Illegally healed from ALS


From here: http://illegallyhealed.com/keeping-als-at-bay-with-cannabis/

Keeping ALS at Bay with Cannabis

Justin Kander, 4th July 2015

Amyotrophic lateral sclerosis (ALS) is one of the most degenerative motor neuron diseases in existence. Most people with ALS die within three to five years after symptom onset, and the disease often progresses very rapidly. Bob Strider wants others to know this prognosis is not written in stone, and cannabis can be a truly effective option for many ALS patients.

Bob has had an especially storied life. He graduated from Harvard University, and from 1965 to 1969 acted as a voice intercept operator for the United States Army, working out of Germany to monitor Russian communications. In 1991, Bob moved to the capital of the Czech Republic, Prague, where he essentially remained for two decades. The environment was very supportive of Bob’s passion for biking, and he often put in 400 kilometers a week.

In 1998, Bob began experiencing the first symptoms of ALS. These symptoms included a loss of function in his right arm and problems swallowing. By 2012, his overall health had gotten really bad, and Bob knew he had to try something better. He had been smoking large amounts of cannabis for years, which he believed was responsible for the slow progression of the disease. However, Bob felt cannabis oil would work even better.

Bob literally took his healing into his own hands. In 2012, he set up two grow rooms and a lab in order to produce cannabis oil. This was especially difficult given Bob’s limited mobility, but hope fueled his physical labor and he had a lot of help from friends. Once he had produced cannabis oil, Bob began with a quarter gram per day. Within the next week he quickly escalated his daily intake to half a gram, then a full gram.

Due to his lifelong use of psychoactive cannabis, Bob was able to accelerate his dosing regimen faster than most patients. He continued at a gram a day for about 60 days before beginning to use a lower dose due to supply concerns.

Within 10 days, Bob had his right arm back, and could even throw a football. His overall condition improved tremendously. He stopped using all pharmaceuticals, including the codeine and aspirin he needed for pain. Unlike pills, the oil had a number of remarkable side effects. The high blood pressure Bob had struggled with for years completely dropped, to the point where he had to control his oil intake to make sure it did not get too low.

Indeed, CB1 activation is linked with hypotensive effects. Nummular eczema, asthma, and a herpes infection also all disappeared. Scientific studies indicate the potential of cannabinoids to benefit these conditions through broncodilatory, anti-inflammatory, and anti-viral capabilities. Also, a January 2015 review implicated cannabinoids in the potential treatment of many neuroinflammatory disorders, including ALS.

In September 2014, Bob returned to Massachusetts, partially because he wanted to share what he had learned about treating ALS with cannabis. While Bob still has problems with swallowing and some other symptoms, he says continued treatment almost makes him feel like he is getting younger. He believes that if he can increase his dose of decarboxylated and raw, acidic cannabinoids, he can more completely reverse the disease.

One reason Bob is excited about the potential of raw cannabinoids, and cannabis extracts as a whole, is due to the experience of one of his friends in Prague. The friend had been diagnosed with Stage IV melanoma that had spread to his liver and brain. He began simmering the bottom leaves of cannabis in milk at a low heat all day, creating a bhang-like infusion. For years he continuously drank the milk and rubbed it on the surface-level lesions. Six years later he is cancer free, and the only treatment he used was that milk preparation. This is not unheard of, as Dr. William Courtney had alluded to a cancer being eliminated with cannabis juice in a 2012 HuffPost Live segment.
The ability of an ALS patient to survive decades beyond the expected lifespan is also not unique. A Florida patient named Cathy Jordan is almost 30 years into her ALS diagnosis, a feat she attributes to cannabis.

It is critical that patients are not restricted in how much cannabis they can access. For people with seriously advanced illnesses, they often need several ounces of raw cannabis a month to ingest the necessary quantities of oil and raw juice. When patients have access to the right medicines at the right quantities, truly miraculous things can happen.

Posted in Cannabis and MND, Latest posts

Sativex – the big pharma ripoff

Legal access to medicinal cannabis within the UK is limited to the pharmaceutical cannabis based medicine Sativex. This can only be prescribed to Multiple Sclerosis sufferers and is at your doctors discretion, so differing postcodes can effect access.
It should also be noted that although the NHS in Wales will subsidise Sativex, the NHS in England will not, so typical treatments can cost up to £500 a month.
All other cannabis use or production in the UK is Illegal.
However, in 2006 the Home Office licensed Sativex so that:
– Doctors, at their own risk, could privately prescribe,
– Pharmacists could possess and dispense, and named patients with a prescription could possess.
From here: http://medicalmarijuana.co.uk/legal/uk-medical-cannabis-guidelines/

So, the only way to get medicinal cannabis in the UK is to ask your doctor for a private prescription for Sativex.

Unfortunately, many doctors are reluctant to prescribe Sativex because of ignorance and misunderstandings over the legality and benefits of cannabis as a medical treatment. Furthermore, Sativex is prohibitively expensive, despite the fact that it is basically exactly the same drug as good quality street cannabis oil tincture, which is readily available and retails at a fraction of the price.

EIGHT things you need to know about Sativex:-

1. With the connivance of the UK Home Office and government, GW Pharmaceuticals has been allowed to develop a monopoly cannabis business against all the provisions of the Misuse of Drugs Act 1971 and the UN Single Convention on Narcotic Drugs 1961. Cannabis is a very effective and safe medicine for a wide variety of conditions but in order to facilitate GW’s monopoly, the British public has been systematically misled and misinformed by government propaganda. Most seriously, people in pain, suffering and disability, seeking to provide their own cannabis medicine, have been ruthlessly and cruelly pursued by a corrupt law enforcement policy.

2. Sativex IS cannabis. It is pharmacologically identical to the plants from which it is made. It is NOT just an extract of THC and CBD, it contains all the cannabinoids, terpenes, flavonoids and other compounds included in cannabis. As GW founder and chairman, Geoffrey Guy, says “Most people in our industry said it was impossible to turn cannabis into a prescription medicine. We had to rewrite the rule book. We have the first approval of a plant extract drug in modern history. It has 420 molecules, whereas every other drug has just one.”

3. Sativex DOES get you high, just as every form of cannabis (except industrial hemp). See the Sativex Summary of Product Characteristics (SPC) which describes “euphoric mood” as a “common” side effect.

4. GW’s licence to cultivate cannabis issued in 1998 was for research purposes only. Since at least 2003, GW has been involved in commercial exploitation of cannabis and has therefore been acting unlawfully. The Home Secretary RETROSPECTIVELY LEGALISED GW’s licence by statutory instrument dated 13th March 2013. For the 10 years prior to that, GW, its directors and employees should have been subject to the same criminal penalties as anyone else producing a class B drug.

5. GW is engaged with the Home Secretary in an unlawful conspiracy falsely to distinguish Sativex from cannabis.Note that when re-scheduling Sativex in schedule 4 it has used a 75 word definition whereas every other drug in all five other schedules is defined by one word. The definition of Sativex even includes its method of delivery by an oral-mucosal spray. No other drug is scheduled by its method of delivery.

6. GW is engaged with the Home Secretary in an unlawful conspiracy to protect its unlawful monopoly of medicinal cannabis with the support of the British police which acts as armed enforcers of a private commercial interest.

7. The Home Office overrides doctors prescriptions for medicinal cannabis produced by Bedrocan, the Dutch government’s official producer. Home Office officials intimidate and threaten GPs who write such prescriptions.

8. Sativex is fantastically expensive. The NHS is charged at least 10 times the price for Sativex that organised crime sells cannabis for on the streets and between six and 17 times what Bedrocan is available for.

From here: http://www.leafscience.com/2014/03/08/7-things-need-know-sativex/

Posted in Cannabis and MND, Latest posts

Article: Highlights in Marijuana Science 2015

Highlights from 2015 in Marijuana Science, by Michael Vipperman

2015 was a big year for marijuana, socially and politically, with massive progress made towards ending the unjust incarceration of its users. However, it was also a big year in terms of scientific research. Here are my pick of the top marijuana-related scientific papers of the year.

Mokrysz C, Gage S, Landy R, Munafo M, Roiser J, Curran H. 2015. “Neuropsychological and educational outcomes related to adolescent cannabis use, a prospective cohort study” Eur Neuropsychopharmacol 24(2): S695

What they found: teens who heavily used marijuana exhibited an IQ decline, but it was attributable to confounding factors. Once enough factors are controlled for, marijuana use is not associated with IQ decline.

Why this matters: teenagers already undergoing an IQ decline are more likely than those not to become dependent on marijuana, leading to a spurious association between marijuana and IQ decline in poorly controlled studies. This study demonstrates that marijuana does not cause a cognitive decline, alleviating concern about its use among adolescents.

White H, Bechtold J, Loeber R, Pardini D. 2015. “Divergent marijuana trajectories among men: socioeconomic, relationship, and life satisfaction outcomes in the mid-30s” Drug and Alcohol Dependence 156: 62-69

Bechtold J, Simpson T, White H, Pardini D. 2015. “Chronic adolescent marijuana use as a risk factor for physical and mental health problems in young adult men” Psychology of Addictive Behaviors 29(3): 552-563

What they found: once confounding factors are controlled for, marijuana use by adolescents is not associated with health problems or poor socio-economic outcomes in adulthood

Why this matters: prohibitionists, as well as advocates of legalise-and-regulate models, continue to assume that we need to keep marijuana away from adolescents to protect them from harm, but these studies show that marijuana use alone is not associated with harm beyond the influence of confounding factors. The associations between early marijuana use, pathology, and poor outcomes are spurious, and marijuana is not the problem — rather, adolescents with certain problems are more likely to use marijuana, and to be at risk for additional factors. The persisting fears are unfounded, and we do not need to concern ourselves with restricting access by age.

Alshaarawy O, Anthony J. 2015. “Cannabis smoking and serum C-reactive protein: a quantile regressions approach based on NHANES 2005-2010” Drug Alcohol Depend 147: 203-207

What they found: marijuana smoking is associated with lower levels of C-reactive protein, a marker of inflammation.

Why this matters: marijuana’s anti-inflammatory effects have been known for millennia, but remain poorly understood by many researchers and the public. This is not the first study showing reduced CRP in marijuana users, but the more the better. Most of the disorders which people believe marijuana to alleviate, or suspect it of causing, are mediated by inflammation. Claims that marijuana protects against disease, or exacerbates it, rest in large part upon its effects on inflammation. If it cannot be shown that marijuana causes inflammation, then the biological plausibility of it causing harm would be impugned.

Chiurchiù V, Leuti A, Maccarrone M. 2015. “Cannabinoid signaling and neuroinflammatory diseases: a melting pot for the regulation of brain immune responses” Journal of Neuroimmune Pharmacology 10(2): 268-280

What they found: marijuana has profound immunoregulatory and anti-inflammatory properties which may ameliorate or protect against numerous inflammation-related disorders.

Why this matters: well, we already knew this, but one more review is always nice. Neuroinflammation is incredibly important in nearly all modern disease, and marijuana’s ability to attenuate it without causing immunosuppression would seem to validate its status as a “wonder drug.” Those who wish to attribute disease to marijuana use will have to show how and in what circumstances marijuana can increase inflammation; skeptics can instead take the position that it is not surprising to find evidence of inflammation in people who depend on anti-inflammatories, and therefore rest assured that marijuana is not causing the disorders with which its heavy use is correlated.

Giacoppo S, Galuppo M, Pollastro F, Grassi G, Bramanti P, Mazzon E. 2015. “A new formulation of cannabidiol in cream shows therapeutic effects in a mouse model of experimental autoimmune encephalomyelitis” Daru 23: 48

What they found: topical CBD reduced inflammation and even resulted in remyelination of spinal neurons in mice with experimental autoimmune encephalomyelitis

Why this matters: another study showing profound immunoregulatory and anti-inflammatory effects from a constituent of marijuana. Here it was found that topical application of a cream containing 1% CBD was sufficient to reverse inflammation-mediated paralysis and to heal damaged spinal neurons. This shows that smoking, vaping and eating are not the only effective routes of administration for combating neuroinflammation. That topical application of cannabinoids can improve skin conditions such as psoriasis and acne was previously shown, but remyelination of a demyelinated spinal cord is a very impressive finding.

Arain M, Khan M, Craig L, Nakanishi S. 2015. “Cannabinoid agonist rescues learning and memory after a traumatic brain injury” Ann Clin Transl Neurol 2(3): 289-294

What they found: administering a CB1 agonist to rats following head injury reduced the extent of brain damage

Why this matters: THC is a CB1 agonist, and is believed to protect against brain injury. This study supports that position.

Bonnet A, Marchalant Y. 2015. “Potential therapeutic contributions of the endocannabinoid system towards aging and Alzheimer’s Disease” Aging Dis 6(5): 400-405

What they found: the endocannabinoid system is a promising target for protecting against the neuroinflammation which contributes to disorders such as Alzheimer’s Disease

Why this matters: marijuana stimulates the endocannabinoid system, and is believed to protect against Alzheimer’s Disease. This paper reviews some of the mechanisms involved.

Tao Y, Tang J, Chen Q, Guo J, Li L, Yang L, Feng H, Zhu G, Chen Z. 2015. “Cannabinoid CB2 receptor stimulation attenuates brain edema and neurological deficits in a germinal matrix hemorrhage rat model” Brain Res 1602:127-35

What they found: CB2 activation protected against brain edema, and improved morphological and neurofunctional outcomes following germinal matrix hemorrhage, one of the most common and devastating cerebrovascular events that affect premature infants. Microglial activation and TNF-α release were found to be reduced.

Why this matters: yet more evidence of neuroprotective effects of cannabinoid receptor stimulation in yet another serious condition, specifically implicating the anti-inflammatory effects of CB2 activation.

England T, Hind W, Rasid N, O’Sullivan S. 2015. “Cannabinoids in experimental stroke: a systematic review and meta-analysis” J Cereb Blood Flow Metab 35(3): 348-58

What they found: reviewing 144 experiments, cannabinoids, including both THC and CBD, significantly and consistently reduced infarct size resulting from stroke in rats.

Why this matters: the relation between marijuana use and stroke remains controversial. The cases have been made both that marijuana may prevent some strokes, and that it may be a risk factor for one or more kinds of stroke. While this review cannot address the questions of incidence or prevalence, it suggests that the use of marijuana may reduce severity among users who experience a stroke (whether or not they would have had one anyway). Future studies into incidence, prevalence and severity of stroke in human marijuana users are necessary.

Blázquez C, Chiarlone A, Bellocchio L, Resel E, Pruunsild P, Garcia-Rincon D, Sentner M, Timmusk T, Lutz B, Galve-Roperh I, Guzman M. 2015. “The CB1 cannabinoid receptor signals striatal neuroprotection via a PI3K-Akt/mTORC1/BDNF pathway” Cell Death Differ 22(1): 1618-1629

What they found: the AKT pathway is involved in cannabinoid neuroprotection in the striatum

Why this matters: numerous mechanisms mediating cannabinoid neuroprotection were already established, such as reduction in microglial activation, inhibition of excitotoxic cytokine release by astrocytes, recruitment of regulatory t-cells, etc. This research adds activation of the AKT pathway to that list, improving our understanding of how the neuroprotective effects of cannabinoids actually take place at a cellular level. Activation of AKT also seems to clarify the relationship between marijuana use and dopamine signalling, because dopamine receptors also activate AKT. This may indicate that some of marijuana’s effects are dopamine-like without mediation by dopamine itself.

Bossong M, Mehta M, van Berckel B, Howes O, Kahn R, Stokes P. 2015. “Further human evidence for striatal dopamine release induced by administration of ∆9-tetrahydrocannabinol (THC): selectivity to limbic striatum” Psychopharmacology (Berl) 232(15):2723-9

What they found: increase in dopamine signalling following THC administration is very limited, and insufficient to explain the association of early onset marijuana use with schizophrenia.

Why this matters: researchers have been claiming for decades with no good human evidence that marijuana works “like other drugs of abuse” by stimulating dopamine release, leading to dependency. This narrative is not only terribly reductive, but false. While there is a small increase in striatal dopamine release following THC administration, it is an order of magnitude less than that associated with other drugs, and is far from the most important of marijuana’s effects. Hopefully now we can lay to rest the canard of THC having its effects by stimulating dopamine. Given that alterations to dopamine signalling are considered the “final common pathway” in psychosis, this is of particular relevance to schizophrenia research: the mechanism once believed to explain the association cannot explain it. Confounding by factors such as childhood trauma increasingly seem to be the more likely explanation for the association.

Cortes-Briones J, Cahill J, Skosnik P, Mathalon D, Williams A, Sewell R, Roach B, Ford J, Ranganathan M, D’Souza D. 2015. “The psychosis-like effects of Δ(9)-tetrahydrocannabinol are associated with increased cortical noise in healthy humans” Biol Psychiatry 78(11): 805-13

What they found: THC increased neural noise, and this effect was strongly related to its psychosis-like effects.

Why this matters: chaotic neural signalling can lead to strange sensations and experiences. It remains controversial whether using marijuana increases the risk of psychosis. This study suggests that psychosis-like effects of THC are due to an increase in neural noise, most likely due to transient reduction in the activity of GABAergic interneurons, which implies that the pathways implicated in the pathophysiology of schizophrenia, which have not been clearly shown to be exacerbated by marijuana use, are not necessary to produce the effect. This would suggest that THC’s effects might be mistaken for, but neither cause nor exacerbate, schizophrenia-related pathology.

Power B, Dragovic M, Badcock J, Morgan V, Castle D, Jablensky A, Stefanis N. 2015. “No additive effect of cannabis on cognition in schizophrenia” Schizophr Res 168(1-2): 245-51

What they found: cannabis use or dependence among schizophrenics does not worsen their cognitive function. The association between marijuana use and cognitive function is confounded by other factors and does not survive careful control.

Why this matters: there is concern that marijuana use can cause cognitive impairment, or exacerbate cognitive impairment in those with pre-existing problems such as schizophrenia. This study shows that this is not likely to be the case, which should alleviate concern about the use of marijuana by those with or at risk for schizophrenia.

Carey C, Agrawal A, Zhang B, Conley E, Degenhardt L, Heath A, Li D, Lynskey M, Martin N, Montgomery G, Wang T, Bierut L, Hariri A, Nelson E, Bogdan R. 2015. “Monoacylglycerol lipase (MGLL) polymorphism rs604300 interacts with childhood adversity to predict cannabis dependence symptoms and amygdala habituation: evidence from an endocannabinoid system-level analysis” J Abnorm Psychol 124(4): 860-77

What they found: people who were sexually abused were much more likely to subsequently become dependent on marijuana if they had two copies of a common version of the gene for an enzyme (MGLL, aka MAGL) involved in the synthesis of 2-AG, the most potent endocannabinoid.

Why this matters: the relationship between childhood trauma and marijuana dependence is well established. Trauma disorders are also known to be associated with impairment of the endocannabinoid system, and that marijuana use can partially compensate for this by stimulating that system is a reasonable explanation for the association. This study supports this position, by showing that it is not all sexual abuse survivors who are liable to become dependent on marijuana, but those whose endocannabinoid system is genetically vulnerable to impairment if they are exposed to severe stress (for example from sexual abuse). Interestingly, those vulnerable appear to be those with the more common version of the gene in question, which runs contrary to the assumption that risk is related to “bad genes” or restricted to a small minority of the population.

Chakraborty A, Anstice N, Jacobs R, LaGasse L, Lester B, Wouldes T, Thompson B. 2015. “Prenatal exposure to recreational drugs affects global motion perception in preschool children” Nature: Scientific Reports 5: 16921

What they found: children who were exposed to marijuana prior to birth had superior global motion perception to children not so exposed.

Why this matters: the effects of marijuana on early neurodevelopment remain controversial. The mainstream assumption is that marijuana use will impair or interfere with neurodevelopment and thus should be avoided during pregnancy, and that marijuana should be kept away from children. This study challenges that assumption, by showing an improvement in an area also shown to be damaged by alcohol. This is also one more piece of evidence showing that marijuana use may protect against alcohol-related brain damage.

Rivera P, Blanco E, Bindila L, Alen F, Vargas A, Rubio L, Pavon F, Serrano A, Lutz B, Rodriguez de Fonseca F, Suarez J. 2015. “Pharmacological activation of CB2 receptors counteracts the deleterious effect of ethanol on cell proliferation in the main neurogenic zones of the adult rat brain.” Front Cell Neurosci 9: 379

What they found: CB2 receptor activation protected against brain damage from giving alcohol to rats.

Why this matters: one more study suggesting that use of marijuana (which activates CB2 receptors) can protect against the adverse effects of alcohol.

Sabia J, Swigert J, Young T. 2015. “The effect of medical marijuana laws on body weight” Health Economics DOI: 10.1002/hec.3267

What they found: enforcement of medical marijuana laws is associated with a 2% to 6% decline in the prevalence of obesity, suggesting that the availability of medical marijuana saves from $58 to $115 per year per person in obesity-related medical costs alone.

Why this matters: obesity is a major contributor to poor health, and a several percent reduction in the overall rate of obesity is a very significant effect. This provides compelling support for the argument that increasing marijuana availability constitutes a legitimate and pressing public health objective. The authors cite increased mobility due to medicinal effects, and reduced consumption of alcohol due to people switching from alcohol to marijuana, to explain the effect. Unfortunately, they did not consider the regulatory, metabolic or anti-inflammatory effects, but future studies can be expected to follow this up.

Cluny N, Keenan C, Reimer R, Le Foll B, Sharkey K. 2015. “Prevention of diet-induced obesity effects on body weight and gut microbiota in mice treated chronically with Δ9-tetrahydrocannabinol” PLoS One  DOI: 10.1371/journal.pone.0144270

What they found: THC protected mice against developing diet-induced-obesity, and protected against obesity-related changes to the gut microbiota, without altering whole gut transit

Why this matters: it has been known for some time that marijuana users have lower than expected rates of obesity. This study provides additional evidence that THC can counteract the effects of high-risk diets and protect against obesity, and suggests that it is not only increased mobility and reduced alcohol consumption which explain the effect. Even with an equally fattening diet, and without any increase in physical activity, obesity was still prevented, because of THC’s effects on metabolism, inflammation and the gut microbiota.

Lutz B, Marsicano G, Maldonado R, Hillard C. 2015. “The endocannabinoid system in guarding against fear, anxiety and stress” Nature Reviews Neuroscience 16: 705-718

Morena M, Patel S, Bains J, Hill M. 2015. “Neurobiological interactions between stress and the endocannabinoid system” Neuropsychopharmacology  doi:10.1038/npp.2015.166

What they found: the endocannabinoid system regulates response to stress and fear-evoking stimuli, which is essential for long term viability, homeostasis and stress resilience.

Why this matters: dysregulation of the endocannabinoid system is observed in conditions such as PTSD and depression which are associated with marijuana use. Marijuana use is believed to assist in the regulation of this system and can therefore protect against or alleviate certain types of pathology. Reviews such as these are very useful for understanding exactly how this takes place, what cellular systems, proteins and enzymes are involved, etc.

Lynch M, Ware M. 2015. “Cannabinoids for the treatment of chronic non-cancer pain: an updated systematic review of randomized controlled trials” J Neuroimmune Pharmacol 10(2): 293-301

Ware M, Tongtong W, Shapiro S, Collet J-P. 2015. “Cannabis for the management of pain: assessment of safety study (COMPASS)” The Journal of Pain 16(12): 1233-1242

What they found: cannabinoids are safe, modestly effective analgesics in the management of chronic pain.

Why this matters: mild-moderate adverse effects, such as dizziness, were noted, but were not severe, and were generally well tolerated. This supports the use of marijuana in pain management.

Roulette C, Kazanji M, Breurec S, Hagen E. 2015. “High prevalence of cannabis use among Aka foragers of the Congo Basin and its possible relationship to helminthiasis” American Journal of Human Biology DOI: 10.1002/ajhb.22740

What they found: use of marijuana by foragers in the Congo was negatively associated with parasitic infection.

Why this matters: because of marijuana’s anti-inflammatory effects, it has been speculated that it could produce vulnerability to infections, such as by parasites. This study suggests that the opposite is the case, with marijuana possibly providing protection against the parasite (helminths) studied.

Pagliaccio D, Barch D, Bogdan R, Wood P, Lynskey M, Heath A, Agrawal A. 2015. “Shared predisposition in the association between cannabis use and subcortical brain structure” JAMA Psychiatry 72(1): 994-1001

What they found: marijuana use was associated with smaller amygdala volume, but this is not caused by marijuana but relates to underlying genetic associations. Siblings of marijuana users who did not use marijuana themselves have similar amygdalae to their marijuana using siblings.

Why this matters: changes in the amygdala have been suspected of being related to marijuana use, but the evidence has been inconsistent. This study demonstrates that the association is only correlative, and is not causally related to marijuana use.

Weiland B, Thayer R, Depue B, Sabbineni A, Bryan A, Hutchison K. 2015. “Daily marijuana use is not associated with brain morphometric results in adolescents or adults” Neurobiology of Disease 35(4): 1505-1512

What they found: marijuana use is not associated with previously suspected brain changes, such as in the nucleus accumbens, amygdala, hippocampus, and cerebellum, once confounding variables are controlled for.

Why this matters: they were specifically replicating Jodi Gilman’s “worst paper of 2014” which violated various principles of statistical analysis to show that recreational marijuana use was associated with (very small) morphometric changes in the amygdala, which it is not. Her paper was fraudulent, and that was already obvious (her data did not support her conclusions, and even her conclusions did not justify her press release), but the attempted replication and unambiguous rejection of her findings is nonetheless appreciated. Unfortunately, Gilman’s fraudulent results continue to be repeated by prohibitionists as proof that marijuana is harmful. Fortunately, more scientists than ever are objecting to this disreputable conduct, and it is very simple now to contrast this paper’s findings with her findings to judge for oneself.

Those highlights out of the way, the anti-highlight of the year remains the recent bit of scientific infamy I’ve already discussed from King’s College London’s faculty of Psychosis Studies, which had the press claiming that smoking skunk “wrecks your brain,” because of a 2% difference in one brain region between people who prefer bud and people who prefer hash in a badly controlled study. Their data, taken without the ridiculous fear-mongering, shows a marked absence of harm. Small differences associated with preferences are to be expected, whether it’s a preference for green as opposed to black olives, or for green as opposed to black marijuana products. If what they were claiming were true, that high potency strains “wreck brains,” there would be much more than this tiny non-effect to show for it. Unfortunately, King’s College does not deserve its prestigious reputation, and has allowed for blatant dishonesty in the service of justifying mass incarceration.

All in all, this year in marijuana science increasingly clarified what was already apparent, which is that the various harms we were concerned that marijuana might be causing are not, in fact, caused by marijuana use, but most of them involve inflammation, with which marijuana can help.

Posted in Cannabis and MND, Latest posts

Article: anti-Cannabis propaganda at Kings College London

King’s College London Causes Psychosis (with anti-marijuana propaganda) by Michael Vipperman

Psychosis is a state of aberrant salience in which faulty perceptions (hallucinations) and faulty beliefs (delusions) combine to produce problematic behaviour. Many researchers around the world are studying this phenomena to try to alleviate it, but at least one faculty is pretending to study it in order to engineer a panic about a plant which psychotic patients often find to be extremely useful, but which it is politically expedient to blame. Psychosis Studies at King’s College London has released numerous studies which betray fundamental failures of understanding regarding the condition in their faculty’s title, especially the role of negative symptoms in psychotic disorders such as schizophrenia. It is hard to be sympathetic towards these failures, when their interpretations combine wilful use of stigmatising language, misdirection and exaggeration to try to disprove the fact that their patients sometimes use tobacco and marijuana because they find them to be helpful, and to “prove” on the contrary that these plants are the cause of the harms in question, using studies incapable of showing causation. In this article I will review just three such studies, although their other material is riddled with the same problems.

Let’s start with a study in which they contradicted themselves in their own abstract, displaying a shocking lack of willingness to listen to their patients or honestly consider their reasons for use:

Kolliakou A, Castle D, Sallis H, Joseph C, O’Conner J, Wiffen B, Gayer-Anderson C, McQueen G, Taylor H, Bonaccorso S, Gaughran F, Smith S, Greenwood K, Murray R, Di Forti M, Atakan Z, Ismail K. 2015. “Reasons for cannabis use in first-episode psychosis: Does strength of endorsement change over 12 months?” European Psychiatry 30(1): 152-159

To excerpt from the abstract: “At each time-point, patients endorsed ‘enhancement’ followed by ‘coping with unpleasant affect’ and ‘social motive’ more highly for their cannabis use than any other reason… Little support for the self-medication or alleviation of dysphoria models was found. Rather, patients rated ‘enhancement’ most highly for their cannabis use”

Positive psychotic symptoms do not occur in a vacuum, but are associated with negative symptoms, which generally precede by years the onset of first episode psychosis. Negative symptoms consist of absences, such as cognitive impairment, anhedonia or lack of motivation. These are primary sources of suffering for people with psychotic disorders, and arguably constitute “the core of the disorder,” at least if that disorder is schizophrenia. Relief from negative symptoms — enhancement, coping with unpleasant affect, etc — is therefore extremely important, and it’s ridiculous to say that patients’ endorsements for enhancement do not support self-medication. What they found was that their patients find cannabis to alleviate the core symptoms of their condition; what they reported was that self-medication can be rejected, on the basis of which we are to conclude that the relative increase in use among prodromal schizophrenics is proof that marijuana use causes schizophrenia, a hypothesis for which there is a mountain of countervailing evidence they do not consider.

Now let’s look at their work which compares users who prefer relatively stimulating, high THC marijuana over relatively relaxing formulations such as hash:

Di Forti M, Marconi A, Carra E, Fraietta S, Trotta A, Bonomo M, Bianconi F, Gardner-Sood P, O’Conner J, Russo M, Stilo S, Marques T, Mondelli V, Dazzan P, Pariante C, David A, Gaughran F, Atakan Z, Iyegbe C, Powell J, Morgan C, Lynskey M, Murray R. 2015. “Proportion of patients in south London with first-episode psychosis attributable to use of high potency cannabis: a case control study” S2215-0366(14)00117-5

Although their sample showed no association between cannabis use and psychosis, they dichotomised the cannabis users into “skunk using” and “hash using” groups — using the term “skunk” to refer to relatively more stimulating bud (not to a specific strain), apparently only because that’s easier to stigmatise, since “skunk” sounds worse than, say, “girl scout cookies” — and showed that the rate of psychosis was somewhat higher in the “skunk using” group. As above, they reject self medication on the basis that THC does not alleviate positive symptoms of psychosis, while ignoring that it DOES alleviate NEGATIVE symptoms of psychotic disorders. They say: “That people who already have prodromal symptoms would choose a type of cannabis that is high in THC and has little cannabidiol (such as skunk), which might exacerbate their symptoms, rather than a cannabidiol-containing type (such as hash), would seem counterintuitive” — this is only counterintuitive if you completely ignore negative symptoms, and the fact that THC alleviates them. This would be more forgiveable if they hadn’t also published studies in which they had interviewed schizophrenics who TOLD them why they use it. Just to break it down really simply: people suffering from negative symptoms enjoy and value THC because it is stimulating, not because it is relaxing. You can’t in good faith reject “self medication” while ignoring self-medication for the symptoms that are actually the greatest source of suffering in the patients’ lives and only focusing on other symptoms for which, it’s true, THC is not effective, and can even exacerbate (while some people with psychotic symptoms value marijuana, others stay away from it; it makes it worse for some and helps for others). It’s not “counterintuitive” that people in a prodromal period  — those for whom positive symptoms are not yet overwhelming — prefer stimulating cannabis over relaxing cannabis. I would accuse Psychosis Studies at King’s College London of incompetence, but their use of the stigmatising term “skunk,” combined with this flagrant disregard for the well being of their patients has eroded all my sympathy for them, and so instead I’ll just call them corrupt, shameful propagandists actively hurting the public by manipulating data to create undue concern. At that, they are not incompetent, but apparently quite adept.

and now the new study that came out this week:

Rigucci S, Marques T, Di Forti M, Taylor H, Dell’Acqua F, Mondelli V, Bonaccorso S, Simmons A, David A, Girardi P, Pariante C, Murray R, Dazzan P. 2015. “Effect of high-potency cannabis on corpus callosum microstructurePsychological Medicine Published online November 27 2015

As in the above study, they dichotomised users with a preference for stimulating cannabis from users with a preference for relaxing cannabis, and looked for evidence of differences in brain structure between the groups, finding a very small difference in the corpus callosum. That is, users with a preference for stimulating cannabis have 2% thinner corpus callosa than users with a preference for relaxing cannabis. The difference is too small to realistically consider as damage, and the study cannot show causation, but it’s assumed that any difference at all must be proof of harm, and so causation is assumed. The title even says “effect of high-potency cannabis on corpus callosum microstructure,” despite no evidence that this was an “effect of high-potency cannabis,” as opposed to an effect of a slightly thinner corpus callosum making users more likely to prefer relatively stimulating forms of cannabis, or some form of confounding (for example, they did not control for childhood trauma, which is known both to damage the corpus callosum and to greatly increase the rate of marijuana dependence among its survivors).

They conclude:
“Since high-potency preparations are now replacing traditional herbal drugs in many European countries, raising awareness about the risks of high-potency cannabis is crucial.”

Setting aside the fact that cannabis IS a traditional herbal drug, listed in every pharmacopoeia ever written (excluding those pressured to exclude it during the war on drugs), claiming their finding as a “risk of high potency cannabis” is indefensible. There is no scientific justification for their position. Prematurely claiming harm simply because you found — in a small, badly controlled study –that a small difference in one area correlates with one preference as opposed to another will only raise alarm, and make people who are not at risk think they are at risk, or even to create risk where it wasn’t previously by promoting nocebo effects, and inevitably iatrogenic harm.

I conclude:
The faculty of Psychosis Studies at King’s College London is encouraging harmful delusions, to the detriment of everybody. Since we are at a moment of redefining laws governing access to this plant, raising awareness about the actual reasons why people use it, and its actual effects, is crucial. Ignorant and inflammatory anti-marijuana propaganda of this ilk should no longer be tolerated. If psychosis researchers don’t understand what negative symptoms are or why the stimulating effects of THC might be relevant to them, they should have no business writing about the “effects of high potency cannabis” while displaying a name so prestigious as King’s College. If King’s College would like to retain its prestigious status, and not be associated with this sort of indefensible nonsense, this faculty should be defunded immediately.

————————————————————————————————————————————————————————————

Studies showing corpus callosum damage in childhood trauma survivors:

http://www.ncbi.nlm.nih.gov/pubmed/12460690
http://www.ncbi.nlm.nih.gov/pubmed/15465292
http://www.ncbi.nlm.nih.gov/pubmed/16730374/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229094/
http://www.ncbi.nlm.nih.gov/pubmed/18296031

Studies showing that marijuana alleviates negative symptoms:
http://www.ncbi.nlm.nih.gov/pubmed/15374573
http://www.ncbi.nlm.nih.gov/pubmed/12111342
http://www.ncbi.nlm.nih.gov/pubmed/1543037
http://schizophreniabulletin.oxfordjournals.org/content/16/1/69.full.pdf
http://www.ncbi.nlm.nih.gov/pubmed/23624489
http://www.ncbi.nlm.nih.gov/pubmed/15354183

Posted in Cannabis and MND, Latest posts

Article: Is Marijuana bad for you?

Is there any proof that marijuana is bad for the health of its users? by Michael Vipperman

Short answer: No.

Many types of pathology have been suspected of being caused by marijuana use or overuse, but so far none of them have stood up to empirical investigation. This is not for lack of trying.  Three examples:

Throat/Lungs:
It’s intuitively obvious that habitual smoke inhalation would damage the throat and lungs, and habitual tobacco smoking certainly does. But after decades of research, it has become obvious that any damage from marijuana itself is clinically insignificant. Long term heavy users have actually been found on average to have greater lung capacities than non-users. They also exhale marginally more slowly, and since bronchitis is diagnosed by measuring the ratio between lung capacity and rate of exhalation, they are slightly more likely to meet the technical criteria for bronchitis, but this effect is driven primarily by *increased lung capacity* and it is dishonest to claim as proof of harm. Throat irritation and a cough however are real side effects, though rarely severe enough to be clinically significant. Avoiding this irritation is the main advantage of switching to vaporisers instead of smoking, but, for many smokers, the irritation remains an acceptable side effect, and evidence of long term harm is lacking. (1,2)

Diabetes:
The munchies are not a myth (although not everyone gets them, and marijuana actually reduces appetite in a minority of users); on average, marijuana users eat ~50% more calories than non-users, sometimes gorging on “junk” foods. This would increase risk for Type II diabetes, were it not for marijuana’s anti-inflammatory and regulatory effects, which appear to protect the pancreas from damage. Several large epidemiological studies have now reported that there is no association, or a negative association, between marijuana use and diabetes. Marijuana users are evidently able to eat more food than non-users with less harm to the pancreas. (3,4,5)

Brain Damage:
Heavy use of marijuana often makes people feel foggy in the head, can slow reaction time, and moderately impairs some memory functions, so it seems reasonable to infer that this is related to damage. What people often do not realise, however, is that brain damage — whether triggered by a head injury, a virus, a seizure or emotional abuse — is mediated by excitotoxicity, which is when neurons are excited to the point that they fry themselves out. Marijuana reduces brain activity through multiple convergent mechanisms, and dramatically increases the activity of the system the brain uses to protect against excito-toxicity (the endocannabinoid system). This protects against brain damage, and there are many studies to prove it, and no studies which demonstrate brain damage from any level of marijuana use at any age: the brains of even very heavy long term users are no worse off than those of non-users. Marijuana users are even more likely to survive head injuries sustained in car accidents. The reason people are concerned about marijuana’s brain effects is precisely because it reduces activity, but it’s too MUCH activity which causes brain damage, not too little. In other words, not only is there no empirical evidence that marijuana causes brain damage in humans, it is also not biologically plausible that it would. (6,7,8,9,10,11,12,13)

It’s important to stress that the burden of proof is on the positive position, which is the claim that marijuana is causing harm. Absence of evidence should mean absence of concern — public policy should not be founded on the assumption that marijuana is causing harms which are both empirically and theoretically unsupported, despite decades of extensive research funded by organisations such as the National Institute on Drug Abuse. If it was harmful, wouldn’t they have proven it by now?

Is there a critical window of vulnerability in which young people are at risk if they use marijuana?

Short answer: No.

Despite the well documented absence of harm from marijuana use, the possibility has been suggested — and frequently repeated, not only by prohibitionists but also as a concession by marijuana advocates wishing to appear moderate — that teenagers might be experiencing harm from using even if adults are not. Increased concern about effects (of anything) on children makes sense, because anything which could interfere in ongoing neurodevelopment will have a ripple effect, and earlier exposure could have more negative effects than later exposure. This is certainly true of trauma: traumatic experiences in early childhood lead to more diverse symptoms and worse outcomes than traumas later in life. Unlike trauma, however, use of marijuana at an early age is not associated with cognitive impairment or poor health outcomes at a later age once other factors are controlled for. Trauma is, however, strongly associated with early onset of marijuana use, and especially with marijuana dependence, and so studies which examine people who became dependent on marijuana at an early age sometimes find evidence of trauma-related pathology when these people are compared with healthy controls. That is presented as evidence that marijuana is causing harm, even though the harms in question are not found in the majority of early-onset users, or even in the majority of heavy users, but only the most dependent early-onset users, and only in studies which did not control for trauma. Once childhood trauma is taken into consideration (unfortunately, it is usually ignored), the association between early marijuana use and harm evaporates. (14,15,16,17,18,19,20,21,22)

Obviously, the health of young people is very important, and we should not be overly hasty to dismiss possible risks. But there is no proof of any kind of harm at any age from any level of marijuana use, and it is dishonest to insist that there is. Thus there is no empirically sound public health argument for restricting marijuana availability or preventing young people from using it. Anybody who wishes to disagree would do well to perform a review of the literature with the confound of trauma in mind. If you would like more detail, citations, and in depth discussion of each of the harms spuriously associated with early-onset marijuana dependence (brain damage, depression, schizophrenia and IQ decline), contact me and I will furnish you with all you need. There is much to say, but for this article I’m trying to keep things brief: the bottom line is that nobody has ever clearly shown that teenagers who use marijuana are any worse off on average than if they had not used it.

Does marijuana help with stress and trauma-related pathology?

Short answer: Yes.

That marijuana has anti-inflammatory properties and can assist in stress relief is widely known. However, the relevance of these facts to the question of pathology has not been properly considered by most writers on the subject. Childhood trauma is strongly associated with all of the harms spuriously associated with marijuana use, and these harms are driven by neuro-inflammation, which marijuana use reduces. It’s helpful to understand the system marijuana works upon, the endocannabinoid system, which is a system the brain uses to protect itself from inflammation and excitotoxicity. Chronic stress however can cause this system to fail, producing an endocannabinoid deficiency which allows damage to proliferate. Marijuana’s main effect is boosting the activity of this system, which can compensate for or reverse the loss of feedback inhibition associated with chronic stress and trauma. This is why so many people with traumatic childhoods are dependent on marijuana: it helps. The critical question, then, is whether excessive marijuana use can cause the endocannabinoid system to downregulate, leading to a loss of this protection, but, even though this is often claimed by organisations such as NIDA, their own data shows it not to be the case. Marijuana use does not suppress the endocannabinoid system, it enhances it, and this make it extremely useful in inflammatory conditions, such as those related to trauma and chronic stress. (23,24,25,26,27,28,29,30)

Childhood trauma explains the modestly elevated pathology observed in cannabis-dependent adolescents. It explains why they begin using it, why they sometimes become dependent on it, why they have brain damage which sometimes turns up in badly designed studies trying to look for marijuana effects without controlling for trauma, and an examination of the mechanisms involved reveals no biologically plausibility that marijuana is worsening any of these conditions.

So can we please stop saying that it harms children when there’s no evidence of that, and when there’s much clearer evidence that it’s helping?

And can we please not design legislation which makes preventing young people from accessing it a goal in and of itself?

It’s high time we actually focused on improving outcomes for people at risk, and stopped blaming their problems on the things they find helpful.

Short Bibliography (click for full bibliography, with or without excerpts/annotations)

(1) Tashkin DP. 2013. “Effects of Marijuana Smoking on the Lung” Annals of the American Thoracic Society 10(3):239-247

(2) Kempker J, Honig E, Martin G. 2014. “Effects of marijuana exposure on expiratory airflow: a study of adults who participated in the US National Health and Nutrition Examination Study” Ann Am Thorac Soc [epub ahead of print]

(3) Rajavashisth TB, Shaheen M, Norris KC, Pan D, Sinha SK, Ortega J, Friedman TC. 2012. “Decreased prevalance of diabetes in marijuana users: cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) III” BMJ Open 2:e000494

(4) Le Strat Y, Le Foll B. 2011. “Obesity and Cannabis Use: Results from 2 Representative National Surveys” American Journal of Epidemiology doi: 10.1093/aje/kwr200

(5) Rodondi N, Pletcher MJ, Liu K, Hulley SB, Sidney S. 2006. “Marijuana use, diet, body mass index and cardiovascular risk factors (from the CARDIA study)” American Journal of Cardiology 15;98(4): 478-84

(6) Weiland B, Thayer R, Depue B, Sabbineni A, Bryan A, Hutchison K. 2015. “Daily marijuana use is not associated with brain morphometric results in adolescents or adults” Neurobiology of Disease 35(4): 1505-1512

(7) Fagan S, Campbell V. 2013. “The influence of cannabinoids on generic traits of neurodegeneration.” British Journal of Pharmacology 2014: 171; 1347-1360

(8) Sánchez-Blázquez P, Rodríguez-Muñoz M, Vicente-Sánchez A, Garzón J. 2013. “Cannabinoid receptors couple to NMDA receptors to reduce the production of NO and the mobilization of zinc induced by glutamate” Antioxid Redux Signal 19(15): 1766-1782

(9) Nguyen B, Kim D, Bricker S, Bongard F, Neville A, Putnam B, Smith J, Plurad D. 2014. “Effect of marijuana use on outcomes in traumatic brain injury” Am Surg 80(10): 979-83

(10) Katona I, Freund T. 2008. “Endocannabinoid signaling as a synaptic circuit breaker in neurological disease” Nat Med 14(9): 923-30

(11) Tzilos G, Cintron C, Wood J, Simpson N, Young A, Pope H Jr, Yurgelun-Todd D. 2005. “Lack of hippocampal volume change in long-term heavy cannabis users” Am J Addict 14(1):64-72

(12) Block R, O’Leary D, Ehrhardt J, Augustinack J, Ghoneim M, Arndt S, Hall J. 2000. “Effects of frequent marijuana use on brain tissue and composition” Neuroreport 11(3): 491-6

(13) DeLisi L, Bertisch H, Szulc K, Majcher M, Brown K, Bappal A, Ardekani B. 2006. “A preliminary DTI study showing no brain structural change associated with adolescent cannabis use.” Harm Reduct J 3: 17

(14) Cornelius J, Kirisci L, Reynolds M, Clark D, Hayes J, Tarter R. 2009. “PTSD contributes to teen and young adult cannabis use disorders” Addictive Behaviors 35(2):91-94

(15) Butters J. 2002. “Family stressors and adolescent cannabis use: a pathway to problem use” J Adolesc 25(6): 645-54

(16) Hyman S, Sinha R. 2009. “Stress-Related Factors in Cannabis Use and Misuse: Implications for Prevention and Treatment” J Subst Abuse Treat 36(4): 400-413

(17) Barnes G, Barnes M, Patton D. 2005. “Prevalence and predictors of “heavy” marijuana use in a Canadian youth sample” Subst Use Misuse 40(12): 1849-63

(18) Murphy J, Houston J, Shevlin M, Adamson G. 2013. “Childhood sexual trauma, cannabis use and psychosis: statistically controlling for pre-trauma psychosis and psychopathology” Soc Psychiatry Psychiatr Epidemiol 48:853-861

(19) Dube SR, Felitti VJ, Dong M, Chapman DP, Giles WH, Anda RF. 2003. “Childhood abuse, neglect, and household dysfunction and the risk of illicit drug use: the adverse childhood experiences study.” Pediatrics 111(3):564-72

(20) Gupta M. 2013. “Review of somatic symptoms in post-traumatic stress disorder” Int Rev Psychiatry 25(1): 86-99

(21) D’Andrea W, Ford J, Stolbach B, Spinazzola J, van der Kolk B. 2012. “Understanding Interpersonal Trauma in Children: Why We Need a Developmentally Appropriate Trauma Diagnosis” American Journal of Orthopsychiatry 82(2): 187-200

(22) Kaffman A. 2009. “The Silent Epidemic of Neurodevelopmental Injuries” Biol Psychiatry 66(7): 624-626

(23) Alshaarawy O, Anthony J. 2015. “Cannabis smoking and serum C-reactive protein: a quantile regressions approach based on NHANES 2005-2010” Drug Alcohol Depend 147: 203-207

(24) Gaffal E, Cron M, Glodde N, Tuting T. 2013. “Anti-inflammatory activity of topical THC in DNFB-mediated mouse allergic contact dermatitis independent of CB1 and CB2 receptors” Allergy68(8): 994-1000

(25) Cabral G, Raborn E, Griffin L, Dennis J, Marciano-Cabral F. 2008. “CB2 receptors in the brain: role in central immune function” Br J Pharmacol 153(2): 240-251

(26) Greer G, Grob C, Halberstadt A. 2014 “PTSD symptom reports of patients evaluated for the New Mexico medical cannabis program” Journal of Psychoactive Drugs 46(1): 73-77

(27) Neumeister A, Normandin M. 2013. “Elevated Brain Cannabinoid CB1 Receptor Availability in Posttraumatic Stress Disorder: A Positron Emission Tomography Study” Molecular Psychiatry 18(9): 1034-1040

(28) Passie T, Emrich H, Karst M, Brandt S, Halpern J. 2012. “Mitigation of post-traumatic stress symptoms by Cannabis resin: a review of the clinical and neurobiological evidence” Drug Test Anal 4(7-8):649-59

(29) Rossi S, de Chiara V, Musella A, Kusayanagi H, Mataluni G, Bernardi G, Usiello A, Centonze D. 2008. “Chronic psychoemotional stress impairs cannabinoid-receptor-mediated control of GABA transmission in the striatum” J Neurosci 28(29): 7284-92

(30) McPartland J, Guy G, Di Marzo V. 2014. “Care and feeding of the endocannabinoid system: a systematic review of potential clinical interventions that upregulate the endocannabinoid system” PLOS ONE 9(3) e89566

Post-script
I acknowledge that marijuana is not useful in every situation, that some people react badly to it and should not use it, and that young people should be educated about appropriate and inappropriate dosage strategies, and not simply encouraged to use all day every day. However, I insist that our focus should be on preventing trauma and alleviating its effects, not on denying access to a plant which many trauma survivors, of any age, find to be incredibly helpful. If future study reveals conclusive evidence of harm, I will gladly revise my position accordingly, but the more evidence emerges, the less plausible that seems. If it was harmful, there would be proof by now. Don’t pretend that this is totally uncharted territory — thousands of studies have been performed, and yet the claims of harm remain unsupported. It’s time we stopped assuming and insisting that marijuana has health effects which it demonstrably does not have.

Posted in Cannabis and MND, Latest posts

Article: Beneficial effects of marijuana

What does marijuana do? It rebalances everything by Michael Vipperman

The “simplest” accurate description of the effects of marijuana in humans is that it modulates the regulation of homeostasis. Homeostasis is what Goldilocks seeks in the children’s story: not too hot; not too cold; just right. More than just heat and cold, the human body contains many systems which must be held in relative balance. The balance between inhibition and excitation, bone formation and resorption, inflammatory/anti-inflammatory signalling, fat storage and release, blood sugar, blood pressure, hormone levels; all these systems are held in balance by the endocannabinoid system. This system, though involved in maintaining nearly every biological process in all humans, has only received scientific study for roughly the past 20 years, and it was discovered because it’s the site of action for marijuana.

Marijuana does not simply activate (agonise) this system. In addition to full cannabinoid agonists (chemicals which stimulate — agonise; antonym: antagonise — receptors), it also contains partial agonists, antagonists (Thomas, 2007), reuptake and transport inhibitors, enzyme modulators and much else besides, (Russo, 2011) including an assortment of terpenoids and flavinoids responsible for the odour of the flowers; how a marijuana strain smells indicates what mix of chemicals (all of which appear to be pharmacologically active in humans) are present, beyond the most famous two, neither of which have an odour: THC and CBD. The most studied receptors in the endocannabinoid system are called CB1 and CB2, both of which inhibit the other (Callén et al 2012), and both of which are stimulated by THC (a partial agonist at both and other sites) and antagonised by CBD (Thomas et al, 2007). There are also believed to be numerous other receptors involved (Petrocellis, 2009), and their scientific study is yet only preliminary and largely speculative. Far from a single chemical with a single mode of action, marijuana has an entourage effect: many chemicals working together to produce effects not reducible to the action of only one or two of its constituents. One chemical it often contains in relatively large quantities, for example, is caryophyllene, a selective full CB2 agonist which is also found in cloves, rosemary, hops and eucalyptus. Other plants which work on cannabinoid receptors include hot pepper and vanilla. Through their presence in the diet of some marijuana users, these (and other) plants participate in the entourage effects of marijuana in modulating the regulation of homeostasis.

Summary: it rebalances almost every system in the body through multiple inter-related effects which move in several directions at once and which compensate for each other’s effects (confused yet?)

But what does it all DO?

Research into the effects of marijuana has been aided by intense and widespread public interest, but hindered in recent decades by efforts by various parties to suppress any investigation into possible benefits and to spread claims of possible harms (no matter how tenuous), as part of the “war on drugs.” As an ethnographer working with young drug users in person and on the internet, as well as having read widely on the subject, these are the effects I have most often found credibly attributed to marijuana:

Increased appetite, change in the perception of time, relief from pain, intensified awareness (both inside and outside the body), relaxation, euphoria, increased heart rate, lower blood pressure, emotional release, increased vigor, lethargy, inhibited memory, increased creativity, intense introspection, reveries, flights of fancy, lower body temperature, increased sexual pleasure, reduced sexual desire, relief from nausea, greater aesthetic appreciation, magical thinking, heightened interest in spiritual phenomena, and both increased and decreased anxiety (presumably different types of anxiety).

Reported medically relevant effects of marijuana also include bronchodilation, decreased intracranial and intraocular pressure, glucagon release, reduction in insulin tolerance, lymphocyte suppression, antimicrobial, anticonvulsant, antipsychotic, psychotomimetic, anti-inflammatory, antiemetic, antinociceptive and anticarcinogenic effects.

Occasionally marijuana causes many strange and idiosyncratic effects not here described. Some of these may sometimes be labelled as psychotic or spiritual, but these effects are typically short-lived; they do not last and often cannot be produced reliably or consistently, making them difficult, if fascinating, to study.

Many of marijuana’s effects appear to be highly context- and dose-dependent. In small and occasional doses, it is often more stimulating, boosting appetite and providing relief from depression, whereas in very large and frequently repeated doses, these effects may reverse, with less appetite and relative inactivity. While it influences every organ system, its direct effects are largely confined to the maintenance of homeostasis, which it pushes not just in one direction but in several, counteracting and balancing out its own effects. Even a massive overdose will generally have a negligible impact on long term health, though it may be disorienting until it wears off.

The stimulating effects of THC typically last 2-3 hours, whereas the half-life of CBD, which is more relaxing, is 9 hours. Thus, the first dose of marijuana after a period of abstinence will tend to be far more stimulating than subsequent doses, which must compete with the relaxing effects of previous doses, because the relaxation both persists much longer and shares many of the same pathways as the stimulation. Regular ingestion of THC also leads to increased tolerance to its stimulating effects, but not to its relaxing effects, with very heavy use associated with a reversible 20% reduction in CB1 receptor density in some areas of the brain (Hirvonen et al, 2012); THC itself provides a longer term mild relaxing effect than the immediate boost. As cannabinoid activity can produce anxiety, it may well be that developing tolerance to the drug may itself protect against anxiety on a longer time scale; in a sense, by getting high you can get your anxiety out of the way while also benefiting from a variety of relaxing and euphoric effects to counteract it, rather than having to deal with constant, unremitting anxiety. Notably, Hirvonen et al only found the reduction in receptor density in only some areas, so this long term down-tuning does not affect all of the processes influenced by THC, but only some of them. In any case, we need to consider not just the immediate high, but also its persisting effects, if we are to understand the consequences of its use in humans.

Summary: it does lots of things, and sometimes also the opposite. (maybe this will be easier if we go system by system…)

Marijuana in the Brain

The brain’s major inhibitory neurotransmitter is GABA, and the major excitatory neurotransmitter is glutamate; the endocannabinoid system regulates the levels of each of these by selectively suppressing them as called for, hopefully maintaining an appropriate balance. THC temporarily boosts this process, suppressing both inhibition and excitation. With GABA suppressed, a wide variety of effects and processes which would otherwise have been inhibited become more free to play themselves out. This explains the sensory enhancements commonly experienced by marijuana users, with increased sensitivity to smell, sight, sound, texture and much besides, including sexual pleasure. This is probably also the best scientific explanation for its occasionally outlandish effects, from the merely weird to the deeply spiritual to the profoundly unsettling: the mind, unleashed and uncontained, for better or for worse. Glutamate, though itself excitatory, excites neural networks which inhibit various behaviours, and so its suppression may contribute not only to relaxation but also to some of marijuana’s behavioural effects, such as indulgence in magical thinking and the wild dancing. Importantly, glutamate can also damage brain cells (excitotoxicity), and so suppressing it provides some protection brain damage as it occurs in head injury, epilepsy, hypoglycaemia, stroke, alcohol or benzodiazapine withdrawal and a variety of neurodegenerative conditions including multiple sclerosis, Parkinson’s Disease, Alzheimer’s Disease and Huntington’s Disease, among other conditions. Cannabinoid receptors on glial cells are involved in memory storage, recall, and forgetting (Lane et al, 2005), as well as the extinction of conditioned place preferences more specifically (Parker et al, 2004), suggesting that marijuana use may make it easier to adapt to new contexts and to forget old habits. It fundamentally changes how we experience the passage of time; in Hindu mythology, Lord Shiva, poisoned by time, takes marijuana which relieves his anxiety so that he begins to dance, and through his dance the poison is neutralised, thus saving the universe from being destroyed by an imbalance between space and time. Many experiments have shown that marijuana use impairs performance at certain memory tasks, but that this effect disappears after a period of abstinence, and so cannot be described as damage. Rather than merely the absence of remembering, forgetting is an active process by which we let go of extraneous or harmful memories (White, 2001; Pollan, 2002); by boosting forgetting functions through its effects on glial cells, marijuana may provide relief from traumatic memories. (Marcisano, 2001) The creative benefit most commonly cited by artists who use marijuana is in improvisation, getting into the flow so that strange new rhythms can emerge, fascinate and delight. (Fachner, 2003) More research is necessary, but I suspect that increased forgetting and increased improvisation are linked, and that a good description of marijuana’s creative effects might be less rote repetition and more novel recombination; whether that will be desirable or harmful will depend on the task at hand.

Marijuana is very popular among people with ADHD, for whom it may be synergistic with their tendency to hyperfocus, sometimes used to push past ennui into full dynamic engagement (the term for which in the cognitive sciences is “flow”), though it also tends to increase restlessness and can make them even more distractable, especially in larger doses, and so ADHD people often find very small doses to be the most helpful. (Loflin, 2014) One physiological description of ADHD is impaired dopamine transporter function, and the most common pharmaceutical interventions for ADHD are psychostimulants such as amphetamines which stimulate dopamine release directly. Marijuana, on the other hand, does not increase dopamine signalling, but modulates salience through other pathways. For this reason, many ADHD people find that marijuana feels more “natural,” ebbing and flowing with the context, whereas amphetamines often feel forced or artificial. Another difference is that amphetamines often make it very difficult to eat and sleep, whereas marijuana boosts appetite and, for many of its users, provides unusually restful and easy sleep. This is extremely important, because poor sleep and poor diet are major sources of harm among people with ADHD.

Some autistic people have also found marijuana to be of benefit in relieving the overstimulation-related emotional anxiety and tension which can inhibit their behaviour. Recent evidence has emerged that autism may in part be caused by abnormalities in cannabinoid signalling (Földy, 2013), so it seems that the rebalancing effect of marijuana directly interacts with some of the underlying causes of autism. One physiological description of autism is too much glutamate and not enough GABA; by suppressing both glutamate and GABA, marijuana may essentially level the playing field, so that a stoned neurotypical and a stoned autistic person end up on roughly the same level.

In neither ADHD nor autism does marijuana merely suppress symptoms and make a person “normal”; far from it. What it does is to rebalance many metabolic, attentional and neural systems, reconfiguring any problematic balance which may be in place, and producing a new state of consciousness unlike either neurotypical consciousness or the typical expression of either ADHD or autism. That is, it may normalise homeostasis, but to do so is not necessarily normative, in the anthropological sense.

In summary, marijuana rebalances excitation and inhibition in ways which are sometimes highly valued, and which may correct for or prevent imbalances in attentional and cognitive systems.

Marijuana benefits and risks

Marijuana, Neuroprotection and Brain Damage

In addition to preventing glutamate excitotoxicity and neuroinflammation, marijuana also reduces the volume of fluid in the head following head injury, lowers brain temperature (trivia: the popular fever reducer sold as Tylenol works partially by breaking down into a cannabinoid reuptake inhibitor, and therefore shares a pathway with marijuana (Bertolini, 2006)) and prevents prion accumulation (Dirikoc et al, 2007), all of which are ways by which it’s known marijuana can protect against brain damage. It also reduces risk of such neurodegenerative conditions as Parkinson’s Disease and Alzheimer’s Disease through other mechanisms besides. (Ramirez et al, 2005; Eubanks et al, 2006) However, because of the pressure from the US government to publish (or fabricate) harms from marijuana, several widely publicised studies have been used to claim that marijuana causes brain damage. In every case, these studies either suggested nothing of the kind when properly interpreted, or were confounded enough to be worthless, and there is, at time of writing, absolutely no credible evidence of any form of brain damage from marijuana use in humans. In a classic example, one team of researchers forced rhesus monkeys to inhale large volumes of smoke, depriving them of oxygen in the process, and attributed their mental decline to marijuana rather than to oxygen deprivation. (Heath et al, 1980) Not surprisingly, subsequent studies failed to reproduce their finding. (Slikker et al, 1990; Paule et al 1992) Other studies have shown mental deficits and brain abnormalities in some young heavy marijuana smokers (Meier, 2012; Smith, 2013, Gilman et al 2014), but it’s highly likely that both the observed deficits and the marijuana use were caused by the same factor, rather than the deficits being caused by the marijuana use, as the deficits are only found in a minority of teenagers who use marijuana, and because there are a variety of sources of deficit which also predict marijuana use. (Tims, 2002) Post traumatic stress disorder (PTSD; often a product of child abuse) is a likely candidate, because it predicts both cognitive deficits (Moradi et al, 2013) as well as adolescent drug use (Maté, 2008; Dube, 2003), including heavy cannabis use. (Cornelius et al, 2009) For people with PTSD, marijuana may correct a chronically dysfunctional stress response (Heim et al, 2000) and make it easier to forget painful memories (Ganon-Elazer 2012; Patel et al, 2004; Marcisano et al, 2001). Regrettably, in none of the studies in which deficits were shown to be correlated with heavy early-onset marijuana use did researchers attempt to control for the enormous confound of past trauma. In light of the indications that marijuana is useful in the treatment of PTSD, to attribute the harms of trauma to a plant being used to alleviate it is particularly bothersome. There has also been a disturbing tendency in news coverage report all findings of alteration as “damage,” even where no deficits, and indeed some potential benefits, were shown. Given the ongoing drug war and propaganda efforts by various governments, the utmost skepticism is warranted in interpreting claims of marijuana-induced brain damage, none of which (to date) survive careful scrutiny grounded in the appropriate scientific literature. Given what we’ve learned about marijuana’s effects the dire claims seem ever more preposterous, especially given the many marijuana users who have distinguished themselves in scientific and artistic communities alike.

Rather than simply accusing hemp flowers of harming teenagers, a more sensible approach might be to listen to teenagers who are heavy marijuana users, to understand why they’re using it and what they’re getting out of it, bearing in mind that they may well be survivors of abuse, which agents of the legal, medical and educational systems may have directly participated in rather than alleviating. Stigma, theft of medicine, segregation and punishment are unacceptable responses to observed suffering.

In summary: marijuana rebalances and soothes a variety of neural processes and can protect against numerous potential sources of damage. No form of brain damage has been demonstrated to have resulted from its use.

Marijuana and Metabolism

The endocrine system consists of glands throughout the body which regulate everything from energy levels to metabolism to sex drive. CB1 receptors can be found throughout this system and influence the release of many hormones. One function of this system is to produce excitation in response to stress. This is necessary for survival, but when it gets out of hand it can be a major source of harm, especially in a fast paced modern economy where stress may be relentless. One effect of marijuana in the endocrine system seems to be to protect against this, by reducing susceptibility to stress-induced activation in the hypothalamus-pituitary-adrenal axis. (Patel et al, 2004) The details of how it does this, as well as all of its other diverse and complex effects throughout the endocrine system, however, remain murky, but are becoming clearer and will likely continue to do so over the coming years.

Marijuana’s ability to boost appetite is well known, and it is used to treat anorexia as well as diet problems resulting from other drug therapies, such as in patients with AIDS or cancer. Part of this effect on appetite may be because GABA suppression increases the rewarding stimulation from food; another part is its ability to block nausea, including the nausea induced by chemotherapy drugs. While there is a stereotype of getting high and then gorging on lots of delicious food, many of my respondents have informed me that they actually prefer to get high after their meal, finding it to improve their digestion and settle their stomach. It’s also common for “the munchies” to not set in until around 45 minutes after dosing, and it’s here that the endocrine effects, specifically in the pancreas, are explanatory. The pancreas secretes the pair of hormones glucagon and insulin to regulate blood sugar by signalling the liver to break down fat into sugar (glucagon) or to store sugar as fat (insulin). These hormones work as a pair to maintain homeostasis, and they stimulate the release of each other through a complex feedback mechanism. In 2008, it was determined that CB1 activation triggers glucagon release and that CB2 activation lowers glucose-dependent insulin release. (Bermudez-Silva et al, 2008) This helps to explain why marijuana users tend to eat more calories but do not gain any extra weight, have less obesity and lower rates of type II diabetes than non-users (Rodondi et al, 2006; Le Strat, 2011; Rajavashisth et al, 2012), and why some diabetics find that marijuana makes it easier to manage their blood sugar, as marijuana rebalances the relative levels of glucagon and insulin, although anti-inflammatory effects are also relevant. Type II diabetics (whose pancreas still functions) tend to have very high levels of insulin, but the liver is unable to use it, and so blood sugar stays high, and the pancreas damages itself by trying to continually produce more and more insulin, eventually leading to organ failure if the diabetes is unmanaged. By boosting glucagon release and lowering insulin resistance, marijuana may alleviate or prevent the progression of type II diabetes and restore balance to the system. The endocannabinoid system is also separately involved in fat storage (Cota, 2003; Osei-Hyiaman et al, 2005) (interestingly, THC is also fat soluble, and so it seems to be storing itself through this process, and is released back into the bloodstream during exercise (Wong et al, 2013)), and some studies have found marijuana users to have more fat in visceral tissue. (Hézode et al, 2008; Muniyappa, 2013) Cannabinoid antagonists have also been shown to reduce obesity, and not only do rodents given these drugs eat less, they also lose more weight than their reduced feeding can account for. (Pagotto et al, 2006) What exactly this means for users of marijuana (which contains both cannabinoid agonists and antagonists) remains unclear (more fat storage through one mechanism, and less fat storage through another), but the findings of lower rates of obesity and diabetes among marijuana users — despite correlations between marijuana use and a variety of life-style risk factors, including heavier eating — are very promising. Marijuana use is certainly not a major source of harm in this system, and may be of benefit in a variety of (very common) circumstances.

Cannabinoid signalling is also involved in many reproductive functions in both males and females, including in foetal development, and there are even CB receptors on sperm themselves. While the effects of marijuana on sperm and reproductive functions are not well understood, it appears that regular marijuana use may moderately reduce both menses and sperm production, and that therefore while many marijuana users can still conceive, it may be prudent for couples having difficulty conceiving to refrain from using marijuana. On the other hand, many find marijuana to improve their experience of sex, and it even allows for orgasm in some otherwise anorgasmic women. Not enough is known about its effects on pregnancy to be confident as to when it may be of benefit or harm to the foetus, (Pagotto et al, 2006) but it is commonly used to alleviate the nausea associated with morning sickness.

A stereotype of marijuana users is that they are lazy and that the drug makes them inactive. Traditional Hindu practices assume that this is the case, and discourage its use by home-owners, while allowing it to ascetics in the process of renouncing worldly attachments. (Morningstar, 1985) Some marijuana users certainly seem drawn to renunciation, and may show little interest in material advancement, especially when using heavily. Many others, however report that its effects are stimulating, and there have been many elite athletes who used marijuana, including martial arts legend Bruce Lee, basketball legend Kareem Abdul-Jabbar, Olympic gold medallists Michael Phelps and Ross Rebagliati, and more than half of the Oregon Ducks football team. Clearly, its effects are not disastrous to fitness or to the ability to exercise. Noted astronomer Carl Sagan and physicist Richard Feynman both used marijuana to stimulate visionary states and the flow of ideas; a great many other musicians, writers, scientists and artists have admitted to doing so as well. Many of the same have admitted at other times that marijuana can interfere with their performance or leave them distracted and tired. Its effects can be very inconsistent, and depend on the user’s metabolism, dosing strategy and the chemical composition of the strain being used.

In summary, marijuana rebalances energy levels, fat storage, reproductive functions, appetite and metabolism, and can correct for imbalances such as in type II diabetes, anorexia and a variety of stress-related disorders.

Marijuana and Mental Health

The use of marijuana is often seen in people who suffer from a wide variety of mental health problems (Wittchen et al 2007), for which it is often used to self-medicate, for better or for worse. It is known to sometimes relieve depression (Denson, 2006), emotional anxiety (Fusar-Poli et al, 2010) and intense stress (Ganon-Elazer, 2012). However, through its powerful and pervasive effects, it may well trigger an episode of any number of conditions, such as underlying psychoses. Some use marijuana precisely to provoke an inexplicable or extreme mental state, which may be interpreted as either spiritual or psychotic, or to produce greater and longer lasting states of elation and activity (mania), and many religious and shamanic groups have employed it to facilitate communication with spirits, to transport the user to heaven, to destroy karma, to deepen a trance, and much else besides. Marijuana surely is a drug favoured by lunatics and maniacs, not only to end their lunacy or mania but sometimes to provoke it. Does that make it dangerous to people who do not want these effects? Especially, perhaps if they despise the moon?

Much has been made of the association between cannabis use and schizophrenia. Schizophrenia (literally: broken mind) is a diagnostic category which consists of an unknown number of poorly understood mental types, characterised by positive symptoms such as delusions, hallucinations and disordered thinking, and negative symptoms such as not finding pleasure in anything and not being interested in talking to the other humans. Best estimates suggest that around 1 in 100 people will be exhibit schizophrenia at some point during their life, or 1.4 in 100 people who have ever used marijuana. (Zammit, 2007) This makes it a moderate risk factor, but less severe than being a first or second generation immigrant, having a father over the age of 55 at the time of birth, being raised in an urban area, or infection with Toxoplasma gondii, a parasite common among cat owners. (Bourque et al, 2011; Torrey et al, 2012) All of the above effects are dwarfed by familial predisposition, and Proal et al recently found that schizophrenic marijuana users are just as likely to have schizophrenic relatives as schizophrenics who do not use marijuana, suggesting that marijuana is not a cause of schizophrenia at all, but it’s just that schizophrenics are more likely than non-schizophrenics to use marijuana. (Proal et al, 2014) If we wish to reduce risk factors for schizophrenia, we may be better served by banning cats. Other research has suggested that “cannabis induced psychosis,” most characterised by paranoia, is at least partially a direct result of legitimate paranoia occasioned by the war on drugs, rather than the plant itself. (Hamilton et al 2014) There is some evidence that marijuana users with psychosis display more positive symptoms (such as paranoia) and less negative symptoms (such as anhedonia) (Zammit, 2008); this is especially interesting because mainstream psychiatry lacks an effective treatment for the negative symptoms, and it may be that many people are self medicating with marijuana for precisely this reason. Not only do people with psychosis use more marijuana than people without psychosis, but Giuffrida et al found that the body may be responding to schizophrenia by increasing endocannabinoid expression, and that this was associated with a reduction in symptom severity. (Giuffrida et al, 2004) Should we be surprised that some schizophrenics are drawn to a plant which mimics some of the body’s defence mechanisms against their symptoms? Lastly, while THC may occasionally produce psychotomimetic effects (that is, very stoned people may appear to be psychotic until they sober up), CBD appears to be anti-psychotic, (Zuardi et al, 2006) and so modulating the endocannabinoid system, for example with a high-CBD strain of marijuana, may be clinically useful in managing the positive symptoms of psychosis as well as the negative ones. In short, the evidence does not support the claim that using marijuana puts you at greater risk for harms from psychosis; perhaps even the opposite is the case, but more research is necessary. Indeed, prohibition is, itself, undeniably a far greater source of harm, for example by severely exacerbating such problems as racial oppression. (Fellner, 2000) Whether the same would be true for the prohibition of cats remains to be tested.

Among people living under the description of bipolar disorder, marijuana is the number one drug of choice, and those who use marijuana have less depression and more mania than those who do not. (Leweke, 2008) This is not surprising, given marijuana’s potential to increase positive symptoms and decrease negative ones. As there are strong cultural forces which value the creativity and charisma of mania and demonise depression, and because people living under the description of bipolar disorder typically identify with their hypomanic self rather than with a sober baseline, (Martin, 2007) marijuana is often used to improve mood and productivity, as well as to deal with stress in highly demanding contexts, with occasionally destabilising or dangerous consequences. To understand its effects in bipolar disorder, therefore, it is necessary to compare its users to others facing similar contexual pressures — for example, are university students (or entrepreneurs) more or less likely to “burn out” if they use marijuana? It’s also important to remember that marijuana has anti-depressant effects and is used to produce stimulation among people who do not have bipolar disorder, as well as by those who do. It’s not surprising that people with bipolar tendencies use it for the same reasons that others use it, even knowing it may increase the likelihood or intensity of a manic episode. Such people would do well to monitor their use (or to recruit friends and family to help monitor their use), and to consider refraining from using if they have a history of making dangerous decisions while manic.

In summary, marijuana rebalances mood, anxiety and attention in ways which may correct for or prevent certain forms of imbalance, but which may also upset a tenuous balance.

Marijuana in the Heart and Lungs

Much attention has been paid to the effects on the lungs of smoking marijuana, because of the severe and well known harms from smoking tobacco. Marijuana smoke contains many of the same carcinogens as tobacco smoke, and some in far higher concentrations (Moir et al, 2008), and so it was expected that it would be a cause of lung disease, as those chemicals are believed to cause cancer and emphysema in tobacco smokers. This however turns out not to be the case; marijuana smokers do not have elevated rates of lung cancer or emphysema, the two main debilitating effects of chronic tobacco smoking, and none of its long term effects on lung function are of clear clinical significance. (Tashkin, 2013) The analogy therefore can be rejected: marijuana is not dangerous in the ways that tobacco is dangerous. In fact, tobacco smokers who also smoke marijuana have lower rates of cancer and emphysema than do tobacco smokers who do not smoke marijuana, (Aldington, 2007) suggestive of the medicinal and/or protective effects of the flower vapours. Some marijuana smokers experience significant irritation and pain in the lungs which worsens over years of smoking, which may lead to a severe cough, and which is consistent with chronic bronchitis, but this often disappears if they switch from smoking to vaporising, even after decades of heavy smoking (vaporising is a method in which the plant matter is heated enough to convert the active compounds into a gaseous form, but below a temperature which would burn the plant matter, thereby avoiding the toxic byproducts of combustion). The lack of association between marijuana smoking and cancer, despite the well documented ample presence of known carcinogens, is strong evidence of its anti-carcinogenic effects; the chemicals it contains seem to compensate for the harmful effects of smoke inhalation (this is far from the only evidence of anti-carcinogenic effects (Ligresti et al, 2006), but it is suggestive as to their extent and efficacy in the wild). Marijuana, as a bronchodilator and an anti-inflammatory, has also been used in the treatment of asthma, and many asthmatic marijuana users have reported that their symptoms reduced during their period of use. (Williams, 1976)

Another major cause of death in tobacco smokers is heart disease, and, like the lung effects, there’s no evidence of elevated levels of coronary disease in marijuana smokers, despite the presence of various toxins in marijuana smoke. In the heart, the effects of marijuana are quite clear: decreased blood pressure, increased heart rate, often by as much as 30% , with CB1 and CB2 receptors as elsewhere working in opposite directions to control blood vessel dilation and other aspects of cardiovascular function. For most users this is not an appreciable concern, although it’s not uncommon for marijuana users to abort exercise because of strange feelings in their heart, or specifically because they feel that their heart is pumping too quickly or strongly. Some people with chronically low blood pressure find that they react badly to marijuana, and it is common for people under the acute influence of alcohol — which also lowers blood pressure — to become dizzy or nauseous if they proceed to smoke marijuana. Doing so may result in “the spins,” a very uncomfortable feeling where the world appears to be spinning and only spins faster if one closes one’s eyes. It is highly advisable therefore not to smoke marijuana while already drinking, especially if one is not a regular marijuana user and may be taken by surprise by the blood pressure crash. Smoking and then drinking does not appear to be nearly so dangerous, partly due to relative ease of dose control (you can sip your drink, but you cannot unsmoke a joint).

In people at elevated risk, a heart rate boost of 30% can trigger a heart attack. It has been estimated that marijuana smoking may increase risk for the next hour of myocardial infarction (heart attack) by a similar extent to having sex or exercising. Therefore, if your doctor has told you to abstain from sex due to the danger to your heart, you should consider also abstaining from marijuana. However, just because it’s more likely for a heart attack to take place during that window doesn’t mean it increases the risk of a heart attack happening at all. Indeed, a study of 3886 people who had already had at least one heart attack found no statistically significant association between marijuana use and death over an 18 year period (Frost et al, 2012), so there’s no great cause for worry. Instead, it seems to be the case that, if someone was going to have a heart attack anyway, it’s liable to happen within an hour of getting high, because of marijuana’s circulatory effects. CB1 activation has also been shown to worsen the damage from repurfusion (the shock caused by oxygen returning to cells temporarily deprived of it due to a heart attack), whereas CB2 protects against this damage, as well as against plaque instability and inflammation, such as in atherosclerosis (remember, THC activates both CB1 and CB2, so it both helps and hinders at the same time). CBD, meanwhile, has other non-cannabinoid receptor mediated cardioprotective effects. A high-CBD strain of marijuana may therefore be more beneficial for people at risk for heart attack than a high-THC strain. (Russo, 2006) For those concerned about heart and lung effects, vapourising or eating marijuana may be preferable to smoking it, as that will greatly reduce exposure to a variety of toxins. That said, the appropriate level of concern for smoking marijuana is probably more comparable to the dangers of toasting bread instead of eating it raw than it is to smoking tobacco, and many users will continue to consider this an acceptable trade-off for the convenience and ease of dose-control which come from smoking. (Montecucco, 2012)

In summary, marijuana rebalances dilation and contractility in the heart and lungs and may correct for or prevent such imbalances as usually result from smoke inhalation.

Marijuana in the Bones, Muscles and Joints

Unlike the many hard objects we encounter outside the body, our bones are constantly being broken down and remade. In young people there is typically more growth than break-down; this levels off and then reverses with age, and, as bone formation is driven by estrogen, post-menopausal women, women who have had their ovaries removed, or others who have very low estrogen, are at increased risk of bone loss and fracture. Cannabinoids regulate this system, stimulating bone formation via CB1 activation and slowing the rate of break-down via CB2 activation, and so marijuana may compensate for factors which could otherwise drive osteoporosis. (Scutt, 2007; Bab, 2009) As an anti-inflammatory and muscle relaxant, marijuana can also improve flexibility and provide relief for everything from soreness after exercise to certain types of arthritis. Indeed, endocannabinoid activation has been found to occur naturally following exertion, and is believed to allow for longer periods of exertion in what’s known as the “runner’s high.” (Sparling et al, 2003) I have observed marijuana use in the wild stimulating the user to begin exercising or facilitating continuation of exercise despite fatigue. I have also seen the opposite: half hearted attempts at exercise followed immediately by cessation. On the one hand, it may be that marijuana makes it easier to continue doing what one was already doing, such as either running or lying on the couch. On the other hand, it sometimes triggers a reversal, from low energy to high energy or vice versa. Like the endogenous runner’s high, using marijuana when fatigued may produce a “second wind” and allow the user to continue. The cardio-pulmonary dilation, discussed above, is also relevant, as it may improve oxygen availability during exercise.

In summary, marijuana rebalances bone growth, muscle fatigue and inflammation in ways which may correct for or prevent certain forms of imbalance, such as age related bone loss and pain after exercise.

Marijuana and the Immune System

THC has been experimentally shown to inhibit certain immune functions — in particular, lymphocyte activity — and to augment others, (Cabral, 2001) and marijuana also contains a variety of antimicrobial agents. (Nissen, et al, 2010) These immunological effects can protect against numerous auto-immune disorders, increase healing and down-tune immune responses. It is likely the case that marijuana can protect against certain kinds of infections under certain conditions, and that it can increase vulnerability to other infections under other conditions. Cannabis oil, especially applied topically, may be an effective treatment for acne, psoriasis (Wilkinson 2007), contact dermatitis (Karsak et al, 2007) as well as a variety of other inflammatory or allergic responses, and against certain infections because of its direct anti-microbial effects.

In summary, marijuana rebalances inflammation and other immune responses and may correct for or prevent certain forms of imbalance, such as autoimmune disorders.

Conclusion:

Marijuana has very complicated effects throughout the body. Many of these effects are often highly valued and sought for a wide variety of reasons. Some of these effects can in some situations can be undesirable, and THC by itself has been implicated in a variety of potential harms, including anxiety, psychosis-like mental effects, heart attack and immune suppression. It is necessary therefore to emphasise the importance of using cannabis flowers instead of isolated chemicals such as pure THC, because of the ways in which the other chemicals in the flowers compensate for, counteract, or amplify the effects of THC. (Russo, 2011) Whether marijuana will boost or inhibit each bodily system depends on the state of the body at the time of use, the chemical makeup of the marijuana being used, and the dosing strategy. Smoking one small hit one evening per week may well have the opposite effect of consuming cannabis oil throughout the day every day; the former may be primarily stimulating whereas the latter may lead to a generalised relaxation and slowing of metabolism. As either/both may be desired by each user, preferences in plant variety and dosage strategy vary accordingly. Some people react badly to the plant, whether for mental, cognitive, hormonal or ideological reasons, and some are allergic to it; for many others, it can be profoundly helpful, providing a way by which to take some conscious control over the regulation of homeostasis and to seek a balance which will work for us.
The above is my best understanding of what marijuana does. Although I have here leaned mostly upon scientific journal articles, which I have tried both to understand and to interpret, I am not in fact an advanced specialist in every relevant discipline — nor, I suspect, is anyone else; my academic background is as an ethnographer, and so I consider my primary responsibility to be towards the humans using the plant, for whatever reasons, and with whatever consequences, and I engage with the scientific literature in order to better understand and interpret the observations I have made in the wild, the many curious things I have been told in interviews both formal and informal. I am absolutely certain that there is very important information about the effects of this plant which I do not understand or which I have not yet seen. If you know of anything useful, or suspect that something I have said is inaccurate, incomplete or in other ways merits revision, I would be happy to hear your suggestions. May my best endeavours to faithfully convey my observations be useful to you.

 

 

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Posted in Cannabis and MND, Latest posts

10 facts about Cannabis and MND

Cannabis does not cure Motor Neurone Disease, but it alleviates discomfort, relieves symptoms, appears to slow progression – sometimes dramatically – and can allow sufferers to regain some motor function.

  1. Cannabis is proven to be an effective treatment for some of the symptoms of Motor Neurone Disease (MND), namely spasticity, loss of appetite, weight loss, insomnia, pain, anxiety and depression.
  2. Cannabis is calming  and therapeutic and has no side effects other than mild intoxication.
  3. The proven beneficial effects of cannabis include: analgesic, lowers blood pressure, increases brochodilation, reduces saliva, anti-inflammatory, appetite stimulant, muscle relaxant, anti-spasm, anti-spasticity, neuroprotectant and promotes brain growth.
  4. Because of anti-cannabis legislation and prejudice there is a dearth of research into its effects on MND and other disorders.
  5. However, pre-clinical findings, together with strong anecdotal evidence, suggest that cannabis slows progression of MND.
  6. There is currently no other treatment for MND which is a) as effective or b) as safe and risk free.
  7. In fact, although a number of recent clinical trials offer hope that new drugs to slow progression will become available in the next few years, Riluzole is the only other drug currently licensed for the treatment of MND, with limited benefits (extends life by 2 or 3 months) and no symptomatic relief.
  8. However, in the UK, medicinal cannabis is illegal except for the GW Pharma product Sativex, which is difficult to obtain and prohibitively expensive.
  9. Meanwhile street cannabis is cheap, is generally of reliable quality and is freely and readily available.
  10. The best method for using Cannabis for the treatment of MND appears to be cannabis oil, either taken orally as a tincture or inhaled using a vaporiser.
Posted in Cannabis and MND, Latest posts

Thoughts on the Labour Purge #2

I’m assuming the current Labour purge of Corbyn supporters will not succeed. If it does, the damage to the integrity and credibility of the party will be so severe I doubt it will ever recover.
Of course – perhaps that’s what the coup plotters want. After all, there are less than 200 of them, all of whom doubtless stand to profit personally from the destruction of the Labour left.
But if the purge fails, and Corbyn wins with the huge majority predicted, certain actions need to be taken immediately to protect the party from future anti-democratic attacks.
Here are a few ideas:-

1. The party’s “rule book” must be rewritten as a constitution, and vague ambiguities removed from its terminology so that, for example, there can be no question in the future of barring members on spurious, selective, unproven and undemocratic grounds.

2. The MPs who have been campaigning against the democratically elected leader of their party must be asked to make a choice – work with the leader, or face deselection.

3. An investigation needs to be undertaken into the power and money behind the right wing Labour pressure groups Progress and Saving Labour and any other similar organisations. Links to private finance corporations like Pfizer, private healthcare providers, and right wing organisations like the Henry Jackson society need to be exposed and outlawed as against the ethos and principles of a left wing socialist political party.

3. A code of practice needs to be adopted by the Labour Party to which MPs, activists and members suscribe, which prohibits lies, smears, slurs, dirty tricks, threats or abuse. Examples of breaching the code would include levelling unfounded accusations at party members – for example calling Corbyn supporters Nazi stormtroopers – and making allegations that the party leader is anti-women or anti-Semitic without offering any evidence to back up these insinuations.
Legitimate criticisms/protests would of course be welcomed, provided they put forward supporting evidence and always allowed a right to reply.
Breaking the code of practice could lead to a tribunal to decide if the person should be barred from the party, but safeguards such as the necessity of clear evidence, a right to representation, and the right of appeal would guard against abuse of tribunals and sanctions by future plotters seeking to oust their enemies.

These are just a few ideas to start with.
Let’s hope we can get the Labour Party back as a Democratic Party of the left. There really are just a couple of hundred individuals actively participating in the PLP/NEC shady behind-the-scenes machinations. They are few. We are many. Even with the entire mainstream media backing them, we stand a good chance to fight them off if we just stick to our principles and refuse to back down.

Remember – principles ARE power!
But power without principles is corruption.

Posted in Latest posts

Dr Liz Davies: ‘Goodbye’ Goddard though I never said ‘Hello’

This is another fantastic post by Dr. Liz Davies, the courageous campaigner for justice for  the victims of child sex abuse.

In 2014,  I wrote about the need for an Inquiry into Organised Child Abuse  , citing the need to re-examine various child murders and to search for missing dossiers of evidence,  but over 25 years I have mainly promoted the need for a national police led multi-agency child protection investigation team. Abusers are well organised nationally and internationally – but protectors have difficulty co-ordinating an investigation effectively when crimes are committed across local, national or international borders.

Although I was brought up Catholic and am now agnostic, I was well indoctrinated with the principles of faith, hope and charity. I have now lost faith in the so called ‘protective’ systems and given uphoping for anything different to happen however many reports I write or interviews I attend with the authorities, journalists, politicians and anyone else who seems to be listening. Only charityis left which to my mind, in its broadest sense, means assisting individual Islington survivors to help them battle with the impact of the abuse and to gain solidarity from connecting with their siblings, friends from care and other survivors now gaining in strength across the country. We know all we need to know about child sexual abuse. We know why abuse has continued over the decades and who profits from it. We know it is a remunerative industry which continues to thrive on the suffering of children and their families. We know that it cannot continue without colluders and facilitators procuring and delivering vulnerable children into the hands of  perpetrators.

‘Goodbye’ Goddard though I never said ‘Hello’

Posted in Latest posts

Michael Foster, Owen Smith and the demonisation of Corbyn

 

When the debate is lost, slander becomes the tool of the loser
Socrates

Since Jeremy Corbyn became Labour leader he has faced an onslaught of orchestrated attempts to depose him – disloyalty from his cabinet and the PLP, ridicule  and bullying by his own MPs at PMQs, smears of antisemitism and misogyny, accusations of condoning abuse, and legal and party challenges to his leadership.

The media have colluded in this onslaught with a barrage of overwhelmingly biased, selective and inaccurate reporting – as revealed by two recent studies at the London School of Economics and Goldsmiths College – of which Michael Foster’s Nazi slur is only the latest example.

Corbyn and his supporters are being subjected to a deliberate campaign of demonisation – a technique routinely used in political propaganda.
Demonisation, and ‘black’ propaganda, were used with great effect by the Nazis to scapegoat the Jews and to justify the holocaust.
It is therefore particularly dishonourable that Foster as a descendant of holocaust survivors should resort to such techniques and cynically exploit his Jewish heritage in order to score political points against the Corbyn movement within the Labour party.

To conflate Corbyn and his supporters with Nazi stormtroopers is a disgrace to the memory of the people who suffered under the Nazis. The holocaust is not something to be bandied around whenever one disagrees with an opponent. Foster’s comments, and the Mail’s accompanying photographs of Nazi rallies and brownshirts, are a shocking misappropriation of the moral high ground.
In my opinion, such a disrespectful trivialisation of the holocaust is as unethical and unprincipled as holocaust denial itself.

Having family who died in the camps is not a green light for baseless, slanderous allegations. I am Jewish. I lost family in the camps too, and it is exactly because of this that I care about respecting the truth – and the memory of the victims.
This is also why I care about social justice, and why I support Jeremy Corbyn.
Because he is honest and decent. He stands up for what he believes in and against injustice and inequality. He doesn’t smear and attack his rivals, despite severe provocation. And he sticks to his principles.

In contrast to Corbyn, Owen Smith doesn’t seem to actually hold firm principles. Prior to his selection as leadership candidate, Smith was pro austerity, anti welfare, pro private finance, pro private healthcare, a Blair man through and through.
Since his selection he declares himself to be a left-wing radical and unveils a raft of policies that mimic Corbyn’s.

If Smith is a man of principle, how can he shift his allegiances with the changing of the winds? And why does he stay silent over the abuse of democracy which his leadership challenge to Corbyn is very much a part of?

If he cares about abuse in the Labour party, why has he not condemned Foster’s deplorable comments, or the bullying to which Corbyn has been subjected by his fellow Labour MPs, or the smears and slurs on Corbyn and his followers?

I agree with the comment on today’s Victoria Derbyshire show about the “toxic” environment in the Labour Party.
Coups, dirty tricks, disinformation, smears, spurious legal and bureaucratic challenges – these are the tactics of bullies, abusers and oppressors, as Jews, of all people, should be hyperaware.
These are unfortunately also the tactics that the Labour establishment are using to try to remove the democratically elected party leader by any means possible, no matter how dirty or underhand.
Toxic indeed

 

Posted in Latest posts