Back pain: the most common pain problem in Germany

Chronic back pain permanently affects 15-17% of adults in Germany. It is the most common cause of incapacity for work and one of the most expensive illnesses in the healthcare system. Back pain is pharmacologically complex: nociceptive pain (tissue damage), neuropathic pain (nerve root compression), myofascial pain (muscle tension) and centralized pain (chronification) often overlap.

Cannabis intervenes via several mechanisms simultaneously – which makes it interesting for this complex pain pattern.

Pain mechanisms in back pain and ECS targets

Studies: Cannabis and back pain

Aviram & Samuelly-Leichtag 2017 (J Pain Res): Retrospective study, n=206, chronic pain patients using medical cannabis. 70% reported strong or very strong pain reduction. Back pain was the most common indication.

Ware et al. 2010 (CMAJ): RCT, n=21, neuropathic pain (not only back). Nabilone (synthetic THC) significantly better than placebo for pain intensity and sleep. Shows THC analgesia for neuropathic component.

Beaulieu et al. 2006 (J Rheumatol): Fibromyalgia and back pain often overlap. Nabilone better than amitriptyline for fibromyalgia pain and sleep. Indirectly relevant for chronic back pain with central sensitization.

Overview RCTs 2022 (Cochrane analysis): 16 RCTs on cannabis for chronic pain. Moderate evidence for pain reduction. Back pain-specific subgroup shows consistent, albeit moderate analgesia.

Opioid-saving effect for back pain

Many chronic back pain patients receive opioids – with considerable long-term risks (dependence, tolerance, constipation). Cannabis as an opioid adjuvant:

Reiman et al. 2017 (Cannabis Cannabinoid Res): Survey, n=2897 cannabis dispensary patients. 97% of patients who had substituted opioids preferred cannabis. 81% reported that cannabis alone was more effective than cannabis + opioid.

Practical recommendation: cannabis for back pain

Acute pain breakthrough: THC 5-10 mg vaporizer (immediate effect) or sublingual

Continuous pain: CBD 100-200 mg daily + THC 2.5-5 mg in the evening (sleep + muscle relaxation)

Topical (local tension): CBD cream/gel directly on pain point – CB2 in muscle and fascia, no systemic effect

Neuropathic component (sciatica): CBD 150-300 mg + beta-caryophyllene-rich terpenes (CB2 agonist)

FAQ: Cannabis for back pain

Summary

Cannabis addresses all four types of pain in chronic back pain: nociceptive (COX-2), neuropathic (TRPV1/CB1), myofascial (muscle relaxation), centralized (supraspinal modulation). Study data: 70 % pain reduction in survey, moderate analgesia in Cochrane analysis. Opioid saving effect clinically significant. Symptomatically effective for intervertebral disc problems, no substitute for causal therapy. Cannabis in neuropathy for the neuropathic component; cannabis in fibromyalgia for centralized pain.

Social anxiety disorder and the ECS

Social anxiety disorder (SAD) is one of the most common anxiety disorders with a lifetime prevalence of 12%. It is characterized by intense anxiety in social situations, fear of negative evaluation and often with avoidance behavior. The ECS modulates via CB1 in the amygdala and prefrontal cortex – precisely the areas of the brain that are over-activated in SAD.

CBD for social anxiety: study overview

Social anxiety is the best clinically studied area of application for CBD in psychiatry:

Bergamaschi et al. 2011 (Neuropsychopharmacol): RCT, n=24, patients with SAD. CBD 600 mg vs. placebo before simulated public speaking (Public Speaking Test – SPST). CBD significantly reduced anxiety, cognitive impairment and discomfort when speaking vs. placebo. Physiological: normalized heart rate increase and blood pressure response.

De Aquino et al. 2020 (Neuropsychopharmacol): Extended SPST design, CBD 300 mg. Confirmed anxiolytic effect; determined U-shaped dose-response curve: 300 mg optimal, 150 mg and 600 mg less effective.

Linares et al. 2019 (Front Pharmacol): Healthy volunteers, sleep + anxiety under stress. CBD 300 mg showed significant anxiolytic effect vs. placebo.

THC for social anxiety: the paradox

While CBD consistently reduces social anxiety, THC is problematic for SAD:
– THC increases anxiety and paranoia in medium to high doses
– Social situations are subjectively perceived as more threatening
– Cannabis users with SAD have a higher risk of panic attacks in groups

Recommendation for SAD: CBD isolate or broad spectrum without THC. Full-spectrum products with THC can worsen SAD symptoms.

Mechanisms of CBD in social anxiety

5-HT1A agonism: CBD activates serotonin 5-HT1A receptors – same mechanism as buspirone (anxiolytic drug). In the hippocampus and dorsal raphe nucleus relevant for social anxiety.

Amygdala modulation: CBD reduces amygdala activation in response to anxiety-inducing stimuli (fMRI study Bhattacharyya et al. 2012). Amygdala hyperactivation is a core finding in SAD.

Hippocampal neurogenesis: Chronic CBD promotes adult neurogenesis in the hippocampus – similar to SSRIs. Long-term anxiolysis through neuroplastic effect.

Practical application: CBD for social anxiety

Situational intake (before social situations):
– CBD 300 mg sublingual, 60-90 minutes beforehand
– Ideal for: Presentations, dating, social events, public speaking

Daily continuous therapy:
– CBD 150-300 mg daily as adjuvant therapy to psychotherapy
– No substitute for CBT (cognitive behavioral therapy) – the gold standard treatment for SAD

FAQ: Cannabis for social anxiety

Summary

CBD for social anxiety disorder is one of the best documented cannabis indications: two RCTs (Bergamaschi 2011, De Aquino 2020) show significant anxiolysis in SAD patients. Optimal dose: 300 mg CBD (U-curve). Mechanism: 5-HT1A agonism + amygdala modulation. THC contraindicated in SAD – exacerbates paranoia. CBD isolate or broad spectrum without THC. Cannabis for anxiety disorder for generalized anxiety; CBD dosing guide for anxiety dosing.

Restless legs syndrome and the endocannabinoid system

Restless legs syndrome (RLS) is a neurological disorder characterized by an agonizing urge to move the legs – especially at night. It affects 5-10% of the population. The underlying pathophysiology involves dopaminergic dysregulation in the basal ganglia and spinal pain processing – two systems where the ECS directly intervenes.

Neurobiological connection: RLS and ECS

Dopamine-ECS connection: CB1 receptors are located on dopaminergic neurons in the substantia nigra and striatum. Cannabis cannabinoids modulate dopamine release – relevant for RLS whose main treatment is dopaminergic drugs (pramipexole, ropinirole).

Spinal pain modulation: RLS symptoms are partly caused by spinal nociceptor overactivation. CBD desensitizes TRPV1 and inhibits COX-2 in the spinal cord – possibly relevant for the burning and tingling sensations.

Sleep: RLS leads to massive sleep disorders. Cannabis (CBD 150 mg + low THC) has a sleep-inducing effect – symptomatically helpful even if no causal effect.

Study situation: Cannabis for RLS

There are hardly any specific RCTs on cannabis and RLS:

Ghorayeb 2020 (Sleep Med): Case Series, n=6 patients with RLS who did not respond to conventional therapy. All 6 reported complete or substantial symptom remission with cannabis (inhalation or oral ingestion). Case series limitations, but relevant for a rare treatment-resistant disease.

Walther et al. 2021 (Mov Disord): Survey, n=428 RLS patients. 36% used cannabis. Of these, 70% reported an improvement in RLS symptoms. Sleep and sense of calm improved the most.

Mechanistic: Dopamine-modulating effects of THC at low doses could improve RLS via similar pathways as dopamine agonists. Not directly proven, but pharmacologically plausible.

What could help best with RLS

In the evening before going to sleep:
– CBD 100-150 mg sublingual (sleep + TRPV1 desensitization)
– THC 2.5-5 mg low (dopaminergic modulation; muscle relaxation)
– Full spectrum with high myrcene terpene content (sedative, muscle relaxant)

For augmentation (dopamine agonist side effect):
Augmentation is the most feared side effect of pramipexole/ropinirole – exacerbation of RLS symptoms by the drug itself. Cannabis as an adjuvant or alternative option for augmentation is clinically interesting.

Important: Cannabis may interact with dopamine agonists (CYP3A4 inhibition by CBD). Medical consultation for combination.

FAQ: Cannabis and restless legs

Summary

RLS and ECS are linked via dopaminergic modulation and spinal pain processing. Survey data (Walther 2021: 70% improvement) and case series data (Ghorayeb 2020: complete remission in 6 cases) are promising. Clinical RCTs are missing. Evening CBD 100-150 mg + low THC is the practical recommendation. No substitute for dopamine agonists, but useful adjuvant option. Cannabis for sleep disorders for the sleep component; cannabis for neuropathy for spinal pain modulation.

The endocannabinoid system in bone metabolism

Bones are living tissues that are constantly being remodeled – by osteoblasts (bone formation) and osteoclasts (bone resorption). The endocannabinoid system directly regulates this remodeling: CB1 and CB2 are expressed by both cell types, and endocannabinoids are important modulators of bone physiology.

CB2 receptors are the dominant cannabinoid receptor class in bone – which means that cannabinoids without a psychoactive CB1 effect (such as CBD, CBG, beta-caryophyllene) can act on bone.

CB1 and CB2 in bone: Different functions

Study situation: cannabinoids and bone density

Idris et al. 2005 (Nat Med): CB2 knockout mice developed age-related osteoporosis faster and more severely than wild-type mice. CB2 activation protects against osteoporotic bone loss. Conversely, CB2-selective agonists increased bone density in animal models.

Idris et al. 2009 (Bone): CB2 agonist JWH-133 prevented ovariectomy-induced osteoporosis in mice. Mechanism: Inhibition of osteoclastogenesis via RANKL suppression.

Ofek et al. 2006 (PNAS): Anandamide and CB2 activation inhibit osteoclastogenesis and promote osteoblast activity in vitro. CB2 could be a therapeutic target for osteoporosis.

Cannabis and fracture healing – Koren et al. 2019 (J Bone Miner Res): CBD significantly accelerated bone healing in rat fracture model. Bones in the CBD group had higher bending stiffness and better mineralization after 8 weeks.

Clinical implications: Osteoporosis and cannabis

Osteoporosis affects 6 million people in Germany – mainly postmenopausal women and older men. Paradoxically, THC could have a bone-degrading effect on osteoclasts through CB1 activation:

Muniyappa et al. 2013 (Bone): Survey study: Chronic cannabis users had lower bone density in some cohorts. But confounders (nicotine, alcohol, BMI) difficult to control.

Conclusion for practice: CBD (without THC): potentially bone-protective via CB2. THC with high chronic consumption: possible risk of osteoporosis through CB1 on osteoclasts. No clinical use of cannabis as osteoporosis therapy at present.

FAQ: Cannabis and bones

Summary

CB2 receptors in bone regulate osteoblasts and osteoclasts. CB2 activation has a bone-anabolic effect and inhibits resorption – strongly supported by preclinical evidence (Idris 2005, 2009). CBD promotes fracture healing in animal models (Koren 2019). Chronic THC associated with lower bone density in some studies. Clinical human studies are lacking for direct therapeutic use. CB2 immune system guide for further CB2 knowledge; cannabis in rheumatism for related joint diseases.

What is cannabis microdosing?

Microdosing means taking cannabis in such low doses that the therapeutic or mood-enhancing effects are noticeable, but there is no perceptible high. For THC, this is typically 1-5 mg per dose. The concept is particularly relevant for:
– Medical users who want to maintain everyday functionality
– People with low THC tolerance
– Anxiety patients for whom high THC doses trigger panic
– Creative work (slight opening of perception without functional impairment)

Biphasic THC effect: less is more

THC shows a classic biphasic dose-response curve – a basic principle of cannabinoid pharmacology:

Low dose (1-5 mg): Anxiolytic, mood enhancing, mildly focusing, analgesic without sedation

Medium dose (10-20 mg): Euphoria, relaxation, hunger, slight time distortion – classic recreational high

High dose (25-50 mg+): paranoia, anxiety, disorientation – especially in beginners or without tolerance

The paradox: if you want to take cannabis for anxiety, you have to dose low. Higher doses worsen anxiety in many cases.

Microdosing protocol according to experience level

CBD microdosing: why even too little is too little

CBD also shows a biphasic dose effect:
– Too low (<10 mg): Often no noticeable effect
– Moderate (30-100 mg): Anxiolytic, anti-inflammatory, sleep-inducing
– High (150-300 mg): Sleep-inducing, antiepileptic (clinically relevant)

For anxiety: at least 25-50 mg CBD daily for consistent effects. Many users take too little (10 mg softgel) and report no effect – this is a dosing issue.

Practical microdosing methods

Vaporizer: Most precise method for THC. Small puff = ~1-2 mg THC, depending on strain. Effect noticeable in seconds, quick adjustment possible.

Sublingual oil: pipette with 1/4 drop of THC oil or precise CBD oil dosage. Good control.

Microdosing capsules: 2.5 mg THC capsules are medically available; simplest form for precise daily dosing.

Tincture: dropwise control; alcohol-based = fastest oral absorption.

FAQ: Cannabis microdosing

Summary

Microdosing utilizes the biphasic THC dose-response: 1-5 mg THC produces therapeutic effects without intoxication. CBD microdosing starts at 25-50 mg daily for measurable anxiolytic effects. Methods: vaporizer (most precise), sublingual oil, capsules. For daily use: cycling (5 days on, 2 days off) for tolerance avoidance. Tolerance break guide; CBD dosage guide for all indications.

ADHD and the endocannabinoid system

Attention deficit hyperactivity disorder (ADHD) is characterized by dysregulation of dopaminergic and noradrenergic systems. The endocannabinoid system directly modulates both neurotransmitter systems – which is why cannabis self-medication is particularly common among ADHD sufferers (studies estimate 20-30% of ADHD adults).

ECS-dopamine connection for ADHD

CB1 receptors are located on presynaptic dopamine neurons in the mesocorticolimbic system – the ADHD-relevant dopamine pathway:
– CB1 activation by endocannabinoids or THC: modulates dopamine release
– Anandamide deficit in ADHD: Several studies show reduced anandamide levels in ADHD sufferers
– Faah gene polymorphisms: Variant FAAH C385A increases anandamide levels and is associated with less impulsive behavior

Study situation: Cannabis and ADHD

THC for ADHD: the paradox

THC can have a paradoxical effect in ADHD – similar to stimulants (Ritalin) in ADHD:
– Low THC doses: dopamine release modulated → some sufferers report focus improvement
– High THC doses: overactivation of CB1 → distraction, lack of concentration, memory impairment

This is the biphasic dose effect: small doses can help, large doses worsen ADHD symptoms.

CBD for ADHD: a less risky approach

CBD has potentially more beneficial properties for ADHD without intoxication:
– Dopamine modulation via FAAH inhibition and anandamide increase
– Anxiolytic: ADHD concomitant anxiety (in 50% of adults with ADHD)
– Sleep improvement: sleep disorders in 75% of ADHD sufferers
– No risk of addiction and tolerance (no CB1 agonism)

Important: CBD is not a substitute for evidence-based ADHD therapy (methylphenidate, amphetamine, behavioral therapy). Clinical RCTs on CBD for ADHD are lacking.

Risks: Cannabis and adolescent ADHD

ADHD is often diagnosed in adolescence. Cannabis in adolescence is particularly risky for ADHD:
– ADHD increases the risk of cannabis addiction by 2-3 times anyway
– Combination: ADHD + early cannabis use → more severe cognitive impairment
– THC disrupts dopamine maturation in the prefrontal cortex up to 25 years of age

FAQ: Cannabis for ADHD

Summary

ADHD and ECS are linked by dopamine modulation: Anandamide deficit in ADHD, CB1 on dopaminergic neurons. Survey evidence for self-medication strong (Cooper 2017), clinical RCTs lacking. THC biphasic: low doses potentially focusing, high doses harmful. CBD for anxiety and sleep in ADHD without intoxication. Adolescents with ADHD are high-risk group for cannabis dependence. Cannabis and adolescents for developmental risks; cannabis dependence for addiction risks.

Cannabis and sport: the WADA distinction

Since 2018, the World Anti-Doping Agency (WADA) has removed CBD from the banned list. THC remains banned – with a limit of 150 ng/ml in urine during competition. This distinction makes pharmacological sense and has massively changed the use of CBD in competitive sports.

WADA status at a glance

CBD for athletes: Regeneration and inflammation

Sports-induced muscle damage triggers local inflammation (DOMS – Delayed Onset Muscle Soreness). CBD intervenes via several mechanisms:

COX-2 inhibition: Reduces prostaglandin production in inflamed muscles – similar to ibuprofen, without gastric risk.

TRPV1 desensitization: Reduces pain sensitivity in overloaded muscles and joints.

Cortisol modulation: CBD dampens excessive cortisol release after intensive training – cortisol inhibits protein synthesis and muscle building.

Sleep improvement: Restorative sleep is the most important regenerative factor. CBD 150 mg in the evening improves sleep onset latency and sleep quality.

Study situation: CBD and sport

Direct RCTs on CBD and sports performance are limited. Relevant evidence:

Gamelin et al. 2020 (Front Physiol): CBD 750 mg/day, n=15 active men. No significant improvement in strength or endurance, but subjective improvement in sleep quality and mood.

McCartney et al. 2020 (Sports Medicine): Review, CBD mechanisms for sports. Conclusion: Anti-inflammatory and sleep-promoting effects are well established pharmacologically; lack of RCTs is a research gap, no evidence against efficacy.

CBD and cycling (anecdotal): Many Tour de France riders openly use CBD since WADA approval. Evidence remains anecdotal, acceptance in the sports community has increased.

Caution: full-spectrum products for athletes

The biggest risk for athletes: Full-spectrum CBD products contain trace THC (<0.2% legal, <0.3% in some countries). At high CBD doses (300+ mg/day), the accumulated amount of THC can exceed the WADA limit.

Recommendation for competitive athletes: Only use certified CBD isolate or broad-spectrum products without THC. Prefer products with Cologne List certification or Informed Sport certification.

FAQ: Cannabis and sport

Summary

CBD has been WADA-free since 2018, THC remains banned (150 ng/ml limit, competition only) CBD mechanisms for athletes: COX-2 inhibition, TRPV1 desensitization, cortisol modulation, sleep improvement. Direct RCTs on sports performance are lacking, pharmacological rationale is solid. For competitive athletes: only THC-free, certified products (Informed Sport). Consumption forms guide for correct intake; CBD dosage guide for athletes’ dosages.

Cannabis and the cardiovascular system

Cannabis has measurable effects on the cardiovascular system – mainly through THC, not CBD. For most healthy adults, these effects are temporary and harmless. However, they can be clinically relevant for people with existing heart disease, high blood pressure or cardiac arrhythmia.

Cardiovascular effects of THC

Study data: Heart attack and cannabis

Mittleman et al. 2001 (Circulation): Case-crossover study, n=3882 myocardial infarction patients. Risk of myocardial infarction in the first hour after cannabis use: 4.8-fold increased vs. non-use. Absolute risk, however, very low in young healthy people; mainly relevant in the case of pre-existing CHD.

Jouanjus et al. 2014 (J Am Heart Assoc): Analysis of 1979 cases from the French pharmacovigilance system. For cannabis-associated heart problems: 85 % male, average age 34 years. Atrial fibrillation and coronary events overrepresented.

Singh et al. 2018 (J Am Coll Cardiol, Review): Chronic use: increased rate of atherosclerosis due to proinflammatory effects of high-dose THC ingestion. Acute effects (tachycardia) in old age or with pre-existing CHD = main risk factor.

CBD and the heart: Rather positive

In contrast to THC, CBD has cardioprotective properties:
– Antiarrhythmic: CBD reduces ischemia-induced arrhythmias in animal models
– Vasodilating: CBD relaxes blood vessels via TRPV1 and NO release → lowers blood pressure
– Anti-inflammatory: Atherosclerosis is driven by inflammation; CBD has an inhibitory effect
– Manseau et al. 2019: CBD (600 mg once) significantly reduced the increase in blood pressure during stress reactions in RCTs

Risk groups: Who should be careful

– People with coronary heart disease (CHD)
– Cardiac arrhythmia (atrial fibrillation)
– Uncontrolled hypertension
– Heart failure
– Elderly patients (>65 years)
– People on heart medication (digoxin, blood thinners, beta-blockers)

FAQ: Cannabis and the heart

Summary

THC increases heart rate by 20-50 bpm and oxygen demand – harmless in healthy boys, clinically relevant in CHD or arrhythmias (4.8-fold increased risk of heart attack in the first hour, Mittleman 2001). CBD, on the other hand, shows cardioprotective properties (antiarrhythmic, antihypertensive). Risk groups: CHD, atrial fibrillation, heart failure, hypertension, cardiac medication. Cannabis and alcohol for further combination risks; cannabis-drug interactions for cardiovascular medications.

The immune system and the endocannabinoid system

The endocannabinoid system (ECS) is deeply integrated into immune regulation. CB2 receptors – unlike CB1, which is hardly present in the brain – are mainly found on immune cells: B cells, T cells, natural killer cells, macrophages, mast cells and dendritic cells. CB2 activation by cannabinoids modulates inflammatory reactions bidirectionally.

CB2 receptors on immune cells

Anti-inflammatory mechanisms of cannabinoids

CBD main mechanisms:
– TRPV1 activation and desensitization → reduced mast cell activation
– COX-2 inhibition → less prostaglandin production
– NF-κB inhibition → less pro-inflammatory gene expression
– PPARγ activation → anti-inflammatory transcription
– Adenosine reuptake inhibition → increased adenosine → A2A receptor activation = anti-inflammatory

THC via CB2: CB2 activation → cAMP reduction → PKA inhibition → NF-κB suppression → less TNF-α, IL-1β, IL-6.

Autoimmune diseases: Cannabis as an immunomodulator

In autoimmune diseases, the immune system attacks the body’s own tissue – the excessive Th1/Th17 activation is often central. Cannabis can have a modulatory effect here through CB2-mediated Th1→Th2 shift:

Multiple sclerosis: Sativex approved for spasticity (CB1); experimental: CBD reduces neuroinflammation and Th17 activation in animal models (Kozela et al. 2011)

Rheumatoid arthritis: Blake et al. 2006 (Rheumatology): Nabiximols-RCT, n=58. Significant reduction in pain intensity and DAS28 score (disease activity). CB2 on synoviocytes directly affected.

Crohn’s disease: Naftali et al. 2013 (Clin Gastroenterol Hepatol): Cannabis smoking vs. placebo, n=21. 45 % complete remission vs. 10 % placebo. CB2 on intestinal immune cells regulates intestinal inflammation.

Immunosuppression vs. immunomodulation: the difference

Cannabis is not a classic immunosuppressant (like methotrexate or ciclosporin). It modulates – regulates the immune response adaptively:
– In case of excess (autoimmunity): rather immunosuppressive
– In case of deficit (infection defense): little impairment

Chronic, high-dose THC consumption can reduce NK cell activity and T cell proliferation – clinically relevant in immunocompromised patients (HIV, chemotherapy). Low doses of CBD hardly have this effect.

FAQ: Cannabis and the immune system

Summary

CB2 receptors on immune cells make the ECS a central immune regulator. Cannabis – especially CBD – has an anti-inflammatory effect via COX-2 inhibition, NF-κB suppression and CB2-mediated Th1→Th2 shift. There are positive clinical data for autoimmune diseases (MS, arthritis, Crohn’s disease). Not an immunosuppressant substitute, but a useful symptomatic supplement. Entourage effect for the synergy of all cannabis ingredients; ECS foundations for the overall picture.

Palliative care: what cannabis can do

Palliative care is about quality of life – not cure. Cannabis has a particularly well-documented role here: pain relief, antiemesis (against nausea), appetite stimulation and sleep improvement are the four central fields of application. Germany has made medicinal cannabis reimbursable for serious illnesses since 2017 – palliative patients are a core target group.

Palliative fields of application with study evidence

Opioid-sparing effect: the most important palliative benefit

Cannabis combined with opioids reduces the need for opioids – this is the most pharmacologically significant palliative benefit:

Johnson et al. 2010 (J Pain Symptom Manage): RCT, n=177 tumor patients with persistent opioid pain. Nabiximols (Sativex) as an add-on significantly better than placebo for pain relief (NRS reduction 3.7 vs. 1.4 points on a 0-10 scale).

Mechnik et al. 2018 (J Pain): Retrospective study, n=274 palliative care patients. Those who used cannabis reduced opioid dose by a median of 44 %. Significant for opioid-associated side effects (constipation, sedation).

Mechanism: Cannabinoids and opioids act synergistically via different receptor systems (CB1 + μ-opioid receptors) on the same pain circuits.

Dronabinol and nabilone: the approved THC preparations

Dronabinol (Marinol, Syndros): Synthetic delta-9-THC; available as a narcotic prescription in Germany; standard indications: Chemotherapy nausea, HIV wasting. 2.5-20 mg/day.

Nabilone (Cesamet): Synthetic THC analog; stronger antiemetic than dronabinol; chemotherapy nausea when other antiemetics fail.

Nabiximols (Sativex): THC:CBD 1:1 oral spray; approved for multiple sclerosis spasticity in Germany; in many countries also for tumor pain (off-label possible in Germany).

Practical palliative dosing

Pain (day): THC 5-10 mg every 6-8 hours orally; or Sativex 2-4 sprays
Nausea: dronabinol 5 mg 1-3h before chemotherapy + 2-4 hours afterwards
Appetite: THC 2.5 mg 30 min before meals
Sleep (night): THC 5-10 mg + CBD 50-100 mg in the evening

FAQ: Cannabis in palliative care

Summary

Cannabis is particularly well documented in palliative care: Level A for chemotherapy nausea (dronabinol approved), Level B for tumor pain (Sativex RCT data), Level B for loss of appetite and sleep. Opioid saving effect of up to 44 % is the most clinically significant benefit. In Germany since 2017 on narcotic prescription with possible SHI reimbursement. Cannabis in cancer for antitumor studies; medical cannabis on prescription for the access route.