Scholarly articles on use of cbd oil for immune disorders

Article

Katz D 1,2 , Katz I 1,2 , Shoenfeld Y 1,3*

1 The Zabludowicz Center for Autoimmune Diseases, Chaim Sheba Medical Center, Tel-Hashomer, Israel
2 Faculty of Medicine, The Hebrew University of Jerusalem, Israel
3 Incumbent of the Laura Schwarz-kipp chair for research of autoimmune diseases, Sackler Faculty of Medicine, Tel-Aviv University, Israel

Introduction

The tale of Cannabis sativa is as old as time. Through its first days as an herbal remedy, ranging back to 4000 BC and to Emperor Shen Nung’s Rule (2700 BC), to cannabis low point of being banned internationally at 1925 to its recent re-emergence by prof. Mechoulam isolation of the Tetrahydrocannabinol (THC, 1963), Cannabis is slowly gaining its place in medicine 1,2 .

Cannabis sativa, also known as Marijuana has been called many names, yet the variety of names given to Cannabis does not encompass the vast medical opportunities that lie within the cannabis. As of now, 545 ingredients have been identified, of which over 100 classified as unique to Cannabis 3 . The two main and most researched active ingredients are – Tetrahydrocannabinol (THC) which holds a psychoactive properties and on the other hand, Cannabidiol (CBD) which is considered non psychoactive. The components are joined by the two main known endocannabinoids – Ananamide (AEA) and 2-Arachidonoylglycerol (2-AG) (also discovered by prof. Mechoulam and colleagues) 4,5 . The other half of the cannabinoid system (as we know thus far) comprises of CB1 and CB2 receptors, G-protein coupled receptors. The two receptors differ in distribution and function. While the major psychoactive effect of cannabis is attributed to the CB1 receptor and accordingly widely distributed in neurons, while the CB2 receptor has been linked to maintaining homeostasis and commonly appears in cells of the immune system 6,7 .

Cannabis and the Brain Immune System

It is well established that murine microglial cells express both CB1 and CB2 receptors, yet the pattern of receptors expression differs in location as well as in levels of expression. While CB1 receptor is consistently expressed in microglial cells in low levels, CB2 receptor is indetectable in resting state cells and highly expressed in activated microglia 8,9 . The pattern of expression and distribution of CB2 receptor in microglial cell suggest a role in microglial migration, CB2 receptor was found to be expressed heterogeneously throughout murine microglial cells with particularly high density at the leading edges of lamellipodia and microspkies (cellular protrusions that mediate cell migration). Moreover, 2-AG, AEA and abnormal-cannabidiol increase microglial cell migration 10 .

Another aspect of the endocannabinoid system effect on microglial cell is the attenuation of the immune response induced by LPS (Lipopolysaccharide) stimulation, AEA attenuates the immediate release of IL-6 and NO by microglial cell by induction of MPK-1 11 .

A different mechanism of action is suggested by the inhibition of the IL-1 signaling pathway following administration of the synthetic cannabinoid R(+)WIN 55,212-2. Appling R(+)WIN 55,212-2 to astrocytoma cells priori stimulated by IL-1 resulted in dose dependent inhibition of ICAM-1 and VCAM-1 adhesion molecules induction, as well as IL-8 and NFκB. The effect aforementioned is independent from the cannabinoids receptors CB1 and CB2 as suggested by the lack of regulation of CB1 and CB2 antagonist on the immunomodulating effects mentioned above, implying that there is still much to learn in the field of Cannabis and immunomodulation 12 .

Cannabis and the Blood-Brain-Barrier

The blood-brain-barrier (BBB) as well as the blood-spinal cord-barrier (BSCS) and their disturbance is often postulated as a possible mechanism of pathogenesis in neurological autoimmune disease. A possible link of pathogenesis has been suggested in Multiple Sclerosis 13 , Neuromyelitis Optica1 14 , Guillain-Barré Syndrome 15 , Chronic Inflammatory Demyelinating Polyneuropathy 16 and Antiphospholipid Syndrome with neurological involvement 17 .

In murine model of LPS induced vascular and inflammatory changes CBD counteracts the effect of LPS. Mice which received LPS+CBD showed no cerebral vasodilation, no leukocyte migration, reduced TNF-α and COX-2 levels compared to LPS treated mice and more over exhibited reduced dextran extravasation (dextran extravasation is used as a quantification instrument of BBB integrity) 18 .

Similar effect is obtained by administration of Anandamide to TMEV-infected endothelial brain cell. AEA inhibits VCAM-1 induction in vitro, and thus limit leukocyte migration through a transwell filter (coated with collagen type I and fibronectin) model of the BBB. Accordingly, in vivo experiment correlated the result of the in vitro experiments. AEA increased tone (by UCM-707, an AEA uptake inhibitor) inhibited VCAM-1 induced expression, as well as attenuated microglial cell activation 19 .

A role for CB2 receptor was also exemplified by in vivo murine model. Ex vivo CB2-activted leukocytes were injected to LPS treated mice resulting in adhesion reduction of up to 96% using GP1a (CB2 receptor agonist) in comparison with to non GP1a treated mice 20 .

The beneficial effect of cannabinoid also extends to human brain endothelial cells (BMVEC). Using human cells from HIV-1 CNS infected patients and from seronegative controls, a group of researches demonstrated enhanced CB2 receptor expression in HIV infected cells compared to controls. Further investigation of naive human BMVEC revealed that the increased expression of CB2 receptor can also be accomplished separately by IL-1β, TNF-α and LPS. Once induced and activated, CB2 receptor decreased leukocyte adhesion, prevented up regulation of adhesion molecules, promoted 2.2-2.7 increase in tight junction proteins (occludin and claudin-5) and significantly reduced BBB resistance drop induced by LPS 21 .

The coherence of the above mentioned experiments is also exemplified at the genetic level. Human BMVEC isolated from eleptogenic patients were activated using TNF-α to evaluate consequent gene expression. Out of 33 genes that were up regulated by TNF-α, 31 and 32 genes were suppressed using CB2 agonist O-1966 or JWH-133 respectively 22 .

Cannabinoids protective effect goes beyond the BBB and also extends to the BSCB. Pretreatment by JHW-015, a CB2 receptor agonist prevents down regulation of occludin and ZO-1 induced by spinal cord ischemia reperfusion injury (SCII) in murine in vivo model. Moreover, JWH-015 pretreatment reduces BBB leakage (measured by Evans blue) compared to SCII only group 23 .

Cannabis potential ability to protect BBB integrity is of possible great importance, not only in autoimmune neurologic disorders, but in a vast verity of neurological fields as in Alzheimer’s disease and ischemia injury.

Cannabis and Autoimmune Demyelinating Disease

Multiple Sclerosis (MS) is known as the hallmarks of neurological autoimmune disease with prevalence as high as 200:100,000 in some countries in northern Europe 24 .

MS Patients are characterized by high CSF levels of AEA compared to healthy control. In accordance high levels of AEA were also measured in autoimmune encephalomyelitis (EAE), a murine model of MS. Moreover, increased NAPE-PLD (part of AEA production) activity and reduced FAAH (degrades AEA) activity 25 . CB1 receptor deficient mice exhibit substantial neurodegeneration following EAE induction including higher prevalence of residual paresis and axonal pathology in relation to wild type mice 26 .

CBD treatment of TMEV infected mice induces a wide range of immunomodulatory outcomes. CBD reduce the infiltrate of immune cell to the brain parenchyma and decreased microglial activation. Moreover, CBD treatment has a long lasting effect, an 80 days follow up of the treatment group revealed restoration of both horizontal and vertical motor activities to that of the healthy mice and a correlating reduction in the expression of TNF-α and IL-β1 27 .

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MS is positively influenced by a variety of cannabinoids, both natural and synthetic, each demonstrating a different mechanism of action to our knowledge. Among the different cannabinoids we can find Cannabidiol which holds the ability to attenuate a range of neuronal apoptotic pathways 28 , Cannabigerol Quinone which its application on murine neuronal culture results in inhibition of IL-1β, IL-6 and PGE2 release 29 . Also Gp1a, a selective CB2 receptor agonist that modulates EAE development by reducing Th17 differentiation 30 , HU-446 and HU-465 (CBD derivatives) and many more which we won’t elaborate on 31 .

There is scarce evidence regarding clinical use of Cannabis in MS patients. A recent Meta-analysis concluded that cannabinoids (nabilone and nabiximols) were associated with a greater average improvement in spasticity assessed by using numerical rating scale (mean difference, -0.76 [95% CI, -1.38 to -0.14]). Also, the average number of patients who reported an improvement on a global impression of change score was greater using nabiximols rather placebo (OR, 1.44 [95% CI, 1.07-1.94]) 32 . Notably, a new large multi centered blinded study was recently published, in which 489 MS patients participated and received either oral dronabinol (THC) or placebo. The study failed to prove the beneficial outcome of dronabinol use in two main outcomes (time to confirmed EDSS [Extended Disability Status Scale] score progression and change in MSIS-29 [Multiple Sclerosis Impact Scale-29] score). However, while taking into consideration the results of this trail, it is worth mentioning a possible weakness in the trail inclusion criteria. The disease progression in MS as measured by the EDSS scale is not linear, and progression through EDSS 4-5.5 is faster the in EDSS 6-6.6. hus making the EDSS 6+ patient’s population insensitive to treatment during the study period of time, leaving the question of Cannabis medical use in MS patients in need of further research 33,34 . Currently, evidenced based recommendation published in 2014 by the American academy of neurology are: oral cannabis extracts (CBD/THC or CBD alone) are the only products with an A – effective rating, next in line is THC (dronabinol/nabilone) with B rating- probably effective 35 .

Another demyelinating autoimmune disease that shows promise for cannabis treatment is Neuromyelitis Optica (NMO). Plasma levels of 2-AG were found to be elevated in NMO patients compared to healthy patients. Moreover, 2-AG levels were negatively correlated with pain sensitivity, while AEA correlated positively with pain sensitivity 36 .

Multiple Sclerosis and Neuromyelitis Optica are the milestones of medical cannabis implantation in neurologic autoimmune disease, yet only the foundation has been accomplished up to now and further clinical investigation is the core of establishing Cannabis Sativa and its products as a new therapeutic solution.

Cannabis Adverse Effects

Cannabis addiction is one of the main adverse effects of chronic cannabis use, though once considered as only “psychological addiction”, recent evidence revels a physiological ingredient to the addiction 37 . Epidemiological studies indicate that about 9% of adult marijuana users will develop cannabis addiction, while adolescent’s percentages of addiction is as high as 17% 38 .

Another adverse effect of great importance lurking chronic cannabis users is the consequence anatomical changes, a 2013 meta-analysis concluded that chronic cannabis consumption results in reduction of hippocampal grey mater 39 . Accordingly a new research conducted at 2015 demonstrated reduced hippocampus and amygdala volumes 40 .

Acute adverse effects (some may be found beneficial in some indications) include anxiety, dysphoria, psychosis/hallucinations, tachycardia, and stimulation of appetite 39 . Further side effects are listed in table 1.

System Adverse Effect Statistics a References
Neurologic ↓hippocampus & amygdala volumes
↑ Incidence of acute ischemic stroke
Age 15-54
Age 25 -34
Age 45 – 54
Drowsiness
Dizziness
↓Educational performance (adolescents)
Lower IQ
RR 1.13 (1.11-1.15)*
RR 2.26 (2.14 – 2.38)*
RR 1.45 (1.42 – 1.54)*
OR 3.68 (2.24-6.01)*
OR 5.09 (4.10-6.32)*
↓11% (% GCSE† points)*
Linear trend, t test
t: -3.36***
32,40-43
Psychiatric Psychosis Schizophrenia
Anxiety
Depression
OR 1.41 (1.20–1.65)*
OR 1.9 (1.1–3.1)*
OR 1.98 (0.73-5.35)*
OR 1.49 (1.15–1.94)*
32,44,45
Cardiovascular Tachyarrhythmia
Palpitation
Angina
RR 1.5 (1.1–2.1)*
↓ 48% (↓time to, during exercise)**
38,46,47
Pulmonary (cannabis smoking) Chronic Bronchitis symptoms
↑health services for respiratory infections
25%-33% of smokers 46,48
Gastrointestinal Nausea
Diarrhea
Vomiting
Abdominal pain
Constipation
OR 2.08 (1.63-2.65)*
OR 1.65 (1.04-2.62)*
OR 1.67 (1.13-2.47)*
32, 49,50
General Dry mouth OR 3.50 (2.58-4.75)* 38
Cannabis dependence
Withdrawal syndrome
Adults, Adolescents
Anxiety
Insomnia
Appetite disturbance
Depression
Irritability
9%, 17% (percentage of users who will
become addicted)
38
51
Pregnancy Maternal anemia
Decrease birth weight
↑Intensive care unit
pOR 1.36 (1.1 – 1.69)*
pOR 1.77 (1.04 – 3.01)*
pOR 2.02 (1.27 – 3.21)*
52

Table 3: Perfusion analysis from 1H-NMR in 12-month-old female mdx mice.

Reperfusion mean has been calculated during the first 25 minutes after release of ischemia. Wild-type mice, n=6; mdx mice, n=7. **p < 0.01.

(a)The set-up of the tourniquet was sufficient to induce an absence of perfusion in both groups. After release of tourniquet, a rapid and important increase of perfusion was detected and the reperfusion of mdx mice was greater than wild-type mice. A single peak of reperfusion was however observed in mdxmice, when a first rapid and strong peak followed by a second attenuated peak of reperfusion was observed in wild-type animals.
Because the release of ischemia induced movements of the leg, images affected by these movement artifacts, at the moment of ischemia release, were removed from analysis of muscle perfusion.

(b) In the first 5 minutes after ischemic stress release, below a threshold of 250 mL/100 g reperfusion (concerning mostly wt mice), PCr resynthesis rate was dependent on perfusion, an increase in reperfusion leading to a decrease of τPCr. In contrast, above the threshold of 250 mL/100 g reperfusion (concerning mostly mdx mice), PCr resynthesis rate was poorly affected by the increase of post-ischemia reperfusion.

a: Perfusion analysis was performed through from 1H-NMR as described in the Material and Methods section; b: Correlation between reperfusion and PCr resynthesis rate (from 31P-spectroscopy analysis) during the first 300 seconds (5 minutes) after ischemia; n = 6 (wt, a, b); n = 7 (mdx, a, b); τPCr: time of creatine rephosphorylation.

Conclusion

Nowadays Cannabis tends to be considered as a “buzz word”, with global recognition of the potential embodied in medical Cannabis, more and more countries legalize the use of medical cannabis, leaving many physicians overwhelmed due to the rapid changes. In this article we aimed to review the laboratory and clinical evidence regarding Medical Cannabis and neurological autoimmunity diseases.

Unfortunately, lack of clinical data prevents a definitive conclusion. Nonetheless, clinical trials conducted upon MS and NMO patients suggests a future role for medical cannabis in MS and NMO treatment by obtaining relief in patient symptoms. Yet, the trails aforementioned only paves the beginning, much research is yet to be done in order to evaluate the therapeutic effects of cannabis in treating autoimmune neurologic diseases versus.

Unfortunately, lack of clinical data prevents a definitive conclusion. Nonetheless, clinical trials conducted upon MS and NMO patients suggests a future role for medical cannabis in MS and NMO treatment by obtaining relief in patient symptoms. Yet, the trails aforementioned only paves the beginning, much research is yet to be done in order to evaluate the therapeutic effects of cannabis in treating autoimmune neurologic diseases versus.

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Another promising aspect is cannabis protective effect on the BBB, having great potential not only in the field of autoimmunity but also in a variety of other pathologies with attributed BBB damage pathogenesis. The field of cannabis immunomodulation and BBB protection is an exciting new medical pathway, but only further research is to say what will be Cannabis sativa place in medical history.

Abbreviations

THC : Tetrahydrocannabiol; CBD : Cannabidiol; AEA : Ananamide; 2-AG : 2-Arachidonoylglcerol; LPS : Lipopolysaccharide; IL-6 : Interleukin 6; NO : Nitric oxide; MPK-1 : Mitogen-activated protein kinase 1; IL-1 : Interleukin 1; ICAM-1 : Intercellular Adhesion Molecule 1; VCAM-1 : vascular cell adhesion molecule 1; IL-8 : Interleukin 8; NFκB : Nuclear factor kappa-light-chain-enhancer of activated B cells; BBB : Blood – brain – barrier; BSCB : Blood – spinal cord – barrier; TNF-α : Tumor necrosis factor α; COX-2 : Cyclooxygenase-2; TMEV : Theiler’s Murine Encephalomyelitis Virus.

Molecular Mimicry: The Role of Cannabis in Healing Autoimmune Disease

Sarah Russo is a writer, cannabis consultant, and a social media and content manager. She got her degree in environmental studies and social justice, with a focus in plant medicine from the Evergreen State College. She has previously worked for Project CBD and the Society of Cannabis Clinicians. She has also acted as an herbal medicine educator in natural remedy apothecary shops. Some of her main goals are diversifying the cannabis movement by integrating the plant into the greater herbal medicine compendium as well as encouraging sustainable agricultural practices.

While advancements in science have enabled a greater understanding of our health, getting to the root cause of a chronic disease can be challenging. Autoimmune conditions are an area of medicine that remain largely misunderstood. Presently, there are more than 80 registered autoimmune disorders, affecting various parts of the body. More conditions may also turn out to be autoimmune related.

Autoimmunity (AI) is an “attack on self”, where the immune system gets triggered and thinks that the body’s healthy tissues are invaders. Our immune system is mediated by beta cells which produce antibodies to foreign invaders. Beta cells produce antibodies to prevent infection or fend off bacterial and viral pathogens. T-cells are in charge of cell-mediated immunity are derived from the thymus and other immune tissues. They attack foreign invaders in the body. In an autoimmune response, T-cells take action as if the body’s own cells were foreign in order to bring the body back into homeostasis. This self-attack is known as “molecular mimicry” and is the root of any autoimmune disease.

The location of the autoimmune attack will vary based on the condition. For example, if there is autoimmunity in the joints, rheumatoid arthritis may result. If molecular mimicry occurs in the thyroid, it may lead to Hashimoto’s. For skin disorders like psoriasis, the dermal layer is the target. Autoimmune conditions may attack more than one part of the body at the same time. Lupus can manifest in the skin, digestive system, joints, and the brain.

The reason why the self-attack switch is turned on is relatively unknown. Common consensus is that those with autoimmunity have a genetic predisposition for these types of conditions. Then a particular event like an infection, parasite, leaky gut syndrome, or a traumatic experience sets off the autoimmune reaction.

The triangle of autoimmune triggers. Gut dysbiosis and genetic and environmental factors play mayor roles in the development of autoimmune diseases.

AI can remain latent in the body, resulting in ailments that have not been properly pinpointed. Autoimmune related situations can linger in the body unexposed for many years, which can result in digestive complaints and various associated problems. Frequently, autoimmune diseases are misdiagnosed because their symptoms can mimic other ailments.

There has been a dramatic increase in the prevalence of autoimmune diseases since World War 2. Autoimmune conditions more commonly affect women than men. The National Institute of Health estimates that 23.5 million people in the USA have an autoimmune disease, while cancer affects 13 million in the country. The true number of those affected by autoimmunity is likely higher, due to misdiagnosis and general lack of understanding about the complexity of AI related conditions.

Conventional medicine ideology believes that the immune system cannot be controlled and once the autoimmunity switch has been triggered, it is impossible to revert back to the body’s normal state. However, many alternative medical professionals feel that autoimmune conditions may be reversed or greatly resolved. In typical treatment protocols, patients are not given information about dietary changes and are generally told that pharmaceutical medications are required to get better.

Conventional treatments for autoimmune disorders

Currently, prescription medication for autoimmune diseases aim to “turn off” the immune system all together. Immunosuppressive drugs are synthetically created antibodies which attack the autoimmune antibodies. Immunosuppressive drugs can create many potential side effects. These medications may make someone more susceptible to infection, and may lead to the development of cancer. According to Dr. Bonni Goldstein, a cannabis friendly doctor in Southern California, many patients who try immunosuppressive medications end up discontinuing them due to unfavorable side effects. In her experience, patients seek holistic treatment options for autoimmune diseases.

Steroids are a commonly prescribed medication for autoimmunity to lower inflammation and suppress the immune system. They are meant to be taken on the short term. Julie Holland, a pro-cannabis psychiatrist based in New York, says that the goal shouldn’t be to be globally immunosuppressed, “With steroids, you are sweeping the dirt under the carpet. You’re not getting to the root cause at all. It’s as if you’re hitting mute on the alarm, but the alarm is going off for a reason.” Steroids may decrease blood supply to various parts of the body, and create fat deposits in the face or other areas. If someone has autoimmunity and chronic pain, steroids may not help address the root of the discomfort.

In general, immunosuppressive therapy is incredibly expensive and not always effective. The aim should be to modulate the immune system and bring it back into balance, not to turn it off completely.

What options exist for someone with an autoimmune condition if they do not wish to use traditional medications? Holistic approaches for autoimmune conditions are to decrease inflammation, repair the digestive tract, and regulate the immune system. This includes getting rid of stressors and sensitivities on the broad spectrum, including environmental, food, chemical, and others. Managing autoimmune disease requires dietary and lifestyle changes, which have been reported to help reverse these conditions.

Someone with an autoimmune disease may consider cannabinoid therapies for their ability to decrease inflammation, modulate the immune system, and help to bring the system back into balance.

Immune system modulation

The immune system is a delicate balancing act and deeper investigation is needed to better understand the mechanisms of how it works. Herbs and foods that work to modulate the immune system are ideal for someone dealing with an autoimmune condition. Cannabis therapy and dietary changes seem to be safer, cheaper, and possibly more effective for combating autoimmune conditions than pharmaceutical medications.

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Cannabis and other adaptogenic herbs are known to be immune modulating. They act as a regulating tool: they can bring an over or under-reacting immune system back into balance. However, the difference between “immune modulating” and “immune boosting” can be tricky to decipher. It is generally felt that someone with autoimmunity would not want to take anything which boosts the immune system, but this is a point of contention among practitioners.

According to Kevin Spelman, faculty member in Botanical Medicine at National University of Natural Medicine, the definition of immune modulatory is the biphasic effect of an herbal medicine. “Immunomodulatory herbs offer a very beneficial strategy to treat autoimmune conditions. The category of immunomodulation rests on biphasic activity. If someone’s immune response is overly vigilant, there would be a down regulation of immune response. If someone’s immune response is ‘deficient’ there would be an increase of immune activity.” Spelman explained that a patient’s therapeutic response is dependent on how their individual molecular environment is behaving.

Cannabis is a unique biphasic botanical remedy that can bring the system back into balance in numerous regards. Based on current research, cannabis therapies may provide benefit for autoimmune disease in three basic ways: modulation of the immune system, decreasing general inflammation, and helping to assist the digestive system. Cannabis medicine may also treat symptoms of specific autoimmune diseases like ALS, rheumatoid arthritis, ulcerative colitis and Crohn’s, fibromyalgia, Huntington disease, multiple sclerosis, and others. The plant may decrease chronic pain, inflammation, and spasms associated with some of these conditions. There have been few specific investigations on cannabinoid treatment for AI, due to federal prohibition on human clinical trials. However, extensive studies in test-tubes and in animals have reported the anti-inflammatory benefits of cannabinoids for specific AI conditions like multiple sclerosis and rheumatoid arthritis.

Investigation has demonstrated that CB2 receptors regulate many complex pathways of the immune system. Preclinical studies show that triggering CB2 receptors can suppress immune response, which can be beneficial for those suffering with AI. CB2 can also inhibit production of pro-inflammatory cytokines and enhance anti-inflammatory cytokines, which helps to restore a balanced state. However, there are conflicting reports as research has shown that CB2 activation, under certain conditions, may aggravate inflammation.

There has been some preclinical investigation focusing on the role of particular cannabinoids in AI disease models. CBD has been found to modulate the immune system instead of suppressing it. Cannabidiol also slows down T-cell production and suppresses immune system memory, meaning that CBD could cut down on the likelihood of future autoimmune attacks. CBD has also been found to increase the expression of genes that deal with oxidative stress, which may reduce cell damage from autoimmune attacks. As for THC, this cannabinoid is immunosuppressive only at very high doses. In low doses can be helpful as an analgesic and anti-inflammatory. Its ability to activate CB2 receptors may down regulate T cell function and decrease the harmful effects of immune cells.

The role of cannabis terpenes for autoimmunity deserve further investigation as well. The terpene beta-caryophyllene, found in certain strains of cannabis and black pepper, is known to decrease inflammation through its ability to stimulate the CB2 receptor. Myrcene, another terpene, also has antiinflammatory properties.

Based on preclinical evidence, cannabinoids may help bring the system back into homeostasis, protect against damage from AI attacks within the body, slow down overactive T-cell production, and prevent the immune system from being triggered.

Decreasing inflammation

Inflammation is the root cause of many illnesses, and autoimmunity is no exception. Extensive research has been performed on the anti-inflammatory properties of THC, CBD, and other cannabis components. If inflammation response is regulated, there will be less likelihood of an autoimmune attack. More investigation is needed to examine the particular role of cannabinoids for autoimmune disorders.

Cannabinoid therapy has the potential to assist those with autoimmune conditions by decreasing systemic inflammation, with little to no side effects. Preclinical evidence has found that cannabinoids can attenuate autoimmune inflammatory response. In an animal model of multiple sclerosis, CBD decreased the gene transcription that promoted inflammation.

Despite a scarcity of specific human based studies, patients with autoimmune disorders have been able to improve their situation by integrating cannabis medicine into their lifestyle. Dr. Bonni Goldstein has seen a number of patients with lupus and rheumatoid arthritis wean off pharmaceuticals and control their symptoms with cannabis, dietary changes, exercise, and stress reduction. Goldstein gave the example of a young patient with ankylosing spondylitis. Goldstein reported that after two months on cannabis the patient discontinued three of the pharmaceuticals, experienced a significant improvement in her pain symptoms, and was “able to participate in her life again”. Dr. Goldstein encourages patients to try various CBD/THC ratios, and to experiment with raw cannabinoids such as THCA and CBDA. Trial and error is required to find what works best for an individual’s unique situation.

Additional approaches one can take to lower inflammation:

  • A nutrient rich diet: a whole food diet, devoid of processed foods, will naturally decrease inflammation.
  • Exercise: active movement increases circulation of anti-inflammatory cytokines from the skeletal muscles.
  • Sufficient sleep: your body naturally lowers inflammation while you get shut eye.
  • Herbal medicine: turmeric, ginger, cinnamon, nettle, and various medicinal mushrooms can help decrease inflammation throughout the body.
  • Probiotics & Prebiotics: these supplements promote healthy bacteria in the gut, which lowers inflammation and promotes healthy immune response.

While autoimmunity may be a complex and challenging situation in need of deeper investigation, there are holistic approaches one can take to manage their condition. Coping with an autoimmune disease may feel burdensome, but it can also be an opportunity to get back in touch with your body. Aim to treat it in the best way possible. Nature can be your guide.

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Holland, Julie. Entrevista personal. 6 de junio de 2017

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Jacob, Aglaée. “Gut Health and Autoimmune Disease — Research Suggests Digestive Abnormalities May Be the Underlying Cause”. Today’s Dietitian. 2013

Kozela, E, et all. “Pathways and gene networks mediating the regulatory effects of cannabidiol, a nonpsychoactive cannabinoid, in autoimmune T cells” J Neuroinflammation. 2016

Malfait, et al. “The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis”. Proc Natl Acad Sci USA. 2000

Rothbard, Gary. “Steroids: The Good, The Bad, The Worrisome For Autoimmune”. Autoimmune Mom. 2012

Santamaria, Pere.”Cytokines and Chemokines in Autoimmune Disease: An Overview”. Madame Curie Bioscience Database

Yeshurun, M, et al. “Cannabidiol for the Prevention of Graft-versus-Host-Disease after Allogeneic Hematopoietic Cell Transplantation: Results of a Phase II Study” Biol Blood Marrow Transplant. 2015