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Prolonged Cannabidiol Treatment Effects on Hippocampal Subfield Volumes in Current Cannabis Users

1 School of Psychology, Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, Australia.

Samantha J. Broyd

1 School of Psychology, Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, Australia.

Yann Chye

2 Brain and Mental Health Laboratory, Monash Institute of Cognitive and Clinical Neurosciences, School of Psychological Sciences, Monash University, Clayton, Australia.

Chao Suo

2 Brain and Mental Health Laboratory, Monash Institute of Cognitive and Clinical Neurosciences, School of Psychological Sciences, Monash University, Clayton, Australia.

Mark Schira

1 School of Psychology, Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, Australia.

Peter Galettis

3 Discipline of Clinical Pharmacology, School of Medicine and Public Health, University of Newcastle, Callaghan, Australia.

4 The Australian Centre for Cannabinoid Clinical and Research Excellence (ACRE), New Lambton Heights, Australia.

Jennifer H. Martin

3 Discipline of Clinical Pharmacology, School of Medicine and Public Health, University of Newcastle, Callaghan, Australia.

4 The Australian Centre for Cannabinoid Clinical and Research Excellence (ACRE), New Lambton Heights, Australia.

Murat Yücel

2 Brain and Mental Health Laboratory, Monash Institute of Cognitive and Clinical Neurosciences, School of Psychological Sciences, Monash University, Clayton, Australia.

Nadia Solowij

1 School of Psychology, Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, Australia.

4 The Australian Centre for Cannabinoid Clinical and Research Excellence (ACRE), New Lambton Heights, Australia.


Introduction: Chronic cannabis use is associated with neuroanatomical alterations in the hippocampus. While adverse impacts of cannabis use are generally attributed to Δ 9 -tetrahydrocannabinol, emerging naturalistic evidence suggests cannabidiol (CBD) is neuroprotective and may ameliorate brain harms associated with cannabis use, including protection from hippocampal volume loss. This study examined whether prolonged administration of CBD to regular cannabis users within the community could reverse or reduce the characteristic hippocampal harms associated with chronic cannabis use.

Materials and Methods: Eighteen regular cannabis users participated in an ∼10-week open-label pragmatic trial involving daily oral administration of 200 mg CBD, with no change to their ongoing cannabis use requested. Participants were assessed at baseline and post-CBD treatment using structural magnetic resonance imaging. Automated longitudinal hippocampal segmentation was performed to assess volumetric change over the whole hippocampus and within 12 subfields.

Results: No change was observed in left or right hippocampus as a whole. However, left subicular complex (parasubiculum, presubiculum, and subiculum) volume significantly increased from baseline to post-treatment (p=0.017 uncorrected) by 1.58% (Cohen’s d=0.63; 2.83% in parasubiculum). Heavy cannabis users demonstrated marked growth in the left subicular complex, predominantly within the presubiculum, and right cornu ammonis (CA)1 compared to lighter users. Associations between greater right subicular complex and total hippocampal volume and higher plasma CBD concentration were evident, particularly in heavy users.

Conclusions: Our findings suggest a restorative effect of CBD on the subicular and CA1 subfields in current cannabis users, especially those with greater lifetime exposure to cannabis. While replication is required in a larger, placebo-controlled trial, these findings support a protective role of CBD against brain structural harms conferred by chronic cannabis use. Furthermore, these outcomes suggest that CBD may be a useful adjunct in treatments for cannabis dependence and may be therapeutic for a range of clinical disorders characterized by hippocampal pathology (e.g., schizophrenia, Alzheimer’s disease, and major depressive disorder).


Regular and prolonged cannabis use has been associated with morphological 1,2 and functional brain changes, 2–4 cognitive impairment, 5 and increased risk of adverse mental health outcomes, including the precipitation of psychotic symptoms and disorders. 6,7 Neuroimaging evidence has consistently identified the hippocampus, a subcortical brain region critically involved in learning and memory and implicated in psychopathology, as a particular locus of compromise. 1,2 Long-term heavy cannabis users have demonstrated reduced hippocampal volume 8,9 and gray matter density 10 compared to nonuser controls, with some evidence for greater volume loss resulting from greater exposure to cannabis. 1 Alterations to hippocampal shape, 11 neurochemistry, 8 and structural 12 and functional connectivity 13 in chronic cannabis users have also been reported. Recently, we showed that volumetric reduction of specific hippocampal subfields (cornu ammonis [CA]1–4 and dentate gyrus [DG]) was sensitive to cannabis dependence, with an inverse correlation between greater lifetime cannabis exposure and subfield volumes in dependent, but not nondependent users. 14

Cannabinoid type 1 receptors (CB1Rs) are abundant throughout the brain, but occur in high density in specific regions, including the hippocampus. 15 Cannabis-related neurobiological, cognitive, and psychological harms are generally ascribed to Δ 9 -tetrahydrocannabinol (THC), the primary psychoactive constituent of cannabis, which is a partial agonist at CB1Rs. 16,17 Acute administration of THC to humans dose-dependently transiently increases anxiety, impairs cognition, and induces a range of positive and negative psychotic-like symptoms, including paranoia, delusions, and conceptual disorganization. 18–20 While the precise mechanisms underlying these effects are not well understood, animal studies have shown that THC accumulates in neurons, 21 with long-term exposure to THC resulting in neurotoxic changes in hippocampal microstructure. 22 Conversely, cannabidiol (CBD) is the second most abundant cannabinoid in cannabis and has purported neuroprotective, 23 anxiolytic, 24 and antipsychotic 25 properties. Acutely administered, CBD exerts opposing effects to THC upon activation of specific brain regions, including the hippocampus, 26 and ameliorates the induction of hippocampal-dependent cognitive impairment and psychotic-like symptoms by THC in healthy volunteers. 27 CBD has a low affinity for CB1Rs, yet demonstrates the capacity to antagonize CB1R agonists, which may underlie its functional antagonism of THC. 28 Preclinical studies have shown CBD to induce synaptic plasticity and facilitate hippocampal neurogenesis, 29,30 with some evidence suggesting that the proneurogenic action of CBD via the hippocampus may underlie its anxiolytic effects. 30 Although precise neurobiological mechanisms by which CBD may promote neurogenesis remain unclear, modulation of endocannabinoids such as anandamide through CB1Rs has been implicated. 29,31

In recent years, increasingly potent strains of cannabis containing high levels of THC and decreasing levels of CBD have dominated the market, raising concerns for greater THC-related harms in the community. 7,32 Naturalistic studies examining proportional exposure to THC and CBD by hair analysis of chronic cannabis users found that the presence of CBD in cannabis was associated with fewer psychotic-like symptoms, 33,34 improved recognition memory, 34 and increased hippocampal gray matter concentration. 10 We have recently shown apparent normalization of hippocampal volume and n-acetylaspartate (NAA; a marker of hippocampal neuronal integrity) levels in cannabis users regularly smoking cannabis containing CBD, such that they were indistinguishable from controls, while those exposed to THC but not CBD, showed 11% smaller hippocampal volumes and 15% lower NAA concentrations than controls. 8 These findings indicate CBD may protect against neurobiological and psychological harms of regular cannabis use; however, the cross-sectional nature of these studies precludes any inferences about directionality.

The possibility that prolonged administration of CBD to cannabis users may protect against or reduce THC-induced harms is intriguing. The hippocampus is highly neuroplastic and volume growth has been demonstrated following relatively brief interventions (e.g., increase in hippocampal volume by 12% in patients with schizophrenia and 16% in healthy controls following 12 weeks of aerobic exercise, 35 indicating this is an adequate timeframe to observe discernible treatment effects in the hippocampus). Hence, this study aimed to investigate whether prolonged administration of CBD may reverse hippocampal volumetric reduction typically observed in long-term, heavy cannabis users, but recruitment was broadened to enable examination of effects of CBD treatment in a sample with a range of cannabis experience. An ∼10-week pragmatic, open-label trial was undertaken, in which cannabis users within the community consumed 200 mg CBD in capsule form daily, in the context of their ongoing cannabis use. Structural magnetic resonance imaging (MRI) scans were completed at baseline and post-CBD treatment. It was hypothesized that prolonged CBD administration would result in increased hippocampal volume at post-treatment, as subserved by growth in specific subfields such as CA1, subiculum, and DG, due to the high concentration of CB1Rs in these subregions 15 and their involvement in neurogenesis. 36

Materials and Methods


Twenty regular cannabis users (at least once per month for a minimum 6 months) aged 18–55 years were recruited from the community through newspaper and online advertisements. Exclusion criteria were current or past regular (greater than once per month for >6 months in the past 3 years) other illicit drug use or dependence on or treatment-seeking for any substance other than cannabis; history of synthetic cannabinoid use; any neurological disorder or serious head injury; psychiatric history (assessed by the Mini-International Neuropsychiatric Interview Plus 37 ) or medication use; pregnancy or lack of contraception for female cannabis users; and contraindications for MRI. Eighteen participants completed both baseline and post-treatment MRI scans and are reported in this study. Participants provided informed written consent at baseline, post-treatment, and each weekly session (see Procedure, CBD administration, and dose section), and were reimbursed for their participation. The study was approved by the University of Wollongong and Illawarra and Shoalhaven Local Health District Health and Medical Human Research Ethics Committee and registered as a clinical trial (ISRCTN89498802).

Procedure, CBD administration, and dose

Further detail regarding the methodology of this pragmatic trial is provided by Solowij et al. (companion article 38 ). In brief, participants attended two comprehensive testing sessions at the beginning (baseline) and completion (post-treatment) of ∼10 weeks of CBD administration, involving MRI scanning and other assessments (electroencephalography, neuropsychological, and clinical, not reported in this study). Participants were also required to attend brief weekly appointments throughout the trial for monitoring of physiological and psychological well-being, collection of blood and urine samples, and provision of CBD capsules. Participants were not asked to make any changes to their cannabis use patterns during the trial, but were instructed to abstain from cannabis, alcohol, and other substances for a minimum 12 h before baseline and post-treatment testing sessions. Participants were requested to abstain from use of illicit substances other than cannabis throughout the trial and were advised urine drug screens would be conducted to corroborate their self-report. 38

At each weekly session, participants were provided 28 gelatin-coated capsules for oral administration containing 50 mg of 99.5% pure crystalline CBD (of herbal origin) solved in Miglyol 812 and Softisan 378 (Trigal Pharma Ltd.; BioSynthesis Pharma Group Ltd.). Participants were instructed to consume four capsules per day (100 mg in the morning and 100 mg in the evening, totaling 200 mg daily). This was selected as a “medium” dose in accordance with the range of therapeutic doses reported in human studies (e.g., 800–1000 mg/day well tolerated for up to 6 weeks in psychotic individuals 39,40 ), as well as for caution as no previous study had administered prolonged and relatively high doses of CBD to current cannabis users. Participants received an SMS text message each morning and evening reminding them to consume their capsules. At each weekly session, participants returned any unused capsules. Adherence was measured by participants self-reporting the times of any missed doses, using a Timeline Follow-Back Procedure, 41 and corroborated by the number of capsules returned.


Participants’ demographic data were obtained and lifetime substance use quantified through structured interview. The Timeline Follow-Back Procedure 41 was employed at baseline and each subsequent session to obtain a specific and accurate history of substance use throughout the trial (cumulative cannabis, alcohol, and tobacco use across the trial quantified). Cannabis use was converted to standardized units of “cones” (1 joint=3 cones; for quantification. The Alcohol Use Disorders Identification Test, 42 Severity of Dependence Scale, 43 and Cannabis Withdrawal Scale 44 were administered at baseline and post-treatment to assess extent of alcohol consumption, severity of cannabis dependence, and cannabis withdrawal symptoms from abstaining before the test session. Blood and urine samples were collected at each session to enable assay of CBD, THC, and THC metabolite concentrations in plasma 45 (following trial completion), and for corroboration of self-reported substance use by urine toxicology.

Vocabulary and matrix reasoning subscales of the Wechsler Abbreviated Scale of Intelligence 46 were administered at baseline to estimate full scale intelligence quotient (IQ). Psychological symptoms of depression, anxiety, and psychosis-proneness were assessed at baseline and post-treatment using the following standardized measures: Beck Depression Inventory 47 ; State Trait Anxiety Index 48 ; Community Assessment of Psychic Experiences 49 ; and Cannabis Experiences Questionnaire (CEQ). 50 Alternate forms of the Rey Auditory Verbal Learning Test (RAVLT), 51 demonstrated to be sensitive to cannabis-related memory impairment, 52,53 were also administered at baseline and post-treatment.

MRI acquisition and processing

Participants underwent structural MRI scans on a 3T Siemens Skyra with a 48-channel head and neck coil using a T1-weighted gradient echo sequence, MPRAGE, with 900 ms inversion time, TR/TE of 2300/2.1 ms, FA=9, 192 slices 1 mm thick, field of view=256×256 mm, and matrix=256×256, resulting in 1.0 mm isotropic resolution and a total acquisition time of 5 min and 26 sec. Participants also underwent other MRI scan sequences not reported in this study. T1-weighted images were processed using an automated longitudinal hippocampal subfield segmentation protocol available through FreeSurfer neuroimaging software version 6.0 ( 54 This technique relies upon the creation of an unbiased subject-specific atlas, which each within-subject time point is then reprocessed against, to reduce within-subject variability. 55 Furthermore, it has demonstrated greater sensitivity in identifying subtle hippocampal subregional changes than previous cross-sectional processing methods. 54 Images were first processed through the longitudinal FreeSurfer stream, 55 involving motion correction, skull stripping, intensity normalization, Talairach transformation, atlas registration, estimation of total intracranial volume, segmentation of white and gray matter volumes, and parcellation of subcortical structures, including the hippocampus. Hippocampal segmentation was then applied, generating volumes for whole left and right hippocampi as well as 12 subfields for each (parasubiculum, presubiculum, subiculum, CA1, CA2/3, CA4, granule cells in the molecular layer of the dentate gyrus [GC-ML-DG], hippocampal-amygdala transition area, fimbria, molecular layer of the dentate gyrus [ML-DG], hippocampal fissure, and hippocampal tail), as depicted in Figure 1 .

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Cross-sectional slices of a T1-weighted image from one participant with automated segmentation of hippocampal subfields overlaid. Coronal (top), axial (middle), and sagittal (bottom) views. CA, cornu ammonis; GC-ML-DG, granule cells in the molecular layer of the dentate gyrus; HATA, hippocampal-amygdala transition area; ML-DG, molecular layer of the dentate gyrus.

Statistical analyses

Statistical analyses were performed using SPSS version 21.0. Paired t-tests were conducted to assess volumetric change from baseline to post-treatment for total left and right hippocampal volumes and for the 12 subfields comprising each. As this was a novel exploratory pilot study in a small sample with no placebo control, no adjustment was made for multiple comparisons. Correlations examined associations between change in hippocampal subregion volume (post-treatment minus baseline volume, in mm 3 ) and plasma CBD concentration, substance use parameters, psychological symptom, and cognitive measures. Outcomes were further explored by group (heavy versus light users, formulated by median split on lifetime cannabis use) using repeated-measures analysis of covariance (ANCOVA).


Demographic, substance use, and psychological symptom characteristics of the sample are summarized in Table 1 . Participants were predominantly young adult males (median age 25 years; four females), most of whom had completed some tertiary education. Participants had used cannabis regularly for a median of 5.17 years and at baseline were smoking cannabis a median of 25.75 days per month. Cannabis frequency and quantity measures did not significantly differ from baseline to post-treatment, indicating that a consistent level of cannabis use was maintained by participants throughout the trial. Most participants refrained from other illicit drug use during the trial 38 (the one exception was not an outlier on any hippocampal measures and his data were retained in the analyses reported in this study). Median CBD capsule adherence was 93.16% (range 68.67–99.35%). Participants reported experiencing less euphoria when smoking cannabis (lower CEQ Euphoria scores) at post-treatment compared to baseline (p=0.001). Changes in other psychological symptoms and cognition from baseline to post-treatment in this sample are provided in Table 1 and reported in detail in a slightly larger sample by Solowij et al. 38

Table 1.

Participant Demographic Data, Substance Use Measures, and Psychological Symptoms at Baseline and Post-Treatment

  Baseline Post-treatment t/Z a p Effect size (d/r)
Age (years) 25.07 [20.56–46.83]      
Gender (male/female) 14/4      
Handedness (left/right) 2/16      
Education (years) 15.50 [11.00–17.50]      
IQ 114.44 (9.50)      
BMI 22.68 (2.96)      
Alcohol frequency (days/month) 3 [0–14] 6 [0–21] −1.95 0.051 † 0.33
Alcohol quantity (standard drinks/month) 15.50 [0–102] 27.50 [0–127.50] −1.22 0.222 0.20
Cumulative alcohol quantity across the trial (standard drinks) 97.54 (75.76)      
AUDIT 7.83 (5.10) 7.56 (4.97) 0.57 0.579 0.13
Regular smoker (yes/no) 8/10      
Tobacco frequency (days/month) 0.50 [0–30] 5.50 [0–30] −1.48 0.138 0.25
Tobacco quantity (cigarettes/month) 2.50 [0–300] 8.75 [0–225] −0.66 0.508 0.11
Cannabis use          
 Age of first use (years) 17.09 (2.18)      
 Age of onset regular use (years) 19.76 (2.11)      
 Duration regular use (years) 5.17 [0.56–28.83]      
 Estimated lifetime occasions of use (days) 1734 [141–8708]      
 Past month frequency (days/month) 25.75 [2–30] 30.00 [3–30] −1.67 0.096 † 0.28
 Past month quantity (cones) 177.50 [9–1125.00] 165 [8–1080.00] −0.60 0.551 0.10
 Cumulative quantity across the trial (cones) 438 [9.50–2195]      
 SDS 3.33 (2.47) 3.11 (2.19) 0.56 0.586 0.13
 BDI 2 [0–14] 0.50 [0–12] −2.18 0.029 * 0.36
 STAI state 25.72 (5.15) 29.39 (8.24) −2.53 0.022 * 0.67
 STAI trait 32 [20–63] 32 [20–49] −1.52 0.129 0.25
 CAPE total frequency 59.83 (10.18) 56.67 (9.13) 1.99 0.063 † 0.47
 CAPE total distress 23.78 (16.40) 19.39 (12.68) 2.09 0.052 † 0.54
 CEQ Euphoria 44.28 (7.78) 38.94 (6.81) 3.90 0.001 * 0.93
 RAVLT words recalled trials 1–5 52.59 (11.52) 55.41 (9.96) −1.88 0.079 † 0.47

Mean (SD) or median [range].

AUDIT, Alcohol Use Disorders Identification Test 42 ; BDI, Beck Depression Inventory 47 ; BMI, body mass index; CAPE, Community Assessment of Psychic Experiences 49 ; CEQ, Cannabis Experiences Questionnaire 50 ; IQ, intelligence quotient; SD, standard deviation; SDS, Severity of Dependence Scale 43 ; STAI, State Trait Anxiety Index 48 ; RAVLT, Rey Auditory Verbal Learning Task. 51

Mean and significance values of all hippocampal volumetric comparisons are presented in Table 2 . Paired samples t-tests revealed no significant change in total left or right hippocampal volume, nor in nine hippocampal subfields. However, a significant increase in left parasubiculum volume was observed (p=0.035), with trend-level increases in the left presubiculum (p=0.058) and left subiculum (p=0.066). In addition, a trend toward decreased volume in the right presubiculum was found (p=0.056). Subsequently, to increase reliability, total volumes of all subicular subfields (parasubiculum, presubiculum, and subiculum) were pooled to create a “subicular complex” 56,57 for each hemisphere. Paired samples t-tests showed a significant increase in left subicular complex volume (p=0.017; Cohen’s d=0.63), but no change in the right subicular complex (p=0.471; Cohen’s d=0.17). Changes in left and right subicular complex and substructures are detailed in Table 3 .

Table 2.

Hippocampal Whole and Subfield Volumes (mm 3 ) at Baseline and Post-Treatment

  Baseline Post-treatment p
Whole hippocampus
 Left 3940.65 (333.06) 3962.13 (344.81) 0.180
 Right 4127.15 (356.02) 4119.00 (375.98) 0.682
Subicular complex
 Left 885.18 (81.89) 899.17 (85.15) 0.017 *
 Right 865.83 (99.15) 862.06 (102.53) 0.471
 Left 64.36 (9.79) 66.18 (10.57) 0.035 *
 Right 64.97 (12.77) 64.29 (12.11) 0.418
 Left 342.48 (24.29) 347.77 (24.62) 0.058 †
 Right 334.71 (44.03) 330.36 (46.80) 0.056 †
 Left 478.33 (60.32) 485.22 (62.14) 0.066 †
 Right 466.15 (49.03) 467.40 (51.55) 0.697
 Left 706.73 (73.16) 710.41 (77.20) 0.322
 Right 750.62 (73.80) 754.35 (78.14) 0.380
 Left 252.73 (42.57) 254.05 (42.93) 0.371
 Right 284.33 (33.23) 283.08 (34.48) 0.533
 Left 326.63 (41.35) 326.89 (40.76) 0.911
 Right 353.30 (46.98) 352.50 (49.61) 0.760
 Left 360.98 (40.63) 360.80 (40.24) 0.935
 Right 383.47 (45.14) 383.72 (48.72) 0.931
 Left 62.54 (8.67) 62.76 (8.97) 0.812
 Right 65.30 (6.82) 64.78 (7.02) 0.359
 Left 96.37 (15.78) 97.26 (15.77) 0.482
 Right 92.46 (23.75) 92.11 (23.58) 0.848
 Left 667.82 (61.27) 670.34 (61.26) 0.450
 Right 695.79 (60.06) 698.67 (64.04) 0.413
Hippocampal fissure
 Left 155.92 (27.44) 157.35 (21.56) 0.725
 Right 156.50 (18.92) 152.37 (20.76) 0.379
Hippocampal tail
 Left 581.66 (62.20) 580.44 (63.11) 0.777
 Right 636.05 (71.03) 627.74 (66.95) 0.126

Mean (SD) and paired t-test significance values. Subicular complex is the sum of parasubiculum, presubiculum, and subiculum volumes.

CA, cornu ammonis; GC-ML-DG, granule cells in the molecular layer of the dentate gyrus; HATA, hippocampal-amygdaloid transition area; ML-DG, molecular layer of the dentate gyrus.

Table 3.

Percentage Change in Volume from Baseline to Post-Treatment and Effect Sizes for Left and Right Subicular Complex and Substructures

  % change Effect size (d)
Left subicular complex 1.58 0.63
 Left parasubiculum 2.83 0.55
 Left presubiculum 1.54 0.48
 Left subiculum 1.44 0.47
Right subicular complex −0.44 0.17
 Right parasubiculum −1.05 0.20
 Right presubiculum −1.30 0.51
 Right subiculum 0.27 0.10

% change calculated as ([post-treatment volume–baseline volume]/baseline volume)×100.

Correlations did not reveal any significant association between left subicular complex or subregion volume change and plasma CBD concentration, cumulative CBD dose (calculated by number of capsules returned by participants), or weeks of CBD treatment. Right subicular complex volumetric change was significantly correlated with plasma CBD concentration in the final trial week (ρ=0.62, p=0.006), as well as a trend-level association with mean CBD plasma concentration over the trial (ρ=0.45, p=0.064), suggesting that higher plasma CBD was associated with increased growth in this area, despite the overall tendency toward a decrease in this region from baseline to post-treatment ( Table 3 ). Age was not significantly correlated with any subicular change, other than at trend level in the left parasubiculum (ρ=−0.43, p=0.073), indicating growth in this subregion was more pronounced in younger participants, potentially implicating a role of brain maturation. Subicular complex or subregion volume change did not significantly correlate with any substance use measures; importantly, change in left subicular complex volume was not associated with changes in alcohol use frequency or quantity from baseline to post-treatment (both p>0.601), nor with cumulative quantity of cannabis, alcohol, or cigarettes used over the trial (all p>0.114). Left subiculum volume was correlated with lifetime duration of cannabis use at baseline (ρ=−0.54, p=0.021; trend for left subicular complex volume ρ=−0.44, p=0.066), suggesting that smaller volumes at baseline were associated with greater cannabis exposure, and these normalized with CBD treatment. A significant inverse correlation was observed between change in right subiculum volume and change in desired level of intoxication when smoking cannabis (scale 1–10 [what level of intoxication do you usually like to reach?], which tended to decrease from baseline to post-treatment: 7.14 vs. 6.97, respectively; r=−0.51, p=0.031; trend level also for left parasubiculum, r=−0.43, p=0.074; and left subicular complex, r=−0.42, p=0.080). This suggests that increased volume in these subicular regions was associated with lesser desired level of “high” following CBD treatment. No significant correlations between subicular complex or subregion volumes and psychological symptom or cognitive (RAVLT) measures were found.

Hippocampal volume change was further explored between and within groups of heavy and light users (median split on lifetime occasions of use, n=9 [seven male, eight right handed] each). Group differences in cannabis use measures are presented in Table 4 . Heavy and light users significantly differed on lifetime cannabis use, frequency and quantity of cannabis use at baseline and post-treatment, cumulative cones smoked across the trial, as well as years of education (median years: heavy=12.50 and light=16.00; p=0.003), but did not differ in age (p=0.070) or IQ (p=0.056), any plasma CBD concentration measure (all p>0.063), nor in alcohol or tobacco use or change over the trial (all p>0.136). Years of education was not correlated with any hippocampal volume measure, so was not included as a covariate in analyses. Heavy and light users did not significantly differ on any hippocampal total or subregion volume measure at baseline, other than at trend level for the left fimbria (p=0.056). Repeated-measures ANCOVAs were conducted with group as a between-subjects factor and intracranial volume and cumulative cones smoked across trial as covariates. As reported in Table 5 , no significant main effects of time were found for any total hippocampal or subregion volume. However, significant time by group interactions were observed in the left presubiculum (p=0.015) and right CA1 (p=0.012). Figure 2a and 2b depict a marked increase in volume in these subregions from baseline to post-treatment in heavy users, yet a slight decrease in lighter users, with both groups showing more similar volume post-treatment. Post hoc repeated measures ANCOVAs (controlling for cumulative cannabis use across the trial) were performed within heavy and light user groups separately. Significant main effects of time were found only in heavy users for the left presubiculum (p<0.001; light users p=0.80), left subicular complex (p=0.003; light users p=0.393), and trend level for left subiculum (p=0.064; light users p=0.344), indicating that the overall finding of increased left subicular complex volume across the trial was driven by the heavy user group. In addition, a significant main effect of time was observed in heavy users for the right CA1 (p=0.036; light users p=0.577).

Time by group interaction for (a) left presubiculum (*p=0.015) and (b) right CA1 (*p=0.012) volume, controlling for intracranial volume and cumulative cannabis use (cones smoked) across the trial. Error bars represent standard error.

Table 4.

Heavy and Light User Group Differences in Cannabis Use Measures

  Heavy (n=9) Light (n=9) Z p
Duration regular use (years)        
 Baseline 6.53 [4.13–28.83] 3.39 [0.56–5.53] −3.18 <0.001 *
Estimated lifetime occasions of use (days)        
 Baseline 2608.50 [1734.00–8707.91] 452.00 [141.00–1448.00] −3.58 <0.001 *
Past month frequency (days/month)        
 Baseline 30.00 [9.00–30.00] 12.00 [2.00–30.00] −2.68 0.006 *
 Post-treatment 30.00 [13.00–30.00] 16.00 [3.00–30.00] −2.62 0.010 *
Past month quantity (cones)        
 Baseline 375.00 [75.00–1125.00] 42.00 [9.00–463.75] −2.48 0.011 *
 Post-treatment 472.50 [58.50–1080.00] 55.00 [8.00–600.00] −2.56 0.008 *
Cumulative quantity across the trial (cones)        
 Post-treatment 1282.00 [317.00–2195.00] 113.00 [9.50–815.00] −2.96 0.002 *

Median [range] and Wilcoxon signed-rank test significance values.

Table 5.

Adjusted Mean (Standard Error) of Hippocampal Whole and Subfield Volumes for Heavy and Light User Groups

  Heavy (n=9) Light (n=9)    
  Baseline Post-treatment Baseline Post-treatment Time p Time by group p
Whole hippocampus
 Left 3822.57 (60.57) 3872.15 (62.23) 4058.73 (60.57) 4052.10 (62.23) 0.197 0.198
 Right 4025.95 (71.47) 4036.63 (68.91) 4228.35 (71.47) 4201.36 (68.91) 0.157 0.507
Subicular complex
 Left 857.42 (20.96) 884.06 (22.77) 912.94 (20.96) 914.28 (22.77) 0.683 0.104
 Right 871.28 (22.48) 865.40 (20.59) 860.38 (22.48) 858.71 (20.59) 0.254 0.780
 Left 61.74 (3.30) 62.71 (3.74) 66.98 (3.30) 69.64 (3.74) 0.591 0.471
 Right 66.50 (2.69) 65.56 (2.16) 63.44 (2.69) 63.03 (2.16) 0.195 0.322
 Left 336.55 (9.00) 350.70 (9.00) 348.41 (9.00) 344.83 (9.00) 0.752 0.015 *
 Right 336.50 (14.10) 334.65 (14.92) 332.93 (14.10) 326.07 (14.92) 0.341 0.436
 Left 459.13 (15.99) 470.64 (16.76) 497.54 (16.76) 499.80 (16.76) 0.612 0.375
 Right 468.29 (9.99) 465.20 (8.04) 464.01 (9.99) 469.61 (8.04) 0.977 0.829
 Left 678.61 (15.72) 686.20 (16.18) 734.85 (15.72) 734.63 (16.18) 0.064 † 0.424
 Right 714.39 (15.91) 731.81 (18.79) 786.84 (15.91) 776.89 (18.79) 0.119 0.012 *
 Left 238.72 (12.66) 240.03 (12.30) 266.74 (12.66) 268.08 (12.30) 0.390 0.995
 Right 273.97 (9.03) 271.91 (8.77) 294.69 (9.03) 294.25 (8.77) 0.347 0.788
 Left 313.37 (10.03) 313.59 (9.16) 339.90 (10.03) 340.20 (9.16) 0.409 0.990
 Right 333.44 (12.77) 334.74 (13.22) 373.17 (12.77) 370.26 (13.22) 0.140 0.573
 Left 346.29 (9.99) 347.79 (9.24) 375.68 (9.99) 373.81 (9.24) 0.400 0.614
 Right 364.66 (11.43) 368.37 (11.87) 402.29 (11.43) 399.07 (11.87) 0.085 † 0.378
 Left 59.46 (2.85) 60.61 (3.46) 65.63 (2.85) 64.92 (3.46) 0.486 0.453
 Right 63.67 (2.19) 62.73 (2.46) 66.94 (2.19) 66.83 (2.46) 0.523 0.631
 Left 88.24 (4.83) 88.38 (4.77) 104.50 (4.83) 106.14 (4.77) 0.836 0.697
 Right 86.02 (8.33) 81.41 (7.80) 98.90 (8.33) 102.81 (7.80) 0.201 0.055 †
 Left 647.81 (13.35) 655.02 (12.26) 687.84 (13.35) 685.65 (12.26) 0.164 0.304
 Right 679.17 (11.95) 689.94 (13.56) 712.41 (11.95) 707.41 (13.56) 0.224 0.106
Hippocampal fissure
 Left 160.18 (10.97) 157.78 (9.29) 151.66 (10.97) 156.91 (9.29) 0.365 0.501
 Right 159.09 (8.39) 149.02 (8.84) 153.92 (8.39) 155.72 (8.84) 0.159 0.370
Hippocampal tail
 Left 592.66 (25.66) 596.47 (25.11) 570.66 (25.66) 564.41 (25.11) 0.661 0.426
 Right 639.38 (29.88) 630.33 (27.22) 632.72 (29.88) 625.14 (27.22) 0.416 0.926

Repeated measures ANCOVA main effect of time and time by group interactions, controlling for intracranial volume and cumulative cannabis use (cones smoked) across the trial. Subicular complex is the sum of parasubiculum, presubiculum, and subiculum volumes.

Exploratory correlations within heavy and light user groups separately indicated associations with mean, maximum, and final trial week plasma CBD concentrations in heavy users only, for the right subicular complex (CBD plasma: mean, r=0.71, p=0.032; maximum, r=0.68, p=0.045; and final week, ρ=0.82, p=0.007), right presubiculum (mean, r=0.85, p=0.003; maximum, r=0.69, p=0.040; and final week, ρ=0.70, p=0.036), and right subiculum (final week, ρ=0.68, p=0.042), indicating greater positive change (increased volumes) with higher CBD concentrations ( Fig. 3a, b ). In heavy users, final week CBD plasma was also correlated with change in the whole right hippocampus (ρ=0.87, p=0.002, as shown in Fig. 3c ; p=0.002 also with removal of outlier) and in the right GC-ML-DG (ρ=0.70, p=0.036), and trend level with right CA1 change (ρ=0.63, p=0.067), suggesting that growth in these areas may be CBD treatment related.

Significant associations in heavy users between (a) mean plasma CBD concentration and right presubiculum volume change; (b) mean plasma CBD concentration and right subicular complex volume change; and (c) final week CBD plasma concentration and right total hippocampal volume change. CBD, cannabidiol.


This study reports outcomes from the first trial of prolonged CBD treatment to cannabis users within the community. We performed an automated longitudinal hippocampal subfield segmentation to examine the potential for chronic CBD administration to restore characteristic hippocampal volumetric reduction in regular cannabis users. We found an overall significant increase of left subicular complex volume from baseline to post-treatment, subserved by growth in the left parasubiculum, presubiculum, and subiculum, with medium-large effect sizes. We compared heavy and light users to explore the influence of prior cannabis exposure on CBD treatment outcomes, finding that the increased left subicular complex volume was driven by heavy users, particularly the marked growth that occurred in the left presubiculum, which normalized post-treatment volumes toward those observed in light users. Similarly, only heavy users showed a significant increase in right CA1 volume over the trial. Despite an overall trend toward decreased right presubiculum volume from baseline to post-treatment, significant associations between higher plasma CBD concentration and increased growth in this region were apparent, particularly in heavy users. Plasma CBD concentration was also significantly correlated with right subicular complex and total right hippocampal growth in heavy users.

These findings suggest a regionally specific restorative effect of CBD upon the subicular and CA1 subfields for heavy cannabis users, in the context of ongoing and relatively consistent cannabis use during the trial. The subicular subregions receive projections from CA1 and function as the primary hippocampal output structures, interfacing with the entorhinal cortex and a range of cortical and subcortical sites. 58 Functionally, CA1 neurons are critically involved in the representation of temporal and spatial contextual information and retrieval of episodic memory, 59,60 while a dorsal-ventral functional segmentation has been suggested for subicular subregions, whereby dorsal subiculum is involved in spatial representation and memory and ventral subiculum is involved in hypothalamic–pituitary–adrenal regulation of stress, anxiety, and reward. 61

Subicular and CA1 subregions are implicated in pathophysiological models of various conditions. 62 For example, atrophy of the presubiculum, subiculum, and CA1 are the earliest sites of hippocampal degeneration in Alzheimer’s disease 62–64 ; subiculum, presubiculum, and right CA1 volume reduction have been demonstrated in patients with schizophrenia 65 and bipolar disorder; 65–67 and subiculum and CA1 shape alterations have been found in patients with major depressive disorder 68,69 and schizophrenia 70 relative to healthy controls. Substantial evidence has revealed a pattern of progressive hippocampal pathophysiology in patients with schizophrenia, beginning with extracellular glutamate dysregulation driving hypermetabolism in CA1, which precipitates attenuated psychotic symptoms, and extends to the subiculum during the transition to frank psychosis. 71–73 Longitudinal studies in ultra-high-risk patients have demonstrated focal atrophy of CA1, at a rate of 6% per year, differentiates those who progress onto syndromal psychosis and those whose attenuated psychotic symptom remit, with an extension of atrophy to the subiculum then other subfields as the illness progresses. 73,74 The rate of CA1 volume reduction specifically was found to predict worsening of symptom severity over time, 74 highlighting the importance of preventing degeneration in this subregion. Furthermore, in schizophrenia patients, subiculum volume reduction has been associated with increased negative symptoms, 65 and left presubiculum atrophy has been correlated with impairments in episodic memory. 75

Interestingly, 12 weeks of antipsychotic treatment was found to increase subicular (but not CA1) volume (encompassing all subicular subregions) by an average 32 mm 3 (2.55%) in patients experiencing a first-episode psychosis, while a healthy young adult control group (of a similar age to the sample reported in this study; mean [standard deviation]: 22.2 [4.9]) showed negligible change in this region (−0.53%) over the same period. 76 This suggests natural fluctuation in subicular volume or the influence of ongoing brain maturation across our similar trial length and participant sample is unlikely, supporting a CBD treatment effect. Given the parallels observed in schizophrenia pathophysiology and neurobiological changes conferred by chronic cannabis use, 77,78 and interest in the antipsychotic properties of CBD, 25 our finding of volumetric restoration in the subicular and CA1 regions is promising, and this therapeutic indication for CBD may extend to benefitting other clinical groups (e.g., schizophrenia).

The greater volumetric increase in heavy cannabis users is consistent with psychological symptom and cognitive outcomes from this trial, showing that dependent users experienced a significantly greater reduction in depressive and psychotic-like symptoms and improved cognition compared to nondependent users (reporting on n=20 participants 38 ). In addition, we recently demonstrated protective effects of chronic CBD treatment against the development of negative psychotic-like symptoms in a preclinical model of schizophrenia, with no effect in control animals. 79 While a ceiling effect may have occurred in lighter users, our findings nevertheless provide further support for the contention that CBD may confer greater therapeutic effects in a more compromised brain.

Our findings suggest a restorative effect of CBD on hippocampal substructures in cannabis users, even within the context of continued cannabis use. In the absence of ongoing use, as might occur in a motivated treatment-seeking sample, greater neurotherapeutic benefit may be expected. During the trial, participants reported feeling less high after using cannabis and this was corroborated by significant reduction at post-treatment on the CEQ Euphoria subscale. As such, CBD may be a valuable adjunct to psychological treatments for cannabis dependence. Furthermore, subjective ratings of preferred level of cannabis intoxication were negatively associated with increased subicular region growth.

A critical limitation of this study was that it was a pragmatic, open-label trial without a placebo control. While it is unlikely that brain structural measures are amenable to expectancy effects, our findings should nevertheless be interpreted with caution. In addition, the sample was relatively high-functioning, and some participants’ cannabis use was infrequent. If therapeutic effects of CBD are more likely to manifest in a disease state, this gives even greater credence to our findings and stronger effects may be expected in a more entrenched sample. As the majority of participants were young adult males, the influence of ongoing brain maturation must be considered and future research should examine age effects as well as potential sex differences in CBD treatment effects. That some hippocampal subfield volume changes were associated with plasma CBD concentrations supports the changes being CBD treatment related. Nevertheless, replication in a larger sample placebo-controlled trial is warranted.

The mechanisms underlying a restorative effect of CBD on hippocampal subfields in cannabis users remain to be elucidated. While neurogenesis is plausible, no change was observed in the DG, the primary hippocampal subregion implicated in neurogenesis. The potential involvement of both CB1Rs and glutamate is worthy of further investigation, given the high density of cannabinoid receptors in the subicular complex and CA1 regions, 15 and evidence suggesting glutamatergic dysregulation to be a driver of subicular and CA1 volume changes associated with psychosis. 72,73 The differential pattern of volume change observed across left and right hippocampi is also of interest. While the majority of studies examining cannabis-related hippocampal pathophysiology which have reported hemispheric lateralization effects found volume reduction to be more pronounced in the right hippocampus, 10,80,81 inverse associations between left hippocampal volume and cannabis exposure (e.g., cumulative use 9 and quantity per week 82 ) have also been reported. Mechanisms for hemispheric differentiation remain unclear, and future research should seek to examine potential lateralization effects in CBD treatment response.

In conclusion, our findings are the first to demonstrate an ameliorating effect of CBD treatment upon brain structural harms characteristic of regular cannabis use. Furthermore, these results speak to the potential for CBD treatment to restore hippocampal pathology in a range of clinical populations (e.g., schizophrenia, Alzheimer’s disease, and major depressive disorder).

Abbreviations Used

ANCOVA analysis of covariance
AUDIT Alcohol Use Disorders Identification Test
BDI Beck Depression Inventory
BMI body mass index
CA cornu ammonis
CAPE Community Assessment of Psychic Experiences
CB1Rs Cannabinoid type 1 receptors
CBD cannabidiol
CEQ Cannabis Experiences Questionnaire
DG dentate gyrus
GC-ML-DG granule cells in the molecular layer of the dentate gyrus
HATA hippocampal-amygdaloid transition area
IQ intelligence quotient
ML-DG molecular layer of the dentate gyrus
MRI magnetic resonance imaging
NAA n-acetylaspartate
RAVLT Rey Auditory Verbal Learning Test
SD standard deviation
SDS Severity of Dependence Scale
STAI State Trait Anxiety Index
THC Δ 9 -tetrahydrocannabinol


This study was funded by the Australian Research Council (ARC Future Fellowship FT110100752 to N.S.) and the research was conducted with the support of the Australian Government Research Training Program Scholarship to C.B. The authors are grateful to Jack Burch, Gabrielle Fynn, Sarah Gallagher, Madeleine Godber, Lisa-marie Greenwood, Elke Macdonald, Julie-Anne Prick, Robba Rai, Karina Rovere, Beth Shaw, Amanda Simon, Hendrika van Hell, and Professors Rodney Croft, Dion Forstner, Shanlin Fu, Alison Jones, Gary Liney, and Nagesh Pai for assistance with participant and trial management, procedures, and logistics. Cannabidiol was provided by the BioSynthesis Pharma Group Ltd. and formulated into capsules by Trigal Pharma Ltd., a company of the BioSynthesis Pharma Group. MRI scans were performed at the Cancer Therapy Centre, Liverpool Hospital, NSW, facilitated by the Ingham Institute.

Author Disclosure Statement

No competing financial interests exist.



Cite this article as: Beale C, Broyd SJ, Chye Y, Suo C, Schira M, Galettis P, Martin JH, Yücel M, Solowij N (2018) Prolonged cannabidiol treatment effects on hippocampal subfield volumes in current cannabis users, Cannabis and Cannabinoid Research 3:1, 94–107, DOI: 10.1089/can.2017.0047.

CBD: Cannabidiol How to Use It.

We have two companies here in the office and its either Full spectrum or THC free. Preferably the full spectrum is best but if there is a chance of drug testing or concern then the THC varieties are fine.

Med7 which is a water soluble and fast absorb THC free (17 mg per ml)


The number of MGs per serving is indicated on our labels for both tinctures and capsules.

The 750mg bottle of 30 gel caps has 25mg CBD per capsule it is full spectrum

The 1,000mg bottle of THC Free gel caps has 40 capsules at 25mg CBD per capsule

The tinctures are in 30ml (one oz) bottles and a recommended dose is 1 ml per day (dropper is marked)

The 1000mg tincture has 33.33mg CBD per dropperful and its full spectrum

The 500mg tincture has 16.66mg CBD per dropperful and its full spectrum

Everyone’s endocannabinoid system and conditions are different. For best results its best to dose two to three times a day in smaller amounts than to use a lot only once a day unless its just for sleep and then a bigger dose at bedtime makes sense.

This is a suggested dosage chart for CBD either brand but if you are not getting results with the lower dose products then go to the higher dose product (i.e. start low and go slow). There is NO psychoactive component to either of the brands full spectrum or not. There is just more cannabinoid support covered in the full spectrum. CBD is 20 x more anti-inflammatory than aspirin and helpful for ADD, anxiety, chronic inflammation, insomnia, autoimmune diseases, energy, focus among other issues.

Mild Conditions

46-85 lbs 86-150 lbs 151-240 lbs 240+ lbs______________

5 mg in AM 5 mg in AM 5 mg in AM 5 mg in AM 5 mg in PM 5 mg in noon 5 mg in noon 10 mg in noon 5 mg at bed 5 mg a bed 10 mg at bed 10 mg at bed

Mid- range Conditions

5 mg in AM 5 mg in AM 5 mg in AM 10 mg in AM 5 mg in PM 5 mg in noon 10 mg in noon 10 mg in noon 10 mg at bed 10 mg a bed 10 mg at bed 15 mg at bed

Severe Conditions

5 mg in AM 5 mg in AM 10 mg in AM 15 mg in AM 10 mg in PM 10 mg in noon 10 mg in noon 20 mg in noon 10 mg at bed 20 mg a bed 20 mg at bed 30 mg at bed

So, these are the starting doses going low and slow you can go up from there. If you are using tinctures or liquids which is what I suggest at first to see what dose feels the best to you. If you are micro dosing small doses more frequently often you can get away with less than just waiting until there is pain or problems and doing a big dose but experiment and see what feels best to you.

If you are at a 25 mg size, then you can try the capsules and then we can get larger dose capsules as well often.

“The most effective neuropathic pain relief occurs after 1 week of daily CBD treatment,” senior author Gabriella Gobbi, MD, PhD, professor of psychiatry, neurobiological psychiatry unit, McGill University, Montreal, Canada, told Medscape Medical News.

CBD has been used therapeutically in doses ranging from 2.85 to 50 mg/kg/day, “meaning that its therapeutic dose is still unclear,” the researchers noted. ( 1 kg is 2.2 pounds) The findings suggest that repeated CBD administration for at least one week is needed to reduce neuropathic pain and associated anxiety, as a single acute treatment is unlikely to be effective.

Here is an article about the endocannabinoid system that might help explain why this works that I wrote for the Revive magazine which also is a lot of good information about cannabinoids.

How Does Cannabis Actually Work?

Most of us were introduced to cannabis as a street drug that was illegal, because it was a gateway drug to really “bad drugs.” We never wondered how cannabis got you “high”, like alcohol or opiates. We did know that we didn’t feel bad after having some, like with alcohol and other pharmaceutical drugs, except the late-night raid on the fridge set the waistline up a few inches. Some of us didn’t like it because we felt strange and a little paranoid, others liked the “high”.

For most people, “how” cannabis works is something we thought chemists and doctors knew. In this instance, we didn’t know why cannabis worked, yet had been used medicinally for over 5000 years. Cannabis, as medicine, can alleviate far more medical problems than most drugs over, under, or behind the counter and without harm to the body. The question of HOW cannabis works medicinally has finally been researched, but getting people to understand a little about it, (including the medical profession), is the purpose of this article.

The focus of cannabis research in the second half of the 20 th century was pretty one sided. The American Medical Society’s Dr William Woodward in 1937, after two hours of testimony before congress stated “ the AMA knows of no dangers from the medical use of cannabis” and he pointed out that the government had no credible scientific evidence to prove it was a problem, including the fact it had been used for hundreds of years and no known overdose or problems. 1 Also discussed at this same meeting was the opium crisis as being far worse menace than cannabis.

The government spent the next 50 years trying to prove cannabis was a problem to justify keeping cannabis illegal. It never had any science to prove the claims that it would lead us to degrading behavior and ruin. The government also stopped all other schools of medicine that didn’t use allopathic approach, no more herbal medicine allowed, no homeopathic medicine allowed as other herbs like cannabis had hundreds of years of safe use. 2 The drug companies gained power in medical schools and education, so cannabis as medicine was forgotten. However, time and time again, the government started research to prove it was a bad drug and the studies came out saying it was not harmful and no reason to make it the toughest on the schedule of drugs. It has been listed next to heroin as Schedule 1 drug despite most of the opiates being listed as a Schedule 2 drug and far more dangerous. The Nixon administration had conducted the largest research to that date and it said cannabis was NOT a gateway drug and should not be a schedule 1 drug and further investigation was needed as to HOW it worked. 3 Researchers wanted to do extensive studies to understand why there has never been a known overdose? How was that possible and how does it work? The government’s answer was to destroy all the research studies to that date per President Gerald Ford.4

Fortunately, other counties were more interested in facts, and in Israel Dr Ralph Mechoulam continued his research and in 1964 he figured out the chemical structure of THC, which is one of the 483 chemicals in cannabis that contributes to the “high” obtained from cannabis. The next number of years had us figuring out what in a human body reacts with the THC. This led to the discovery of the Endocannabinoid System (ECS) of a human body. 5 It was discovered that the ECS is the master regulator of human function, or physiology. It’s an overarching system of regulating how your physical body interacts and protects you from the environment around you. Science calls it maintaining homeostasis.

We make our own cannabinoid substances very much like THC and they interact with the endocannabinoid receptors called CB1and CB2. The CB1 receptor is found largely in the brain and the CB2 in the immune system and everywhere in the body. There are no receptors in the areas of the brain that control breathing or slowing the heart like opiates do so that’s why there isn’t an overdose issue. We discovered some of the human endocannabinoids, like 2AG and Anandamide, that help control brain protection and function. So, your CB1 or CB2 receptors are what you want your personal endocannbinoids to influence to get a certain protective or functional response. Examples would be your cannabinoids would influence a CB1 receptor and it would act like a seizure circuit breaker, or inhibit pain signals, control your anxiety, fear and stress, or regulate inflammation.

The ECS regulates information processing, your process for learning and memory, how your gut works, recovery from a stroke or heart attack, and according to Dr Mecoulam “endocannabionoids apparently act in just about every system people have looked at”. 6 So again another example of how it works; you have a traumatic brain injury, your ECS immediately reduces the extent and severity of your brain injury, reducing inflammation, pain, and starting repair. Therefore, the US government grabbed a patent titled “Cannabinoid as Antioxidants and Neuroprotectants” in October 2003 awarded to the Department of Health and Human Services. 7 The patent claims exclusive rights on the use of cannabinoids for treating neurological diseases, such as Alzheimer’s, Parkinson’s and stroke, and diseases caused by oxidative stress, such as heart attack, Crohn’s disease, diabetes and arthritis and other conditions. Weren’t they smart to do that!

Our endocannabinoid system will influence the way we recover from pretty much any illness or problem resulting from inflammation. This includes mental illness, which is just another way of saying the brain is on fire due to inflammation in the brain and elsewhere in the system.

So how does Cannabis and hemp figure into this? In nature there are bio identical plant-based options to support a damaged or overwhelmed endocannabinoid system in humans and all vertebrate species. The two types of cannabinoids that commonly are talked about from cannabis are THC, which accounts for the psychoactive component and much of the pain-relieving properties, and CBD a non-psychoactive chemical which acts as a balancing (or antidote for too much) THC, as well as many other amazing properties. Cannabis and Hemp, (as well as Echinacea and Sunflowers) to date are the only plants we know have any measurable human cannabinoid like substances in them. Cannabis strains (called chemovars) have varying amounts of many different cannabinoids and hemp has mostly CBD and much less, and almost no discernable, THC. So, medicating with cannabis or hemp is like boosting the body’s ECS, a system associated with physiologic health and wellbeing.

So, we started the early 20 th century knowing cannabis worked but not how it worked, and it was in most every pharmaceutical preparation until 1938. Then the government said forget the anecdotal evidence of 5000 years of use, and made cannabis something that made you “stoned, lazy, addicted, violent, mentally impaired for life, or mentally disturbed”, despite the large amount of research to the contrary. Finally, the science tells us that we have an endocannabinoid system in our bodies that often needs help, as it is the guardian of our nervous system and regulates the neurobiology of our pain and ability of the body to maintain balance (homeostasis).

We now know that some of us have had damage, from the environment we have encountered to our ECS, and can’t regulate the environment as easily. This is due in part to toxins severely damaging our guts and immune system. Often overwhelming emotional traumas can’t be forgotten that create pathways or “loops” in some people’s brains and can continually cause anxiety and PTSD, possibly because some vulnerability genetically in their endocannabinoid system. We finally have the legal right to do research in the United States.8

We know now that using cannabinoids from plants, such as cannabis and hemp, are easily available and grown, and don’t need a billion-dollar process and justification for us to take, (such as a pharmaceutical drug needs). They help us repair and enhance our ECS and are safe and effective.

So why is it that not all medical and pharmacy schools are teaching the endocannabinoid system, and current data says most medical schools don’t teach it. Nor is it taught in high school and college biology? 9 Good question, and hopefully the next couple years will show that we are all more educated about our bodies and how to keep our endocannabinoid system safe and working. Also, its hopeful that we will all have the right to use a little help when needed from organic, biodynamic plant sourced medicine that has helped us for 5000 years.

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