Full Report


The Disease

Asthma is a disease of the lungs that consists of 3 clinical aspects: 1) bronchoconstriction, 2) inflammation of the bronchi, and 3) excess mucus production.  The disease is usually characterized by a constant state of hyper-reflexivity of the bronchi to allergic components (allergens—usually pollen and/or animal dander).  When the patient breaths in these allergens, a cascade of events happens.  The allergens bind to allergy cells (mast cells) in the bronchi causes them to release histamine and inflammatory causing agents.  Initially, the patient will experience bronchoconstriction followed by inflammation and resulting swelling, excess mucus production, and a further increase in the sensitivity of the lung to any allergen or breathing problem.  Repeated exposure to the allergens causes the lungs to be in a consistent state of inflammation and, as a result, persistent problems with asthma symptoms.  Medical care of asthma consists of: 1) remedies to reverse the bronchoconstriction (i.e.,  albuterol, etc.), 2) remedies to prevent and/or treat the inflammation (i.e., inhaled steroids, montelukast, etc), and 3) remedies to decrease the allergic response to the allergens (allergy shots, Xolair, etc).  Inhaled steroids are the mainstay for persistent allergy treatment because, as they decrease the inflammation in the lungs, the excess mucus production and airway reactivity decrease and, as a result, the lung’s reaction to allergens decreases, also.

Research Findings

The inflammation of the lungs is caused by the release of inflammatory compounds from the allergy cells in the lung of patients with asthma.  CBD lowers the amount of these inflammatory causing compounds in the lungs in asthma  and raises the level of specific anti-inflammatory causing compounds.  It appears that CBD does not reverse the bronchoconstriction in asthma and should not be used for this purpose.  THC, the compound in marijuana that makes people high, does reverse bronchoconstriction somewhat if it smoked or vaped directly into the lung, however, this can actually cause or worsen an asthma attack in some individuals.  CBD does not worsen asthma and does not have to be smoked or vaped to decrease the inflammation in the lung.  It may be taken orally or under the tongue to have an effect.

Animal Studies

In rodent animal models of asthma, systemic administration of cannabidiol decreases the inflammation of the bronchial tubes and decreases mucus production by lowering 4 different interleukins (IL4, -5, -6, and -13) and TNF-alpha, compounds that are elevated in asthma and cause the inflammation.1,2  In addition, cannabidiol did not lower the levels of IL10 which is protective against bronchial inflammation and helps in decreasing the allergic response.2,3 In a guinea pig model of asthma, pulmonary administration of THC but not cannabidiol was found to reverse the bronchoconstriction associated with asthma.4

Human Studies

Similar the the guinea pig model, pulmonary administration of THC and not CBD was found to produce bronchodilatation in humans.5,6 However, the smoking of TCH or its inhalation using a mist produced bronchoconstriction in some cases.7  Using human bronchial epithelial cells, THC has an anti-inflammatory effect that is mediated through CB2 receptors and the bronchodilation effect is through CB1 receptors.8,9

Bottom line

CBD in animals decreases the inflammation associated with asthma and it may also do this in humans via the CB2 receptor pathway.  THC seems to be a bronchodilator but only if inhaled via smoking or misting, which causes bronchoconstriction in some individuals.   No controlled studies in humans have been performed using hemp oil.  However, at this time, neither CBD nor marijuana is recommended for the treatment of asthma by the FDA.

Bottom line

CBD decreases the inflammation associated with asthma in animals and apparently also in humans.  THC has some ability as a bronchodilator but only if inhaled via smoking or misting, which causes bronchoconstriction in some individuals.   No controlled studies in humans have been performed using hemp oil.  However, at this time, neither CBD nor marijuana is recommended for the treatment of asthma by the FDA.



  1. Jan T, et al (2003). Attenuation of the ovalbumin-induced allergic airway response by cannabinoid treatment in A/J mice.  Toxicol Appl Pharmacol. 2003 Apr 1;188(1):24-35.
  2. Vuolo F, et al (2015). Evaluation of Serum Cytokines Levels and the Role of Cannabidiol Treatment in Animal Model of Asthma.  Mediators of Inflamm.  2015 Vol. 2015: Article ID 538670, 5 pages
  3. Chung F (2001). Anti-inflammatory cytokines in asthma and allergy: interleukin-10, interleukin-12, interferon-gamma. Mediators Inflamm. 2001 Apr; 10(2): 51–59.
  4. Makwana R, et al (2015). The Effect of Phytocannabinoids on Airway Hyper-Responsiveness, Airway Inflamation, and Cough.  Pharm. & Exp. Thera. 2015 Apr; 353:169-180.
  5. Taskin D, et al (1975). Effects of smoked marijuana in experimentally induces asthma.  Am Rev Respir Dis. 1975 Sep;112(3):377-86.
  6. Gong H, et al. (1984). Acute and subacute bronchial effects of oral cannabinoids. Clin Pharmacol Ther. 1984 Jan;35(1):26-32.
  7. Taskin D, et al (1977). Bronchial effects of aerosolized delta 9-tetrahydrocannabinol in healthy and asthmatic subjects.  Am Rev Respir Dis. 1977 Jan;115(1):57-65.
  8. Grassin-Delyle S, et al (2014). Cannabinoids inhibit cholinergic contraction in human airways through prejunctional CB1 receptors.  British Journal of Pharmacology (2014) 171 2767–2777
  9. Shang VC, et al (2016). Δ9-Tetrahydrocannabinol reverses TNFα-induced increase in airway epithelial cell permeability through CB2 Biochem Pharmacol. 2016 Nov 15;120:63-71.

Alzheimer’s Disease

The Disease

Alzheimer’s disease is an progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out the simplest tasks. In most people (~95%), symptoms first appear in their mid-60s, however, there is autosomal dominant genetic form of the disease in which the symptoms onset earlier in life.  Regardless of the cause, two unique findings in the brain are associated with the disease: 1) amyloid plaques deposition between the brain cells and 2) the deposition of protein fibers within the brain cells called neurofibrillary tangles, both of which lead to a loss of connections between brain cells.  Amyloid plaques consist of normal protein fragments that are normally eliminated from the brain but in AD, these proteins accumulate and form hard, insoluble plaques.   Neurofibrillary tangles are made up of microtubules that are normally found in the brain and function to transport materials within the nerve cells so they can function normally.  However, in AD, the protein that makes up these fibers (tau) is abnormal and causes the tubules to collapse, resulting in abnormal nerve cell function.  These pathologically findings cause inflammation and oxidative stress in the brain all of which causes and promotes neurodegeneration.  In general, as the symptoms of AD deteriorate, the plaques and tangles become more pronounced and the neuroinflammation and oxidative stress increase.  Alzheimer’s has been thought to be continually progressive and irreversible, however, recent studies suggest that this may not be completely true.


In the laboratory CBD protects brain cells, prevents nerve degeneration, decreases plaques, is anti-inflammatory, decreases oxidative stress, and improves cell life.  Each of these effects would be beneficial in AD.  In addition, CBD decreases the production of amyloid plaques.  In animal models of AD, CBD has the same effects and, as it has these effects, the memories and thinking process of the animals improve.  CBD even improves the memories and thinking processes of animals with advanced AD. Very little human research using CBD to treat AD has been done.  However, in a small 4-week study of 10 human patients with advanced AD, CBD improved their symptoms.

Laboratory Studies

CBD has been found in-vitro:  to be neuroprotective, to prevent hippocampal and cortical neurodegeneration, to reduce tau hyperphosphorylation, to lower amyloid b levels, to be anti-inflammatory, and to act as an antioxidant. 1-5 In addition, CBD protects against Ab mediated neurotoxicity and microglial- activated neurotoxicity and improves cell viability.6-8 CBD decreases the oxidative stress in neuroinflammation.9  GPR3 is a modulator of beta-arrestin 2 (BA2) and its stimulation by agonists results in over production of BA2 while its stimulation by inverse agonists results in lowering of BA2.10 Beta-arrestin 2 (BA2) is produced by stimulation of GPR3 receptors and results in the production of amyloid in human brain cultures.10

Live Animal Studies

CBD reduces inflammation by reducing NO and interleukin-1b (IL-1b) release.11 IL-1b is involved in neurodegeneration and the over-production of NO, which causes tau hyperphosphorylation.  In addition, CBD is an inverse agonist for GPR3 which when stimulated inversely should result in decreased production of amyloid in brain tissue and subsequently a decrease in the number of plaques.12 Eradiation of GPR3 results in the loss of plaques and the restoration of memory in a mice model of AD.13 In both mice and rat models of AD, CBD was able to reverse the pathological changes found in AD. 4,7,12-20 CBD has been found restore memory and other cognitive defects in animals that have the disease—even in animals with advanced disease.4,7,13,14,17,19,20 Finally, CBD has been shown to prevent the development of AD.21

Human Studies

GPR3 expression is elevated in the sporadic Alzheimer’s disease brain, is highly expressed in areas of the normal human brain implicated in Alzheimer’s disease and this upregulation correlates with the progression of the disease 13,22.  Over a 4-week period involving 10 patients, CBD decreased the amount and severity of delusions, agitation/aggression, irritability, and apathy of patients with AD and improved the amount of sleep in these patients.  In addition, it decreased the amount and severity of caregiver distress. No adverse reactions were noted during the treatment time.23

Bottom Line

CBD significantly reverses the neural pathology in animal models of Alzheimer’s Disease and improves the memory and thinking of the animals.  Whether this will translate to humans is not yet scientifically proven.  However, a small, non-controlled study indicates promise.  At this time, the FDA does not recommend CBD for the treatment of Alzheimer’s Disease



  1. Esposito G, etal.(2006b).Cannabidiol inhibits inducible nitric oxide synthase protein expression and nitric oxide production in b-amyloid stimulated PC12 neurons through p38 MAP kinase and NF-kB involvement. Neurosci Lett 2006, 399:91–95.
  2. Hamelink C, etal. (2005) Comparison of cannabidiol, antioxidants, and diuretics in reversing binge ethanol-induced neurotoxicity. J Pharmacol Exp Ther 314:780–788, 2005.
  3. Esposito G, etal. (2006a). The marijuana component cannabidiol inhibits b-amyloid-induced tau protein hyperphosphorylation through Wnt/b-catenin pathway rescue in PC12 cells. J Mol Med 2006, 84:253–258
  4. Marin-Moreno A, etal. Prolonged oral cannabinoid administration prevents neuroinflammation, lowers b-amyloid levels and improves cognitive performance in Tg APP 2576 mice. J Neuroinflam 9(8) 1-15, 2012.
  5. Mukhopadhyay P, etal.(2011) Cannabidiol protects against hepatic ischemia/reperfusion injury by attenuating inflammatory signaling and response, oxidative/nitrative stress, and cell death. Free Radic Biol Med 2011, 50:1368–1381.
  6. Janefjord E, etal. (2014). Cannabinoid effects on b amyloid fibril and aggregate formation, neuronal and microglial-activated neurotoxicity in-vitro. Cell Mol Neurobiol 34:31–42, 2014.
  7. Marin-Moreno A, etal. Cannabidiol and other cannibinoids reduce microglial activation in-vivo and in-vitro: Relevance to Alzheimer’s Disease. Mol Pharm 79: 964-973, 2011
  8. Harvey B, etal. (2012). Contrasting protective effects of cannabinoids against oxidative stress andamyloid-b evoked neurotoxicity invitro. Neurotoxicology 33:138–146, 2012.
  9. Vallée A, et al. Effects of cannabidiol interactions with Wnt/β-catenin pathway and PPARγ on oxidative stress and neuroinflammation in Alzheimer’s disease. Acta Biochim Biophys Sin (Shanghai). 2017 Oct 1;49(10):853-866.
  10. Thathiah A, etal. β-arrestin 2 regulates Aβ generation and γ-secretase activity in Alzheimer’s disease. Nat Med. 2013 Jan;19(1):43-9.
  11. Esposito G, etal. (2007). Cannabidiol in-vivo blunts b-amyloid induced neuroinflammation by suppressingIL-1b and iNOS expression. Br J Pharmacol 2007 151:1272–1279.
  12. Aso E., et al. Cannabis-based medicine reduces multiple pathological processes in AβPP/PS1 mice. J Laun AS, etal. GPR3, GPR6, and GPR12 as novel molecular targets: their biological functions and interaction with cannabidiol. Acta Pharmacol Sin. 2018 Jun 25.  Alzheimers Dis.2015;43(3):977-91.
  13. Huang Y, etal. Loss of GPR3 reduces the amyloid plaque burden and improves memory in Alzheimer’s disease mouse models. Sci Transl Med. 2015 Oct 14;7(309):309ra164.
  14. Aso E., et al. Cannabinoid Receptor 2 Participates in Amyloid-β Processing in a Mouse Model of Alzheimer’s Disease but Plays a Minor Role in the Therapeutic Properties of a Cannabis-Based Medicine. J Alzheimers Dis. 2016;51(2):489-500.
  15. Casarejos MJ, et al. Natural cannabinoids improve dopamine neurotransmission and tau and amyloid pathology in a mouse model of tauopathy. J Alzheimers Dis. 2013;35(3):525-39.
  16. Esposito G, etal. (2011). Cannabidiol reduces Ab-induced neuroinflammation and promotes hippocampal neurogenesis through PPARg PLoSONE 2011, 6:e28668.
  17. Hughes B and Herron C. Cannabidiol Reverses Deficits in Hippocampal LTP in a Model of Alzheimer’s Disease. Neurochem Res. 2018 Mar 24.
  18. Scuderi C, et al. Cannabidiol promotes amyloid precursor protein ubiquitination and reduction of beta amyloid expression in SHSY5YAPP+ cells through PPARγ involvement. Phytother Res. 2014 Jul;28(7):1007-13.
  19. Cheng D, et al. Chronic cannabidiol treatment improves social and object recognition in double transgenic APPswe/PS1∆E9 mice. Psychopharmacology (Berl). 2014b Aug;231(15):3009-17.
  20. Aso E, et al. Delineating the Efficacy of a Cannabis-Based Medicine at Advanced Stages of Dementia in a Murine Model. J Alzheimers Dis. 2016 Oct 4;54(3):903-912.
  21. Cheng D, et al. Long-term cannabidiol treatment prevents the development of social recognition memory deficits in Alzheimer’s disease transgenic mice. J Alzheimers Dis. 2014;42(4):1383-96
  22. Thathiah A, etal. The orphan G protein-coupled receptor 3 modulates amyloid-beta peptide generation in neurons. 2009 Feb 13;323(5916):946-51.
  23. Shelef AJ, et al. Safety and Efficacy of Medical Cannabis Oil for Behavioral and Psychological Symptoms of Dementia: An-Open Label, Add-On, Pilot Study. Alzheimers Dis. 2016;51(1):15-19.


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