 * 1.0 ± 0.3 * 0.9 ± 0.3 1.0 ± 0.3 * 1.0 ± 0.3 *
Calcium 9.3–11.4 mg/dL 10.4 ± 0.5 10.4 ± 0.4 10.3 ± 0.4 10.4 ± 0.6 10.4 ± 0.4 10.4 ± 0.4
Phosphorus 2.9–5.2 mg/dL 3.8 ± 0.8 3.9 ± 0.8 3.9 ± 0.6 4.0 ± 0.7 3.9 ± 0.6 4.0 ± 0.5
Magnesium 1.4–2.2 mg/dL 1.8 ± 0.2 1.8 ± 0.2 1.8 ± 0.2 1.8 ± 0.1 1.8 ± 0.1 1.8 ± 0.1
Glucose 63–118 mg/dL 92 ± 9 89 ± 9 92 ± 9 97 ± 10 * 93 ± 8 97 ± 10 *
ALT 20–98 U/L 93 ± 86 93 ± 88 114 ± 119 90 ± 89 222 ± 606 166 ± 284
AST 14–51 U/L 31 ± 8 33 ± 13 34 ± 16 30 ± 8 56 ± 99 45 ± 34
ALP 17–111 U/L 160 ± 212 238 ± 268 323 ± 407 * 204 ± 287 186 ± 287 175 ± 248
GGT 0–6 U/L 4 ± 3 3 ± 2 3 ± 2 3 ± 2 4 ± 6 5 ± 4
Bilirubin 0.0–0.2 mg/dL 0.1 ± 0.1 0.0 ± 0.1 0.1 ± 0.1 0.0 ± 0.1 0.0 ± 0.1 0.0 ± 0.1
Total protein 5.3–7.0 g/dL 6.3 ± 0.4 6.4 ± 0.5 6.3 ± 0.4 6.3 ± 0.4 6.3 ± 0.4 6.3 ± 0.4
Albumin 3.1–4.2 g/dL 3.7 ± 0.2 3.7 ± 0.2 3.7 ± 0.2 3.7 ± 0.2 3.7 ± 0.2 3.7 ± 0.2
Globulin 1.9–3.6 g/dL 2.6 ± 0.3 2.6 ± 0.4 2.6 ± 0.4 2.6 ± 0.4 2.6 ± 0.4 2.6 ± 0.4
Cholesterol 138–332 mg/dL 291 ± 64 301 ± 62 302 ± 62 295 ± 71 300 ± 71 308 ± 83
CK 48–260 U/L 148 ± 81 147 ± 59 134 ± 61 139 ± 57 158 ± 80 168 ± 105

Data presented at mean + standard deviations. Asterisk

Box-and-whisker plot of serum alkaline phosphatase (ALP) activity at each time for treatment and placebo oils. Box represents the mean and 25th and 75th percentile and the whiskers represent the 99th and 1st percentiles. * Indicates a significant difference (p < 0.05) from week 0 CBD treatment.


To date, an objective evaluation of the pharmacokinetics of a commercially available industrial hemp product after oral dosing in dogs is absent. This study showed that the terminal half-life of oral CBD, as the most abundant cannabinoid in this specific preparation when in an oil base, was between 4 and 5 h, suggesting it was bioavailable with a dosing schedule of 2 mg/kg at least twice daily. This half-life was shorter than a previous report after intravenous (1.88–2.81 and 3.75–5.63 mg/kg) and oral (7.5–11.25 mg/kg) administration (32). In the intravenous study, CBD distribution was rapid, followed by prolonged elimination with a terminal half-life of 9 h. When examining prior oral CBD bioavailability it was determined to be low and highly variable (0–19% of dose) with three dogs showing no absorption. This may be due to the first pass effect in the liver, and the product was not in an oil base, but a powder within a gelatin capsule being a different delivery vehicle (32). After initially seeing no neurological effects at the 2 mg/kg dose a 8 mg/kg dose was chosen to assess the potential neurological effects since mistaken overdosing can occur clinically, and a higher dose might have been necessary since the prior study showed poor absorption. Although our dogs were fasted the delivery vehicle was olive oil which is a food item. The absorption may be greater and more consistent because of the oil-based vehicle which may be due to the lipophilic nature of CBD, hence delivery with food may be preferable (32, 33). As previously demonstrated, CBD biotransformation in dogs involves hydroxylation, carboxylation and conjugation, leading to relatively rapid elimination suggesting a more frequent dosing schedule (34). The dosing schedule of twice per day was chosen due to the practical nature of this dosing regimen even though the elimination is well within a three or four time a day dosing regimen. Our hope was that the lipophilic nature of CBD would allow for a steady state over time, and future studies examining 24 h pharmacokinetics with different dosing regimens with larger numbers of dogs, and steady state serum pharmacokinetics after extended treatment in a clinical population are sorely needed.

The main objective of this study was to perform an owner and veterinary double-blinded, placebo-controlled, cross-over study to determine the efficacy of CBD oil in dogs affected by OA. Despite our small sample size, short study duration and heterogeneity of OA signs, CBPI and Hudson scores showed that CBD oil increase comfort and activity in the home environment for dogs with OA. Additionally, veterinary assessments of pain were also favorable. Although a caregiver placebo effect should be considered with subjective evaluations by owners and veterinarians (35), the cross-over design limits confounding covariates since each dog serves as its own control. Our statistical model controlled for the possible effect of treatment sequence. The lack of a placebo effect in our study may be due to nine of the 16 owners being intimately involved in veterinary medical care, all of whom have an understanding of the placebo effect making them more cognizant of improvements when providing feedback. In addition, there was a noticeable decrease in Hudson scores and rise in CBPI scores during the initiation placebo treatment suggesting a potential carry over effect of CBD treatment indicating that a longer washout period might be indicated in future studies. This carry over effect may have resulted in some improved perceptions at the initiation of the placebo treatment which were eliminated by week 4 of placebo treatment, underscoring the importance of longer term steady state PK studies in dogs.

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There was no significant difference in subjective veterinary lameness score and weight-bearing capacity throughout the study. Kinetic data was obtained from these dogs (data not shown), however 11 of the 16 dogs had significant bilateral disease (stifle, coxofemoral, or elbow) making evaluation of peak vertical force or symmetry tenuous at best. Unilateral disease in any of the aforementioned joints would be ideal to study the kinetic effects of this or similar extracts for pain relief leading to better objective outcomes. The population we used in our investigation was representative of dogs presenting in a clinical setting for management of OA and represents the typical OA patient.

Currently, NSAIDs are the primary treatment for OA and are associated with negative effects on the gastrointestinal tract and glomerular filtration (2). In the current study, no significant difference was noted in BUN, creatinine, or phosphorus between dogs treated with the CBD oil vs. the placebo oil, while NSAID treatment resulted in a higher creatinine concentration. A mild rise in creatinine from baseline was noted in both groups at weeks 2 and 4, the hydration status of the dogs was unknown; however changes in albumin sodium, and chloride were unchanged suggesting euhydration, and all creatinine values remained within the reference interval. Increased ALP activity is fairly sensitive for hepatobiliary changes in this age group, but not specific. Increased ALP activity noted in nine dogs in the CBD treatment group may be an effect of the hemp extract attributed to the induction of cytochrome p450 mediated oxidative metabolism of the liver (reported previously with prolonged exposure to cannabis) (36–38). Other causes of cholestasis, increased endogenous corticosteroid release from stress, or a progression of regenerative nodular hyperplasia of the liver cannot be ruled out. Without concurrent significant rise in ALT in the CBD treatment to support hepatocellular damage, or biopsy for further clarification, the significance is uncertain. As such, it may be prudent to monitor liver enzyme values (especially ALP) while dogs are receiving industrial hemp products until controlled long term safety studies are published.

A recent survey reported that pet owners endorse hemp based treats and products because of perceived improvement in numerous ailments, as hemp products were moderately to very helpful medicinally (39). Some of the conditions thought to be relieved by hemp consumption were: pain, inflammation, anxiety and phobia, digestive system issue, and pruritus (39). One immunohistochemical study suggested that cannabinoids could protect against the effects of immune-mediated and inflammatory allergic disorders in dogs (40) whereas another uncontrolled study suggested that CBD has anticonvulsant and anti-epileptic properties in dogs (41). The apparent analgesic effect of the industrial hemp based oil observed in the present study may be attributable to downregulation of cylooxygenase enzymes, glycine interneuron potentiation, transient receptor potential cation receptor subfamily V1 receptor agonism (peripheral nerves), and/or g-protein receptor 55 activation (immune cells), influencing nociceptive signaling and/or inflammation (14, 42, 43).

The industrial hemp product used in this study is a proprietary strain-specific extract of the cannabinoids outlined in the methods with relatively high concentrations of CBD and lesser quantities of other cannabinoids as well as small amounts of terpenes that may have synergistic effects often termed the “entourage effect.” This brings to light that fact that different strains of cannabis produce differing amounts of CBD and other related cannabinoids making the results of this study specific to this industrial hemp extract that may not translate to other available products due to differing cannabinoid concentrations in this largely unregulated market.

In conclusion, this particular product was shown to be bioavailable across the small number of dogs examined in the PK portion of the study, and dogs with OA receiving this industrial hemp extract high in CBD (2 mg/kg of CBD) were perceived to be more comfortable and active. There appear to be no observed side effects of the treatment in either the dogs utilized in the PK study at 2 and 8 mg/kg, or dogs undergoing OA treatment for a month duration. There were some dogs with incidental rises in alkaline phosphatase that could be related to the treatment. Further long-term studies with larger populations are needed to identify long-term effects of CBD rich industrial hemp treatment, however short term effects appear to be positive.

Author contributions

L-JG was responsible for data analysis and interpretation, drafting of the manuscript and approval of the submitted manuscript. JB was responsible for the conception of the study and manuscript writing and revisions. CF was responsible for acquisition of data and manuscript revision. WS was responsible for pharmacokinetic evaluation and revision of the manuscript. SM was responsible for statistical analysis, data analysis and revision of the manuscript. LW was responsible for laboratory work including liquid chromatography-mass spectrometry. HB was responsible for interpretation of the blood work and manuscript revision. EB was responsible for acquisition of data, and data analysis. JW was responsible for the conception of study, supervised data collection, statistical analysis, and manuscript editing.

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


The authors would like to thank Renee C. Staffeld and Danny Sack for data entry. The present study was financially supported by ElleVet Sciences, Portland, Maine.

Cbd oil for dogs can you treat cruciate ligament

Cannabidiol (CBD) is a phytocannabinoid from the Cannabis sativa plant. It’s been increasingly used for treating pain in dogs with arthritis due to its anti-inflammatory and analgesic properties.

This article looks at some of the studies on CBD oil for dogs arthritis and sees what the science says.

How Does CBD Oil Help in Arthritis Pain in Pets?

CBD does not directly affect pain receptors. Instead, it works indirectly by turning on endocannabinoid receptors. These are the same type of receptors that THC binds to humans for its psychoactive effects. CBD is non-psychoactive. Hence, CBD products do not cause your pet to get intoxicated.

The CB2 receptor is activated by CBD and is responsible for reducing inflammation. When activated, it inhibits the release of proinflammatory cytokines, which are chemicals that cause inflammation.

CBD is said to be effective in reducing pain and inflammation as per some studies. In one study, dogs with arthritis given CBD significantly reduced pain and improved mobility.

Many vets are starting to use CBD on their arthritic patients. However, CBD is yet to be approved by the FDA for use in animals. This is one reason why it is challenging to find a veterinarian willing to prescribe it.

What Does Science Say About CBD for Arthritis in Dogs?

One study published looked at the use of CBD for dogs with osteoarthritis. The study found that CBD could reduce pain and improve function in dogs with arthritis. CBD was also well tolerated by the dogs, with no adverse effects reported.

Another study looked at the use of CBD for treating dogs with arthritis induced by a torn cruciate ligament. The study found that CBD oilcould reduce pain and improve the quality of life in dogs.

A third study looked at CBD for treating dogs with both osteoarthritis and chronic pancreatitis. The study found that CBD could reduce pain, improve mobility and increase appetite in dogs with both conditions.

CBD is therefore considered a good candidate for treating arthritis in dogs due to its ability to reduce chronic inflammation without the side effects of traditional non-steroidal anti-inflammatory drugs. It makes it more tolerable for dogs with arthritis.

However, while CBD oil has been significant in treating arthritis in pets, research is still ongoing. It’s important to note that CBD has not shown any adverse effects in studies done so far.

CBD Oil Without Consulting Your Veterinarian

A new forecast predicts that the market will soar to $19.5 billion in 2025.

Your pet doctor will be able to recommend a CBD product that is safe and effective for your pet. They can also help you track the results of using CBD oil for your dog’s arthritis and make any necessary adjustments.

So, if you’re considering using CBD oil to treat your dog’s arthritis, speak with your veterinarian to see if it’s the right option for your pet.

Administering CBD to Your Dog for Arthritis Treatment

There are various methods to administer CBD oil to dogs with arthritis. You can give them orally as a tincture or add it to their food. CBD can also be given topically as a cream or ointment.

If you’re using a tincture, make sure it contains a high-quality carrier oil such as olive or MCT oil to help increase absorption of the CBD. Depending on your dog’s needs, you can administer CBD this way once or twice per day.

If your dog is not comfortable with oral medications, you can also mix CBD oil with their food.

CBD ointments and creams can be applied topically two to four times per day as needed. They should be massaged into the affected area until they are fully absorbed.

It’s essential to start with a low dose of CBD and increase it gradually until you see the results you’re looking for. It can take a few weeks to start seeing improvement, so it’s important not to give up too soon.

You must speak with your veterinarian about the best way to administer CBD oil to your dog for arthritis treatment.