CECDS (Clinical Endocannabinoid Deficiency Syndrome)

A Guide to CECDS (Clinical Endocannabinoid Deficiency Syndrome)

A Guide to CECDS (Clinical Endocannabinoid Deficiency Syndrome)

Imagine that you live in a country where medical and recreational marijuana has been legal for years. (I know, humor me for the moment.) This is your first checkup with your new doctor. He’s younger, bright and bushy-tailed, only fresh out of residency last year. But he knows more about the endocannabinoid (eCB) system in humans than any dozen of his elder peers. That’s because medical schools started teaching their fledglings about this remarkable organic structure several years earlier on the coat tails of the Nobel Prize laureates who painstakingly mapped out the mechanisms of disease from clinical endocannabinoid deficiencies in humans.

The endocannabinoid system is a Titan. In fact, it’s bigger than the biggest of all receptor systems found within the human body. This means that eCB ligands and their receptors are literally peppered across and among nearly every single “other” receptor arrangement known to exist in human biochemistry.

Once the “model” of disease was presented it took only another two years before teams the world over were able to replicate these prize findings. Proving to the domains of Man that dis-ease starts FIRST within the intricacies of endocannabinoid physiology.

Our fictitious doctor examines you, asks numerous questions, draws 3 tubes of your precious blood and sends it off to regions unknown within the campus orbit. After about an hour wait he comes back with promising results.

He carefully reads the computer printout and proclaims with a slight smile: “Mitch, you have a severe endocannabinoid deficiency. We need to start you out-today-on a special blend of medical cannabis. In no time you will start feeling much better. I have written for 12 refills. That should do it for the year. See me one month from now to assess how you are doing.”

Within days of starting your new medication you are sleeping better and the fibromyalgia-like symptoms are nearly gone. You notice that while your appetite has improved you are actually losing body fat-another advantage from the medication’s actions on metabolism.

The diagnosis was CECDS, the new “it” disease. The treatment?#

Phytocannabinoids from the plants Cannabis Sativa and Cannabis Indica either in a smokable form, metered inhaler, or in a tasty edible candy. Big Pharma also provides numerous synthetic cannabinoid agonists and antagonists but our imaginary doctor is a purist and believes as many do that whole-plant remedies work best.

OK, wake up everyone this has not yet happened, it’s only speculation. But it may very well turn out to be a premonition of things to come. Nobel prizes are certainly in store as the future will verify.

So let me ask you this: what if real bona fide cures for many diverse human illnesses were to be found in the sap of the marijuana plant? The search to relieve human suffering is as old as time, but some intrepid scientists think we are a step closer.

A handful of pioneering researchers are confident they have found the common ground through which many ailments manifest. Before long we may be seeing distinct prescriptions of cannabinoids being used to cure human illnesses. We could even imagine the Merck Manual adding the definition of a new disease phylum to their already burgeoning tome.


In 2003 an enterprising doctor formulated a unique and novel concept that sought to unite seemingly unrelated disorders to a deficiency of endocannabinoids. Back then proposing such an unusual theory was as inappropriate as using your soupspoon for desert. Nobody was thinking along those lines which makes it all the more fascinating.

After careful observation of the facts, Ethan B. Russo introduced the concept of a clinical endocannabinoid deficiency (CECD) underlying the pathophysiology of migraine, fibromyalgia, irritable bowel syndrome and other functional conditions alleviated by clinical cannabis.

Investigation at that time suggested that cannabinoids can block spinal, peripheral and gastrointestinal mechanisms that promote pain in headache, fibromyalgia, irritable bowel syndrome and muscle spasm.

Five years later Russo followed up with another salvo of information from the available databases. The results were promising:

Migraine has numerous relationships to endocannabinoid function. Anandamide (AEA) potentiates 5-HT1A and inhibits 5-HT2A receptors supporting therapeutic efficacy in acute and preventive migraine treatment. Cannabinoids also demonstrate dopamine-blocking and anti-inflammatory effects. AEA [ANANDAMIDE] is tonically active in the periaqueductal gray matter, a migraine generator. THC modulates glutamatergic neurotransmission via NMDA receptors. Fibromyalgia is now conceived as a central sensitization state with secondary hyperalgesia. Cannabinoids have similarly demonstrated the ability to block spinal, peripheral and gastrointestinal mechanisms that promote pain in headache, fibromyalgia, IBS and related disorders. The past and potential clinical utility of cannabis-based medicines in their treatment is discussed, as are further suggestions for experimental investigation of CECD via CSF examination and neuro-imaging.

Let me clarify some of this discussion for you. The 5HT1 and 5HT2 receptors are serotonin receptors. AEA, which is our body’s endogenous THC-like molecule, acts specifically to stimulate 5HT1 and block 5HT2 receptors in the brain while blocking dopamine receptors.

Guess what? This arrangement is precisely the same as the activity of the new “atypical” antipsychotics which block dopamine (D2) receptors and 5HT2 receptors. The implications in the treatment of mental-emotional disorders is clear. This provides another fertile area of research and reinforces the theory of CECDS.

Also from the above paragraph: AEA in sufficient quantities helps to mitigate migraine by acting on serotonergic pathways. Imitrex, the best seller for migraine treatment, acts in a similar fashion.

Finally, THC acts on NMDA receptors. NMDA receptors are for glutamate an excitatory neurotransmitter. Here we can appreciate the enormous potential of the cannabinoids in treating hyperactive brain regions involving the excitatory glutamate pathways by attenuating their activity.

Cannabinoids act to decrease glutaminergic and other pathway activities in brain regions prone to seizure activity. That’s why CBD is so powerful in treating seizure disorders.

Twelve years later the CECD concept has gained considerable ground and is now thought to be a viable theory on the pathogenesis of numerous clinical conditions refractory to modern medical interventions.


The 21st century has evolved with a tangle of “new” disorders causing human misery and disease. These new diseases have names that we know all too well. Many of these are thought to have an autoimmune component such as fibromyalgia and Crohn’s disease, but investigators are left scratching their collective heads on what to do about them. So far little in the way of medications has worked; the ones that do perform often have serious side effects that can complicate therapeutic decisions.

Perhaps they have been wrong all along and the primary problem is NOT autoimmunity but a deficiency of endocannabinoids manifesting as an autoimmune-like disease. That’s precisely what several investigators hope to prove someday.

Not to be outdone in 2014 Smith and Wagner performed a new comprehensive literature review from the National Library of Medicine among other sources and concluded that;

…underlying endocannabinoid deficiencies indeed play a role in migraine, fibromyalgia, irritable bowel syndrome and a growing list of other medical conditions. Clinical experience is bearing this out. Further research and especially, clinical trials will further demonstrate the usefulness of medical cannabis. As legal barriers fall and scientific bias fades this will become more apparent.


Indeed the legal barriers are legion among those who study cannabis. Still in 2015 as Dr Mechoulam, the father of cannabis research, reminds us there is virtually a freeze on the clinical study of cannabis in humans. Plenty in mice and rats but not too much on the forefront for humans except in Israel. It is however slowly changing. Moving at about the speed of glacier.

Meanwhile Storr et al was making progress on the role of the endocannabinoids and irritable bowel syndrome (IBS). In his recent publication entitled, [t]he role of the endocannabinoid system in the pathophysiology and treatment of irritable bowel syndrome, they had this to say:

We now know that the endocannabinoid system is involved in the regulation of numerous gastrointestinal functions including motility, sensation and secretion under both physiological and pathophysiological conditions. They showed that:

Activation of cannabinoid (CB) (1) and CB (2) receptors under various circumstances reduces motility, limits secretion and decreases hypersensitivity in the gut. Drugs that alter the levels of endocannabinoids in the gut also reduce motility and attenuate inflammation. In this review, we discuss the role of the endocannabinoid system in gastrointestinal physiology. We go on to consider the involvement of the endocannabinoid system in the context of symptoms associated with IBS and a possible role of this system in the pathophysiology and treatment of IBS.[ref]Neurogastroenterol Motil. 2008 Aug;20(8):857-68.[/ref]


Also in 2014 McPartland et al examined the literature and performed the most recent systematic review of clinical interventions that enhance the eCB system–ways to upregulate cannabinoid receptors, increase ligand (neurotransmitter) synthesis, or inhibit ligand degradation.

The “classic” endocannabinoid (eCB) system includes the cannabinoid receptors CB1 and CB2, the eCB ligands anandamide (AEA) and 2-arachidonoylglycerol (2-AG), and their metabolic enzymes. The eCB system’s salient homeostatic roles have been summarized as, “eat, sleep, relax, forget, and protect”.[ref]Biochimica et Biophysica Acta – Lipids and Lipid Metabolism 1392: 153–175[/ref]

Here McPartland schools us on the eCB system and its remarkable involvement in nearly all human activity and physiology. It modulates embryological development, neural plasticity, neuroprotection, immunity and inflammation, apoptosis and carcinogenesis, pain and emotional memory, and most importantly from the viewpoint of recent drug development: hunger, feeding, and metabolism.

Obese individuals seem to display an increased eCB tone, driving CB1 activation in a chronic, feed-forward dysfunction.[ref]Di Marzo V, Piscitelli F, Mechoulam R (2011) Cannabinoids and endocannabinoids in metabolic disorders with focus on diabetes. Handbook of Experimental Pharmacology 75–104[/ref] An antagonist or inverse agonist of CB1 called Rimonabant was approved for the treatment of obesity. It was subsequently withdrawn from the market due to adverse effects.[ref]Pharmacology Biochemistry and Behavior 95: 375–382[/ref]

Other diseases are associated with suboptimal functioning of the eCB system. Russo [see above] proposed that migraine, fibromyalgia, irritable bowel syndrome, and related conditions represent CEDS, “clinical endocannabinoid deficiency syndromes.” Fride [Neuroendocrinology Letters 25: 24–30] speculated that a dysfunctional eCB system in infants contributes to “failure to thrive” syndrome. Hill and Gorzalka [Behav Pharmacol 16: 333–352] hypothesized that deficient eCB signaling could be involved in the pathogenesis of depressive illnesses. In human studies, eCB system deficiencies have been implicated in uncompensated schizophrenia [Neuropsychopharmacology 29: 2108–2114] migraine [Neuropsychopharmacology 32: 1384–1390], multiple sclerosis [Journal of Neurology Neurosurgery and Psychiatry 79: 1224–1229] Huntington’s [Journal of Chemical Neuroanatomy 37: 266–281, Journal of Nuclear Medicine 51: 1413–1417], uncompensated Parkinson’s [Movement Disorders 25: 920–924] irritable bowel syndrome [Neurogastroenterology and Motility 24], uncompensated anorexia [Biological Psychiatry 70: 777–784], and chronic motion sickness [PLoS ONE 5].[ref]PLoS One. 2014; 9(3): e89566.[/ref]


The goal is to increase activity of the eCB system. Another way to say this is to upregulate the structure. Upregulation in this context is to stimulate the system to make more of its neurotransmitters AEA and 2-AG, to proliferate receptors CB1 and CB2, or to inhibit the enzymes responsible for degradation of endocannabinoids.

McPartland’s search covered hundreds of animal and in vitro (test tube) studies and 36 human trials. What his team found was completely unexpected. Many of our “bread and butter” medicines act through the eCB system. Furthermore, alternative practices like acupuncture also implicate the eCB system as do our recreational substances. For example:

Evidence indicates that several classes of pharmaceuticals upregulate the eCB system, including analgesics (acetaminophen, non-steroidal anti-inflammatory drugs, opioids, glucocorticoids), antidepressants, antipsychotics, anxiolytics, and anticonvulsants. Clinical interventions characterized as “complementary and alternative medicine” also upregulate the eCB system: massage and manipulation, acupuncture, dietary supplements, and herbal medicines. Lifestyle modification (diet, weight control, exercise, and the use of psychoactive substances–alcohol, tobacco, coffee, cannabis) also modulate the eCB system.

They concluded:

Few clinical trials have assessed interventions that upregulate the eCB system. Many preclinical studies point to other potential approaches; human trials are needed to explore these promising interventions.

Folks, we are witnessing a possible revolution in human biochemistry and medicine; it appears that the eCB system underlies many disease states. Furthermore, our familiar medicines do not work the way we thought they did. Rather, they in some unusual and unknown way, tweak the eCB matrix to ameliorate dysfunction and cure disease.

If anything were Nobel Prize material this surely is.

In a separate publication I will detail some of our common household OTC and prescription drugs that markedly affect the eCB system.

One special word of caution. The drugs I will be referring to upregulate the eCB system when used ACUTELY. The chronic use of these substances produces the opposite effect: the system downregulates as a response to these drugs. Downregulation may turn out to be a setup for disease. It may even help explain the side effects of some drugs when chronically used.

Cannabis Puts Crohn's Patients Into Remission

Cannabis Puts Crohn’s Patients Into Remission

A fascinating new study has emerged which shows an unexpectedly favorable response to cannabis in those that suffer from one of the most common disorders seen in the gastroenterologist’s office – Crohn’s disease. Crohn’s disease (CD) and ulcerative colitis (UC) are flip sides of the same coin. They fall under the broader heading of inflammatory bowel disease or IBD.


From the Mayo Clinic:

Inflammatory bowel disease (IBD) involves chronic inflammation of all or part of your digestive tract. IBD primarily includes ulcerative colitis and Crohn’s disease. Both usually involve severe diarrhea, pain, fatigue and weight loss. IBD can be debilitating and sometimes leads to life-threatening complications.

Ulcerative colitis is an inflammatory bowel disease that causes long-lasting inflammation and sores (ulcers) in the innermost lining of your large intestine (colon) and rectum.

Crohn’s disease is an IBD that cause inflammation of the lining of your digestive tract. In Crohn’s disease, inflammation often spreads deep into affected tissues. The inflammation can involve different areas of the digestive tract — the large intestine, small intestine or both.

The exact cause of inflammatory bowel disease remains unknown. Previously, diet and stress were suspected, but now doctors know that these factors may aggravate but don’t cause IBD.
One possible cause is an immune system malfunction. When your immune system tries to fight off an invading virus or bacterium, an abnormal immune response causes the immune system to attack the cells in the digestive tract, too. Heredity also seems to play a role in that IBD is more common in people who have family members with the disease. However, most people with IBD don’t have this family history.

I have treated patients with Crohn’s disease and UC using an integrative approach, combining western medicine with Chinese herbs and acupuncture. These tactics helped immeasurably but they fell short of inducing a remission. Patients were usually left taking some form of prescription drug and often times were steroid dependent. Meaning they could never stop taking for example, prednisone. If they were to stop, symptoms would escalate very quickly requiring the drug again to quell the inevitable pain.

Medical Management

From a purely western medical slant, treating patients often involves using several drugs at the same time. The safest and least harmful tactic is to use the less potent preparations first such as the aminosalicylates which are similar in action to aspirin. These drugs are taken orally and act both locally on bowel tissue and systemically. They carry little risk in the long-term management of IBD.

Next are the powerful corticosteroid preparations like prednisone. These have dozens of injurious side effects like massive weight gain, weak bones, high blood sugars, poor wound healing, and many others. If at all possible I avoided prescribing drugs of this class for extended periods of time since the side effects were disastrous. However, sometimes its use was unavoidable.

The next course is much more potent, and they carry numerous toxic side effects. Drugs like Remicade fall into this category. Patients who take Remicade report excellent symptom control but it comes with a huge price tag. These drugs block certain key immune responses which can re-activate latent infections such as hepatitis B or TB, and even generate cancers such as lymphoma after prolonged use. They can also lead to an overwhelming infection, called sepsis, which can be fatal.

Lastly, surgery is indicated for refractory cases. For UC this sometimes means removal of your entire colon and an ileoanal anastomosis: connecting your distal small bowel to the back door so to speak. Or a colostomy bag might be indicated in other cases. At least one surgery is expected for Crohn’s disease sufferers on average. This may not be as extensive as UC surgery, and it only involves the small bowel. Therefore a colostomy is not needed. However, disease frequently springs up months or years later right at the surgical borders of the bowel anastomosis (connection).

Alternatives: Cannabis and LDN

Given these measures it comes as no surprise that the IBD community would embrace a novel drug that had no toxic side effects, had minimal adverse drug effects, and produced a remission in many patients.

Did I just describe a miracle drug? Enter cannabis and LDN or low dose naltrexone. It’s beyond the scope of this article to detail the powerful healing effects of LDN, a safe alternative to more toxic pharmaceuticals. Simply search LDN and see for yourself. I have seen this medication work wonders. Sadly many gastroenterologists dismiss its curative effects as internet tripe. That’s sad and completely inaccurate.

If you have IBD find someone who will prescribe it for you. Give it a fair trial regardless of what your GI doc tells you. You can thank me later.

Now, in spite of the dismissal of LDN we have a new contender for inducing remission in IBD patients. That candidate is cannabis.

A remarkable study was published recently (in 2013) from an Israeli team that clearly showed cannabis smoking not only suppressed many Crohn’s symptoms but it induced remission in 45% of the treatment group of patients. Even more shocking was that these patients were selected because they were treatment failures-no modern drugs were helping them.

From Tel Aviv University, Kfar Saba, Israel, Cannabis induces a clinical response in patients with Crohn’s disease: a prospective placebo-controlled study by Naftali et al:

In their introduction section the author reminds us of the vacancy of controlled clinical trials using cannabis in treating IBD. They undertook a prospective trial to determine whether cannabis can induce remission in patients with Crohn’s disease.

In the purpose section of their study application under ClinicalTrials.gov they had this to say:

…there are no major immune events which do not involve the endocannabinoid system. Cannabinoids shift the balance of pro-inflammatory cytokines and anti-inflammatory cytokines towards the T-helper cell type 2 profiles (Th2 phenotype), and suppress cell-mediated immunity whereas humoral immunity may be enhanced. They are therefore used for various inflammatory conditions including rheumatoid arthritis and asthma. In a mouse model of colitis cannabinoids were found to ameliorate inflammation and there are many anecdotal reports about the effect of cannabis in inflammatory bowel disease.

In other words, marijuana acts by suppressing runaway inflammation which is responsible for the numerous symptoms of IBD.

Complete remission…was achieved by 5 of 11 subjects in the cannabis group (45%) and 1 of 10 in the placebo group (10%; P = .43). A clinical response…was observed in 10 of 11 subjects in the cannabis group… and 4 of 10 in the placebo group. Three patients in the cannabis group were weaned from steroid dependency. Subjects receiving cannabis reported improved appetite and sleep, with no significant side effects.
…a short course (8 weeks) of THC-rich cannabis produced significant clinical, steroid-free benefits to 10 of 11 patients with active Crohn’s disease, compared with placebo, without side effects.[ref]Clin Gastroenterol Hepatol. 2013 Oct;11(10):1276-1280.e1[/ref]

The authors comment that their end point of “remission free” was NOT achieved yet clearly almost half DID achieve that goal!
Based on my own clinical experience with IBD this trial really rocked my world. What it suggests is nothing short of astonishing: smoking marijuana twice daily, in the form of cigarettes containing 115 mg of Δ9-tetrahydrocannabinol, gives the average Crohn’s patient a 50/50 chance of never having to deal again with the “stomachache that never goes away.”

Three Points

Three things need mentioning. One is that the research hails from Israel, the only nation living in the twenty-first century regarding marijuana research. We would not have this information were it not for the courage of the Israelis to open up their science benches to clinical study of cannabis in human disease.

Secondly, this trial was only 8 weeks long, and very small involving only 21 patients, 11 of which were in the experimental group. We will need a larger followup trial aimed at reproducing these results. But if subsequent studies conclude anything close to the findings in the above trial we will have much to celebrate.

Thirdly, these patients were all traditional medication failures. This suggests that cannabis is even more powerful than the shopping list of current pharmaceuticals.

Here’s a few suggestions. A trial involving oral cannabis capsules to directly bathe the GI tract in cannabinoids in the same way that we use the aminosalicylates. Cannabis enemas for UC could also be tried in the same way patients receive prednisone enemas now. Add to that LDN therapy to help modulate the defective immune system that these patients have. I predict that these measures would outperform current drug therapy and significantly alter disease outcomes.

Do Cannabis Smokers Develop Lung Cancer? - A Comprehensive Research Report

Do Cannabis Smokers Develop Lung Cancer? – A Comprehensive Research Report

The question everyone should be asking, “Does cannabis smoking give you lung cancer” is perhaps the most important question you could ask.

In this series I’ve devoted considerable time and effort to give you a realistic picture of the true pulmonary risks associated with smoking marijuana. It is the most comprehensive article to date. I have analyzed much of the research on this subject covering data from nearly five decades.

You, dear reader, need to know exactly where you stand as far as your risk is concerned if you currently smoke marijuana because lung cancer is deadly. You do not want to increase your peril if at all possible.

Let’s face it, some in the research community are already convinced that cannabis smoking is as bad as or worse than cigarette smoking. But is this an accurate portrayal?

There is also a stubborn, yet significant, element of cognitive dissonance among many investigators. That is, their inability to accept (research) evidence that contradicts their firmly held beliefs. In this case it’s the belief that marijuana smoke is toxic. That it significantly increases the risk for bullous disease of the lungs, emphysema, chronic bronchitis, lung cancer, decreased lung function, and increased risk for pneumonias. Let’s see if there’s any truth to these accusations.


For decades investigators have tried to prove what they intuitively suspected to be true. That chronic use of cannabis increases the dangers for lung cancer, and other smoke related pathologies such as COPD, and pneumonia in a similar fashion as tobacco smoking.

Here’s their reasoning: the chronic use of tobacco has dozens of catastrophic, systemic effects. Nearly every organ system is adversely affected by tobacco. But in this discussion we will limit it to chronic obstructive pulmonary disease (COPD) and lung cancer with a brief mention of some others. COPD (emphysema and chronic bronchitis), and lung cancer are two of the most common and serious consequences of tobacco smoking. Smoking tobacco is the main cause of lung cancer and emphysema in the world. In fact, if you don’t smoke tobacco you eliminate two major disease risks altogether.


The theory tells us that tobacco and cannabis combustion by-products are basically the same, but because of the way cannabis is smoked it makes the risks greater. Therefore, smoking weed should give you lung cancer and COPD if you smoke enough-say at least one joint a day for 20-30 years. One joint per day times 30 years equals a 30 joint-year history which is considered heavy usage. Moderate usage is under that peak, say a 20 joint-year history.

Clinicians feel that cannabis smoke is worse than cigarette smoke because cannabis consumers take bigger tokes, hold the smoke longer in the lungs, smoke the joint to its oily conclusion, and generally do not use a cigarette filter for removing some of the gross accumulation of combustion tars.

Here’s the scary part. Back in the 1990’s studies were accumulating that sent some bad reverberations through the research community. Much of the information looked dreadful for cannabis smokers. The data predicted a major role for cannabis smoking and the development of lung cancer. It was not a good decade for cannabis consumers. Much of that data was derived from Dr Tashkin’s work spanning over four decades.

Compelling information such as these (below) were common. From the publication Effects of marijuana on the lung and its immune defenses by Donald P. Tashkin, M.D. UCLA School of Medicine. Secretary’s Youth Substance Abuse Prevention Initiative: Resource Papers, March 1997, Center for Substance Abuse Prevention, pp. 33-51:

– The tar phase of marijuana smoke, as already noted, contains many of the same carcinogenic compounds contained in tobacco smoke, induding (sic) nitrosamines, reactive aldehydes, and up to a 50 percent higher concentration of carcinogenic polycydic (sic) hydrocarbons, induding (sic) benz[a]pyrene (Hoffmann et al. 1975). Benz[a]pyrene, which has recently been shown to promote mutations in the p53 oncogene (Denissenko et al. 1996), is believed to play an important role in human cancer.

– One marijuana cigarette was shown by Wu and colleagues (1988) to deposit four times as much tar in the lung as a single filtered tobacco cigarette of approximately the same weight. The higher content of carcinogenic polycyclic hydrocarbons in marijuana tar and the greater deposition of marijuana tar in the lung act together to amplify exposure of the marijuana smoker to the carcinogens in the tar phase.

Together with numerous other findings Dr Tashkin finished with this:

– The evidence for the harmful consequences of marijuana smoking is preliminary and requires long-term study. In the interim, prudent advice must serve where substantial clinical evidence is lacking. Habitual marijuana use, as often as one joint per day, may result in serious pulmonary consequences. In the short term, breathing may be restricted, coughing may be increased, and resistance may be lowered to opportunistic infections of the lungs such as pneumonia. Respiratory cancer is a likely result in the long term. Heavier use of marijuana is likely to have more potent, adverse health consequences.

That was in 1997. In a more recent publication in 2005[ref]Tashkin DP. Smoked marijuana as a cause of lung injury. Monaldi Arch Chest Dis. 2005 Jun;63(2):93-100.[/ref] Tashkin notes several recent findings that shed more light on this controversial topic. He states that THC itself is a bronchodilator which in theory would be good for an asthmatic. Chronic pot smoking produces a small orbit of long-term pulmonary consequences, including chronic cough with sputum production; histopathologic evidence of widespread airway inflammation and injury; and immunohistochemical evidence of dysregulated growth of respiratory epithelial cells that may be precursors to lung cancer.

He continues that the THC content in cannabis could contribute to some of these injurious changes through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis (programmed cell death). They also noted that the data is limited and inconsistent, there is no solid evidence that marijuana smoking may lead to chronic obstructive pulmonary disease or respiratory cancer.

Furthermore, Tashkin asserts that habitual use of marijuana is also associated with abnormalities in the structure and function of alveolar macrophages, including impairment in microbial phagocytosis (literally “to eat”) and killing that is associated with defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing to pulmonary infection (pneumonia).

Translated this means that chronic cannabis smoke acts as an irritant which over time can cause pre-cancerous changes in the cell architecture of the lungs. It also causes a certain amount of dysfunction of the pulmonary immune system, namely affecting the macrophages, that MAY increase risk for pneumonia. Macrophages, or “big eaters,” consume cellular debris and bacteria and anything else that needs removal. Macrophages are a major part of “pus” in a bacterial infection.

Fast forward to a 2014 review article by Denyse Lutchmansingh entitled, Legalizing Cannabis: A physician’s primer on the pulmonary effects of marijuana summarizes what we knew up to 2014 regarding marijuana’s pulmonary harms.

– Habitual smoking of marijuana is associated with multiple respiratory symptoms such as cough, sputum production, and wheezing .These symptoms are not significantly different from those exhibited by tobacco smokers. Furthermore, endobronchial biopsies of habitual smokers of marijuana and /or tobacco have shown that both marijuana and cigarette smoking cause significant bronchial mucosal histopathology and that these effects are additive. Although marijuana smokers have minimal changes in pulmonary function studies as compared to tobacco smokers, they may develop bullous disease and spontaneous pneumothoraces.[ref]Curr Respir Care Rep. 2014; 3(4): 200–205. Published online 2014 Oct 12.[/ref]

From the above 2 articles, and dozens more like them, we see that chronic marijuana smoking can cause some of the same cellular changes within the bronchial tree that are precursors to cancer or COPD (emphysema and chronic bronchitis). Also a new finding that’s already assumed to be causative: bullous disease of the lung. But we don’t see the significant damage to alveoli that tobacco smoking causes decades later which can lead to emphysema. Nor do we see the noted histopathologic changes transform into actual lung cancer. More on that in a moment.


The literature notes an association of pneumothorax (from bullous disease-see below) with chronic marijuana use. A pneumothorax is a hole in the lung with air in the chest, which can lead to a deflated portion of lung with symptoms such as breathlessness.

Tall, lanky, young males who smoke cigarettes are at the greatest risk for pneumothorax-especially if they like to scream at a football game or a similar event.

It’s nothing unique to pot smoking. The risk is also very small for pot smokers. The literature has only a handful of cases (ten total) of pneumothorax with concomitant cannabis use. And again they are only observations that show cannabis was associated with pneumothorax. Lastly, cannabis smokers appear to be at greater risk for bullous disease which is the development of large bubbles of air in the lung. This can lead to a pneumothorax. This is a hallmark for COPD but it is an association only, no proof of causation exists with pot smoking.

In addition to the associations listed above an interesting French publication from 2014 claims that:

– Cellular, tissue, animal and human studies, and also epidemiological studies, show that marijuana smoke is a risk factor for lung cancer. Cannabis exposure doubles the risk of developing lung cancer. This should encourage clinicians to identify cannabis use and to offer patients support in quitting.[ref]Underner M. Rev Mal Respir. 2014 Jun;31(6):488-98[/ref]

Here it appears that we have evidence showing that marijuana “causes” lung cancer, it doubles the risk. We have two camps, one is more conservative and the other like the above is more apt to conclude that cannabis “causes” lung cancer.

In response to the above article I can only say that the author, like many who accept the cannabis research baton, are using artistic license with the information. In other words they tend to exaggerate the harms or sometimes fabricate the harms. We’ll discuss these exaggerated claims and the reasoning behind them later.

Does pot smoking really double the risk of lung cancer? Is marijuana smoking a risk factor for lung cancer? No and no. No proof exists so far that pot increases the risk for lung cancer as you shall see.



Do the cellular changes documented above in the lungs of pot smokers translate into significant morbidity (disease)? Clinical and epidemiological data on chronic marijuana users provides a solid contradiction. Based on the pathologic changes seen microscopically we would expect to see many new cancers emerge from the din but we don’t. Where are all the lung cancer cases researchers predicted from the millions of new cannabis users who emerged since the 1990s when marijuana was finally accepted as a safe recreational drug?

Indeed where are they? It’s been 25 years starting with the somewhat arbitrary date of 1990. I picked 1990 since many investigators use this date as a marker for when pot smoking accelerated among populations all over the world. Twenty-five years later we should start seeing cancers if marijuana had the same toxicity profile as tobacco. But we don’t, in spite of the French publication mentioned in part one.

In their attempts to prove that pot causes lung cancer investigators kept hitting contradictions. The science (and observations) just didn’t add up to weed being a powerful carcinogen or cancer promoter. Back when cigarettes were suspected of causing lung cancer the epidemiologic data were overwhelmingly positive showing a clear and significant association between tobacco users and the development of lung cancer. We simply cannot find strong associations with weed and lung cancer in the same way.

For the last several decades scientists have made numerous attempts to show such an association but have come up short. Some investigators have accepted this fact and are now trying to unravel the mystery of why marijuana smokers do not run the same risks for lung cancer as that of cigarette smokers. Others who view marijuana with a jaundiced eye speedily conclude that pot smoking causes lung cancer. Same data, different conclusions.

It’s very odd actually. They both (tobacco and marijuana) start out with similar histopathologic cell changes in the lungs from exposure to similar “tars” of combustion. Then one (the tobacco user) goes on to develop lung cancer or COPD. However, the fate for the other user (the cannabis connoisseur) is completely different. The sum total of the evidence since the 1970s shows that the destructive pathologic processes in pot smokers never accelerates into lung cancer, COPD or even pneumonias. That’s what the data show. Unbiased observers agree on this point.

So something else must be going on that “prevents” the further development of cancer after metaplastic changes occur in bronchial tissues that are irritated from cannabis combustion by-products. Luckily for the millions of pot connoisseurs throughout the planet they are simultaneously ingesting a prospectus of potent anti-inflammatory molecules with each tooth-yellowing, tar hit. Those tiny molecules are called cannabinoids and they cure disease, not promote it.

You see the devil is in the details. This is precisely where tobacco and cannabis depart and head their separate ways. To put it differently nicotine and tobacco are toxic, cannabis and THC are not. In fact, some of the cannabinoids are also potent free radical mops and anti-inflammatory substances. These would help to inhibit the formation of cancers and other potentially serious disorders. In fact, we can agree that tobacco and cannabis smoke really are not the same at all.


Incidentally, the infamous Jack Herer (breeder of the Cannabis Cup winning varietal Jack Herer) relates his discussions with Dr Tashkin at UCLA, when he was writing his book, “The Emperor Wears No Clothes.” Herer:

I told Dr. Tashkin from 1981 to 1997 that no one gets lung cancer or any other type of cancer from marijuana because Dr. Vera Ruben [see below] and Dr. Todd Mikuriya had already each separately proven it. I had been doing research for my book since the early 1970s.

Both he and Tashkin completely disagreed with each other. Herer insisted that he (Tashkin) would never find proof that marijuana causes any cancer much less lung cancer. Jack may have been right all along as we will see. He finished with this amusing quote:

“If you want to live longer, smoke more pot (Jack Herer July 4, 2006)”

Maybe that should read EAT more pot and rid yourself of combustion by-products altogether.

Well, as they say that was Zen, this is Dao. Much has changed over the decades. The most recent findings from several large epidemiologic studies covering decades of pot smoking provide an anxiety-relieving golden parachute for chronic pot users. It’s good news for marijuana smokers everywhere.


Remember Quicksilver Messenger Service’s 1971 hit song, Fresh Air? You remember it don’t you? Back when songs weren’t sexed up by corporate suits, it goes like this: “[h]ave another hit of fresh air,” with much oohing before the lyrics. Well, they could have been talking about pot smoke since it looks like the miasma from marijuana is nearly as safe as pine-swept, mountain air. Yes, it sounds a little over-the-top but the latest, and best quality research has exonerated weed as a cause of smoke related (cigarette-type) pathologies. From Tashkin (2013):

– Although marijuana smoke contains a number of carcinogens and cocarcinogens, findings from a limited number of well-designed epidemiological studies do not suggest an increased risk for the development of either lung or upper airway cancer from light or moderate use, although evidence is mixed concerning possible carcinogenic risks of heavy, long-term use… In summary, the accumulated weight of evidence implies far lower risks for pulmonary complications of even regular heavy use of marijuana compared with the grave pulmonary consequences of tobacco.[ref]Tashkin DP1 Effects of marijuana smoking on the lung. Ann Am Thorac Soc. 2013 Jun;10(3):239-47. [/ref]

Meanwhile, we already have powerful epidemiologic studies on ganja smoking Rastafarians in Jamaica published by Dr Vera Rubin over 40 years ago.

– Another foreign investigation (Ruben et al., 1972) conducted in Jamaica (under contract for the National Institute of Mental Health) studied chronic cannabis users and matched nonuser controls. Preliminary findings have shown little evidence of significant differences between the two groups in the extensive anthropological, medical, psychiatric and psychological investigations.[ref](http://druglibrary.eu/library/reports/nc/nc1h_3.htm) 08/08/2015[/ref]

Honestly, if you were going to TRY to find a significant association between cannabis consumption and lung cancer, you could not do better than to study Jamaica’s Rastafarians. As a cultural phenomenon they are nearly weaned on cannabis from day one. As adults they smoke marijuana all day long every day as a means to work more efficiently, relieve heat illness and as part of their religious observations. If they are not at increased risk for lung cancer I think we can safely assume the average pudgy, joint-toking businessman isn’t either.


This just in: chronic marijuana smokers run a negative risk for lung cancer and COPD says prominent UCLA pulmonologist in 2015. From an interview with Dr. Donald Tashkin, professor emeritus of medicine at UCLA, for the LA Weekly:

– Through my studies, we failed to find any positive association. Instead, the association would be negative, between lung cancer and the use of marijuana. The likelihood is, that despite the fact that marijuana smoke contains carcinogens, we don’t see the same heightened risks of cancers that we see in tobacco.[ref]http://www.laweekly.com/music/ucla-professor-finds-marijuana-is-safer-to-smoke-than-tobacco-5658317[/ref]

One of the most significant diseases to emerge from cigarette smoking besides lung cancer is emphysema and chronic bronchitis; both are forms of chronic obstructive pulmonary disease (COPD). Dr Tashkin:

– The other major impact of tobacco smoking on the lungs is the association between smoking tobacco and the development of destructive pulmonary disease [such as COPD], the third cause of death in America.

…smoking marijuana, unlike smoking tobacco, does not cause chronic obstructive pulmonary disease (COPD). Reasoning for this may be that marijuana is a potent anti-inflammatory and suppressive. But COPD is activated by tobacco smoke and other toxic substances.

The National Institute on Drug Abuse (NIDA) supported Tashkin’s cannabis-related research over the decades. Tashkin initially set out to prove that pot smokers are at a significantly increased risk for lung cancer. They readily gave him a grant to conduct a large, population-based, case-controlled study that would substantiate the claim that heavy, long-term marijuana use increases the risk of lung and upper-airway cancers. What Tashkin and his colleagues found, however, sent ripples through the agenda-driven corridors of this institute.

From Rasta Livewire Fred Garner (editor of O’Shaughnessy’s) includes a story that ran initially in O’ Shaughnessy’s in 2005 when Dr Tashkin released findings at the 2005 meeting of the International Cannabinoid Research Society. This blockbuster study was ignored by NIDA, and everyone else. It eventually was published in the October 2006 issue of Cancer Epidemiology Biomarkers & Prevention.

It states rather clearly that marijuana protects people from developing airway cancers.

– As to the highly promising implication of his own study -that something in marijuana stops damaged cells from becoming malignant- Tashkin noted that an anti-proliferative [anti-cancer] effect of THC has been observed in cell-culture systems and animal models of brain, breast, prostate, and lung cancer. THC has been shown to promote known apoptosis (damaged cells die instead of reproducing) and to counter angiogenesis (the process by which blood vessels are formed -a requirement of tumor growth). Other antioxidants in cannabis may also be involved in countering malignancy, said Tashkin.[ref](http://www.africaresource.com/rasta/sesostris-the-great-the-egyptian-hercules/study-smoking-pot-doesnt-cause-cancer-it-may-prevent-it/) 08/09/2015[/ref]

Wait just a minute, it gets better. As mentioned earlier besides lung cancer tobacco smokers risk developing COPD. A separate study looked at lung function (a way to quantify lung damage from COPD) among cannabis and tobacco smokers. Lung function tests are the type that you see at the bedside with a patient blowing into a device with a tiny ball in it. Or it can be much more technical with computer driven machines that measure a multitude of pulmonary functions. Tashkin reports that, as predicted, tobacco-only smokers had accelerated rates of lung function decline. The more tobacco smoked the greater the rate of decline. Nothing new there.

Here’s the interesting part: pot smokers with or without concomitant tobacco use, suffered NO DECLINE in lung function. They stayed on the same trajectory as non-smokers. Dr Tashkin:

– In contrast, no matter how much marijuana was smoked, the rate of decline was similar to normal. Tashkin concluded that his and other studies do not support the concept that regular smoking of marijuana leads to COPD.

In other words your lung volumes will stay at normal, healthy values no matter how much weed you smoke. That’s fascinating, and it really says all that we need to know. Tobacco and cannabis are about as different as you can get.


We have compelling data which has accumulated for over 45 years, but in particular over the last two decades, that even heavy cannabis smoking does not increase your risk for head and neck (previous articles) or lung cancers. Furthermore, the data substantiating increased risk for developing COPD, bullous disease (and pneumothorax), or of reducing lung function from smoking pot (or pot mixed with tobacco), is either poor quality or non-existent.

This is particularly important because some researchers are already assuming these harms are true in their introductions in scientific papers. Up to as recently as 2014 many authors have already concluded wrongly that marijuana smoking causes lung cancer, upper airway cancers, bullous disease and pneumothorax, and COPD where no quality evidence permits these drastic, sweeping conclusions.


Dr Carol Tan’s wise observations and comments provide a much-needed breath of fresh air far from the madding crowd. In her Royal Society publication she highlights the bandwagon argumentative fallacy that seems particularly strong regarding marijuana harms, i.e., that pot smoking increases the risk for numerous pulmonary complications such as those listed throughout this paper.

For example, in her publication Bullous disease of the lung and cannabis smoking: insufficient evidence for a causative link[ref]Carol Tan. J R Soc Med. 2006 Feb; 99(2): 77–80. [/ref], she takes to task the chicken littles yowling that pot smoking is a cause of bullous disease of the lung, called bong lung. (I have a separate series of articles coming out that explain in detail bong lung.)

She judiciously informs us:

– Cannabis smoking appears on teaching slides as a cause of bullous lung disease and consequent pneumothorax. This seems to have become received wisdom—`A striking feature of cannabis smoking is that it is associated with bullous lung disease in young people’ (BMJ 2003;326: 942-3). The authors cite a report of four cases (Thorax 2000;55: 340-2 ). The suggestion appears, albeit in more muted terms, with the same citation in a UK Parliamentary memorandum on adverse effects of smoking marijuana on lung health (Memorandum 59. London: Royal College of Physicians, 2005).

– …Association can easily be interpreted as cause and effect particularly by a mind primed by the literature.

– …The phrase `a striking feature’ with reference to lung bullae is a strong assertion to be referenced only to a report of four patients. Co-authors, reviewers and editors generally provide a series of safety nets to protect us from overstatement but perhaps when sex, drugs and rock and roll are involved, titillation clouds reason.

– …It is of great concern that this belief about cannabis and lung bullae should have gained such wide acceptance without the production of better evidence. Perhaps myths are more easily made than forgotten.

Dr Tan’s comments focus on bullous disease from pot smoking but they could just as easily have been referring to lung cancer, COPD, psychosis, or heart attack. These sweeping assertions, based on flimsy associations from weak epidemiologic studies, condemn marijuana without sufficient scientific backing or foundation.

Many authors, as in the Dr Tan example above, seem to have drunk deeply from their institution’s Kool-Aid. The flavor of Kool-Aid in these hallowed halls often times reads “weed is a drug of abuse, it’s no good.”

Look, the information regarding marijuana harms is often times ambiguous enough without us needing to question agenda-driven conclusions from mildly hysterical clinicians. I believe this is due to a cultural anti-marijuana bias within the minds of some investigators. From my research it looks as if perhaps 50% of the publications seem to promote overstatement in regards to potential harms from chronic marijuana use.

In other words some authors may have a deeply held preconception that pot needs to look bad and appear dangerous regardless of where the science takes you. Because of this prejudice we can be terribly mislead. If I were to simply accept the exaggerated claims especially in the introductions and conclusions of many publications, I might have a completely different impression of marijuana. But it would be the wrong one.

Let’s stop the scare mongering from many in the research community. Instead observe the details of the best quality studies provided above authored by unbiased investigators like Dr Tashkin. Then we start to see a picture emerge that special properties of marijuana’s constituents-the phytocannabinoids-appear to vigorously prevent the conversion of toxic, combustion by-products, into either a cancerous lesion, bullous disease, or into the broad alveolar destructiveness of COPD.

Now isn’t it nice to know that in spite of very serious efforts to throw pot users, and the emerging worldwide legalization effort under the bus, there exists scanty evidence that marijuana causes serious pulmonary harms.

Tobacco smoking, on the other hand, is a toxic and dangerous habit. If you are living in Europe (as opposed to the US) then you probably smoke tobacco with your hash or cannabis. That’s a habit that probably should be abandoned knowing what we now know about these two popular recreational herbs.

CB2 Receptors Help Treat Alzheimers, Dementia and M.S, New Study Finds

CB2 Receptors Help Treat Alzheimers, Dementia and M.S, New Study Finds

Traditional endocannabinoid biochemistry holds that there are two main endocannabinoid receptors while others exist as candidates. The two most studied cannabinoid receptors in the human body are the CB1 and CB2 receptors. Customarily, we are taught that CB1 receptors are located within the central nervous system (CNS) and CB2 are expressed outside the CNS in peripheral systems like spleen tissue ((Lynn and Herkenham, 1994) and immune cells.

The CNS is the brain proper. The cells and nerves coming and going from the brain within the spinal column are still considered “central” until they synapse with intermediate nerve cells located within the spinal cord. Once the intermediate cells synapse (communicate) with peripheral nerves such as motor and sensory information leaving and arriving (the spinal cord), that branch becomes part of the peripheral nervous system or PNS.

Since 1996, scientists had been unable to isolate CB2 receptors in the CNS. They insisted that only CB1 receptors were in the CNS based on the available data. That all changed about a decade later in 2006. We now know that there are CB1 receptors all over the body both centrally (brain) and peripherally (everything else).

There is now compelling data that demonstrates things are not quite so neat and tidy with the CB2 receptor either. There appear to be CB2 receptors located in numerous regions within the CNS including both structural and immune type cells, and in myocardium, gut, endothelial, vascular smooth muscle and Kupffer cells, exocrine and endocrine pancreas, bone, reproductive organs/cells, and in various tumors.[ref]FEBS J. 2013 May; 280(9): 1918–1943. Published online 2013 Apr 22.[/ref]

The newly discovered CB2 receptors within the CNS are “inducible” under conditions of injury and inflammation. That means they can become powerful anti-inflammatory cells in the brain when exposed to injury. In contrast to CB1 receptors that have limited clinical applications due to their potent psychoactive nature, the CB2 receptor system provides fertile ground for drug research.

While this may not sound very interesting, it throws a wrench into the cogwheels of endocannabinoid pharmacology while opening new vistas for drug development. For example, it’s not as easy to explain all brain effects including psychiatric disorders on CB1 receptor behavior. Scientists now have another player to consider, the centrally located CB2 receptor.

In 2006 Onaivi et al, published Discovery of the presence and functional expression of cannabinoid CB2 receptors in brain, in Annals of the New York Academy of Science.

The implications are important clinically. The authors noted:

We have reported the discovery and functional presence of CB2 cannabinoid receptors in mammalian brain that may be involved in depression and drug abuse and this was supported by reports of identification of neuronal CB2 receptors that are involved in emesis. Thus, contrary to the prevailing view that CB2 CBrs [cannabinoid receptors] are restricted to peripheral tissues and predominantly in immune cells, we demonstrated that CB2 CBrs and their gene transcripts are widely distributed in the brain. This multifocal expression of CB2 immunoreactivity in brain suggests that CB2 receptors may play broader roles in the brain than previously anticipated and may be exploited as new targets in the treatment of depression and substance abuse.[ref]Ann N Y Acad Sci. 2006 Aug;1074:514-36.[/ref]


Emesis and drug abuse? That’s right, it would be from the tight embrace of dopaminergic neurons mingled with opiate mu receptors. For example, the opiates such as heroin frequently cause nausea and vomiting when ingested because heroin stimulates not just opiate receptors but also dopamine receptors in an area of the brain that triggers vomiting called the chemoreceptive trigger zone (CTZ). It appears that CB2 receptors are also located in that area. CB receptors are intertwined with dopamine and opiate systems among others. This helps to explain why marijuana helps with nausea.

Dopamine is also thought to be a key player in the reward system which reinforces drug addiction. A NIDA study published in the prestigious Proceeds of the National Academy of Science, Cannabinoid CB2 Receptors in Brain Reward Systems, researchers were able to show that CB2 receptors were located in the ventral tegmental region of the brain. This is an area known for its role in drug addiction and reward.

Activation of these receptors caused a reduction in cocaine self-administration by mice, suggesting a role for these receptors in modulating reward from cocaine. These findings suggest a new target for both understanding how cocaine acts in the brain and for developing effective treatments for cocaine addiction. They also provide insight into the role of the brain’s natural receptors for chemicals found in marijuana and suggest the need for additional research to understand the role these receptors play in normal brain functioning and abuse of drugs.[ref]Proc Natl Acad Sci U S A. 2014 Nov 18;111(46):E5007-15.[/ref]


Neuroinflammation is a hot topic. Rightly so because we all stand ever-greater chances of developing one of these ailments as we age. It plays a role in scores of diseases such as: MS, Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease, viral encephalitis, ischemia, and traumatic brain injury.

Glial cells are the brain’s immune cells. When they become activated from any of the diseases mentioned above (and many others) they secrete numerous chemicals called cytokines and chemokines. These events are part of the immune response, but when exaggerated may have detrimental effects on neuronal function. Often leading to neuronal injury with further glial activation and, ultimately, neurodegeneration. It’s an “overreaction” to a noxious stimulus with overproduction of chemokines and the like which can migrate and injure normal cells in a process called the “bystander effect.” While we need some inflammation for proper immune function it becomes a source for disease when these systems become over activated.

Here they found upregulation (an increase in the activity and number) of both CB2 and FAAH. FAAH, as you recall, is the enzyme responsible for the degradation of anandamide and possibly other analogues of THC. These were found to be protective responses to injury. Hence the increased expression of CB2 receptors in the CNS in response to injury is an anti-inflammatory riposte.

Presently we have three endocannabinoid neuroprotective actors participating on the stage of neuroinflammation as highlighted (in bold) below in quoting Benito et al, in Cannabinoid CB2 receptors in human brain inflammation:

As previously mentioned, this participation would include, in addition to the known neuroprotection exerted by neuronal CB1 receptors, glial CB2 receptors and FAAH. Both proteins seem to be significantly upregulated in microglial and astroglial cells, respectively, in areas of active neuroinflammation. Among these, β-amyloid enriched neuritic plaques in AD, infiltrative areas in viral encephalitis and regions of active demyelination in MS show marked increases in CB2 and FAAH levels of glial expression (reviewed by Benito et al., 2007c).[ref]Br J Pharmacol. 2008 Jan; 153(2): 277–285.[/ref]


AD is the number one cause of dementia in the developed world. In the US, you stand a 50/50 chance of developing AD by 85 years of age. The risk increases further still as one ages past 85. In 2001, more than 5 million people with dementia live in European countries, and more than 4 million people were affected in the US alone. A 100% increase in the number affected is expected in developed regions by the year 2040 (Ferri et al., 2005).[ref]IBID[/ref] At that point medical care expenses will probably bankrupt most country’s healthcare systems.

Other publications such as this one in the Lancet, the UK’s premier, peer-reviewed medical journal, show a slightly different picture but equally depressing:

The number of people living with dementia will almost double every 20 years, to 42·3 million in 2020 and 81·1 million in 2040. Although the expert consensus was for a higher prevalence of dementia in developed regions than developing regions, it is China and its developing western-Pacific neighbors that have the highest number of people with dementia (6 million), followed by western Europe with 4·9 million, and North America with 3·4 million. In 2001, 60·1% of all people with dementia lived in developing countries, rising to 64·5% in 2020 and 71·2% in 2040. At country level, the seven countries with the largest number of people with dementia in 2001 were: China (5·0 million), the European Union (5·0 million), USA (2·9 million), India (1·5 million), Japan (1·1 million), Russia (1·1 million), and Indonesia (1·0 million).[ref]Lancet. 2005 Dec 17; 366(9503): 2112–2117.[/ref]

It was expected that the developed nations were to be at the greatest risk. Why developing countries are at greater risk is uncertain.

The authors speculate on a possible role of the CB2 receptor in AD: CB2 activation could provide beneficial effects in AD through several mechanisms including a decrease in local, microglia-mediated inflammation, and an enhancement of beta amyloid plaque (Aβ) removal. Beta amyloid is one of the hallmarks of AD. Drugs that decrease the formation of beta amyloid have shown promise in treating AD.

Perhaps with enough research dollars poured into the system AFTER marijuana is rescheduled we will find a cure for what has been aptly called the most burdensome healthcare issue in the world.


What caught the team’s attention was the proliferation of CB2 receptors in the encephalitis induced by type 1-human immunodeficiency virus. This inflammatory process is the cause of acquired immuno deficiency syndrome (AIDS) dementia that affects at least 5–7% of AIDS patients per year, in Europe alone (Mollace et al., 2001). In its more advanced and severe form, the disease ultimately leads the patient progressing to a vegetative state (González-Scarano and Martín-García, 2005).[ref]Br J Pharmacol. 2008 Jan; 153(2): 277–285.[/ref]

The above authors speculate that CB2 receptors might participate in the inflammatory response against viral infection of the brain by modifying the microglial production of inflammatory molecules (decreasing the bystander effect) and by controlling the entry of peripheral (immune system) cells into the CNS.

The applications for CB2 receptor agonists in treating this disease is being actively pursued by several drug companies.


The disease destroys the fatty covering on brain neurons called myelin. The myelin acts much like an insulator. With its destruction leading to the hallmark features of the disease: such as painful muscle spasms, tremor, ataxia, weakness or paralysis. All symptoms are thought to be the result of new lesions and expansion of old lesions at the CNS level as a result of myelin phagocytic (eating) activity carried out by certain immune cells. CBD oil has already been approved by the FDA for treating the pain and spasticity of MS.

The endocannabinoid system (ECS) provides a promising target for the development of new drugs for treating MS. Both animal and human research using THC, cannabis extract or Sativex (50/50 THC and CBD) produced significant reductions in neuropathic pain and spasticity. Previously, treatment of MS focused on CB1 activation. Results from these and other studies suggests that CB2 receptors are potential treatment targets for the management of MS. With this knowledge the probability of finding cannabinoid-based drugs devoid of undesirable psychotropic side effects for treating this disease now seems more likely.

Benito: In summary, cannabinoids are known to have a therapeutic effect in MS. New evidence suggests that the CB2 receptor could also be a pharmacological target, as its expression is increased in several cell types known to be directly involved in the pathogenesis of MS. The activity of microglia, astrocytes and infiltrated lymphocytes could be modified by the activation of CB2 receptors.[ref]IBID[/ref]

CB2 receptors have been found in several animal species in addition to humans. The fact that their expression is increased in both animal and human trials, by inflammatory stimuli suggests that they may be involved in the pathogenesis and/or in the endogenous response to injury.

Data obtained in vitro and in animal models show that CB2 receptors may be part of the general neuroprotective action of the ECS by decreasing glial reactivity.[ref]IBID[/ref] It appears that upregulation of CB2 receptors is a common pattern of response to injury in human brains as well. Their presence in microglial cells suggests an important role in disease-driven neuroinflammation.

The authors conclude: The anti-inflammatory effects triggered by the activation of the CB2 receptor make it an attractive target for the development of novel anti-inflammatory therapies.

Can Cannabis Help Treat Tourette Syndrome?

Can Cannabis Help Treat Tourette Syndrome?

Tourette (too-RET) syndrome is a nervous system (neurological) disorder that starts in childhood. It involves unusual repetitive movements or unwanted sounds that can’t be controlled (tics). For instance, you may repeatedly blink your eyes, shrug your shoulders or jerk your head. In some cases, you might unintentionally blurt out offensive words.

Signs and symptoms of Tourette syndrome typically show up between ages 2 and 12.

TS is diagnosed according to the presence of multiple motor and phonic tics. Specific tics related to the above include coprophenomena (such as coprolalia: the uttering of obscene language), echophenomena (copying behaviours) and paliphenomena (repetitive behaviours).

They also generally suffer from obsessive-compulsive disorder (OCD) and sometimes ADHD as well.

There exists a dangerous tic such as hitting one’s head repeatedly against a wall that can cause a serious threat to bodily injury.

Treatment for the movement disorders involves the use of several drugs. The worst of which are the powerful neurolept medications such as the older, classic antipsychotic Haldol®, or the atypical antipsychotics. Both the classic and the atypical antipsychotic drugs themselves can cause disastrous Parkinsonian symptoms or the devastating disorder tardive dyskinesia in chronic users. In other words there are no effective and safe drugs to use in treating these patients.

It’s a terribly debilitating movement disorder. To get an idea on how bad it can become watch the video below where a man uses cannabis to placate his disease. It’s quite remarkable to watch.



In 1998 a possible role for cannabis was already being explored by Müller-Vahl KR in their publication: Cannabinoids: possible role in patho-physiology and therapy of Gilles de la Tourette syndrome.

Their conclusion: our results provide more evidence that marijuana improves tics and behavioural disorders in TS.

A pilot study was performed more recently, by Muller-Vahl et al. It involved a randomized, double-blind, crossover trial [Muller-Vahl et al. 2002]. In conclusion both motor tic severity and OCSs were significantly improved by THC.

In a follow up 6-week study [Muller-Vahl et al. 2003] they used doses of THC up to 10 mg. Small improvements in tic frequency and severity were evident according to assessment using different measures of tic severity.

They concluded: our results provide more evidence that THC is effective and safe in the treatment of tics. It, therefore, can be hypothesized that the central cannabinoid receptor system might play a role in TS pathology. The side effects associated with the use of THC were reported to be mild and transient.

In 2009 Curtis and colleagues, attempted a meta-analysis of current data. Only two trials met their criteria. Based on a paucity of available data they concluded that there was not enough evidence to support the use of cannabinoids in treating tics and obsessive-compulsive behaviour in people with Tourette’s syndrome.[ref]Cochrane Database Syst Rev. 2009 Oct 7;(4):CD006565.[/ref]

Although both trials reported a positive effect from Delta(9)THC, the improvements in tic frequency and severity were small and were only detected by some of the outcome measures. These include the possibility that effect sizes could be artificially inflated, as those participants who drop out may do so due to lack of treatment response [Curtis et al. 2009].[ref]Ther Adv Neurol Disord. 2011 Jan; 4(1): 25–45.[/ref]


Muller-Vahl and colleagues reported no deterioration in verbal or visual memory, reaction time, intelligence, sustained attention, divided attention, vigilance or mood, with the use of THC [Muller-Vahl et al. 2001].


Presently some data exists that demonstrates a decrease in the severity of tics and other TS symptoms using THC. It appeared to be safe and did not cause cognitive decline. However, some trials were disappointing and more work clearly is needed.

Dr Muller-Vahl suggests: if well-established drugs either fail to improve tics or cause significant adverse effects, in adult patients, therapy with Delta9-THC should be tried. At present, it remains unclear whether herbal cannabis, different natural or synthetic cannabinoid CB1-receptor agonists or agents that interfere with the inactivation of endocannabinoids, may have the best adverse effect profile in TS.

A search of the literature for the use of pure CBD, which acts as a powerful neurolept drug, was futile. There do not appear to be any trials that used pure CBD, only THC. I believe CBD would have produced better outcomes. The neurolepts are some of the only drugs that help but sadly come with intolerable side effects. CBD has a nearly side effect free profile especially when compared to any of the current antipsychotic medications, or other drugs used in this challenging condition.

A History of Cannabis Prohibition

A History of Cannabis Prohibition

Clinical research on cannabis is nearly nonexistent in the US and most of the first world. Since 1970, marijuana has been a schedule I drug. So for the last 45 years research into the mysterious workings of this substance has been frozen. That’s because the law tells us that cannabis is medically worthless.

Yet for over 100 years, patients could obtain any number of cannabis products for health and personal use. That all changed in the 1930s, with its deathblow finally culminating from reclassification to schedule I by the beginning of the turbulent 70’s.

But why? Why has cannabis received such onerous attributes? How can a herb that enjoyed 100’s of medical applications during the 19th and early 20th centuries suddenly become medically useless?

That’s not possible unless a strange phenomenon in human behavior called politics becomes enmeshed with it. There is only one force stronger than the rational facts of hard science – politics and the irrational politician.

What actually happened during the last century to transform what could be described as a miracle drug into the devil’s ditch weed?

There are various reasons why cannabis became demonized. Some say it was the emerging paper industry. Threatened by hemp paper as a competitor, such heavyweights as the DuPonts and WR Hearst enlisted to crush the neonatal hemp industry as it was leaving the birth canal.

There are other factors too such as prejudicial fear mongering of “degenerate” Mexican “immigrants” and black musicians who after using marijuana would lose their minds and impulse control. This would lead to “deviant sexual (rape of white women) and other felonious behaviors”.

From a recent publication in the Mayo Clinic  Proceedings entitled Blurred Boundaries: The Therapeutics and Politics of Medical Marijuana by J. Michael Bostwick, MD, a section is devoted on just how strange and Byzantine our government became regarding all things marijuana.

The execution goes like this:

  • The Federal Bureau of Narcotics over the objection of the American Medical Association pushed for the congressional passage of the 1937 Marihuana [sic] Tax Act that taxed cannabis. It may have been meant to placate xenophobic law enforcement officials and legislators from southwestern and western states who associated marijuana’s use with dangerous and criminal activity of Mexicans and migrant workers. Pharmaceutical companies opposed any regulation.
  • On the heels of media propaganda campaigns, removal from the US Dispensatory in 1942 after nearly a century stripped it of any remaining therapeutic legitimacy.
  • In 1970 marijuana was finally declared persona non grata. The controlled Substances Act requires scientific evaluation and testimony before legislative action. In spite of clear medical indications congress declared cannabis illegal in the “absence of such evidence.”
  • In a rapid follow up the FDA reclassified pot into schedule I: an addictive drug with high abuse potential and no currently accepted medical use.

Thus ending the millennial reign of king cannabis.

Dr. Bostwick reminds us that the basic principles of medicine should take precedence over political expediency in the development of a rational strategy for any therapeutic agent, even one as controversial as marijuana. Marijuana being relegated to Schedule I status appears especially irrational when precedence exists for assigning potential drugs of abuse Schedule II status when they also possess manifest medical benefits. Think of the opiates and cocaine for example. Risk versus benefit needs to be considered.

It’s not just the ridiculous scheduling that has made cannabis one of the hardest drugs to research, it’s also the Medusian tangle of bureaucratic limbs to negotiate.

The FDA, for example, authorizes research to proceed on safety and efficacy, the National Institute on Drug Abuse provides the research material, and the Drug Enforcement Agency grants the investigator the actual license to perform the research. Any one of these agencies has the power to halt an initiative in its tracks.[ref]February 2012 Volume 87, Issue 2, Pages 172–186. DOI: http://dx.doi.org/10.1016/j.mayocp.2011.10.003[/ref]

I know of a physician who took 10 agonizing years before being granted permission to use DMT on human volunteers. The average time it takes for cannabis approval is about half that time (but it can be longer). The US government still favors a culture of prohibition. They won’t go down without a fight but it’s the wrong fight in this new era.

CBD Can Help Heal Broken Bones, According to Dr. Rasmussen

CBD Can Help Heal Broken Bones, According to Dr. Rasmussen

Will wonders never cease?

If I were to sit my colleagues down and provide them with a lecture on all of the positive uses for cannabis and CBD they would think I was nuts, and laugh me off the stage. Typically when you hear someone pealing from a soapbox about how great a product is, that it cures dozens of different aliments, you should run the other way. That’s because (allopathic) medicines don’t have huge applications across dozens of organ systems. Like the snake oil sold to thousands at the turn of the century, products come and go. Most are complete nonsense.

Incidentally, snake oil was a rich source of omega 3 fatty acids which DID make it a very useful drug. But in general drugs, tinctures, extracts, whatever, never really cure dozens of different diseases. They may be great for a limited application but that’s where the fantasy ends. At least from the pharmacopeia that I use every day.


Well, there’s a new sheriff in town that is changing how we will use drugs and treat diseases. The new sheriff would be the cannabinoids. I have never seen a class of compounds that seem to have so many powerful disease-fighting properties. Which makes all of this terribly frustrating because nobody can get any research done with human volunteers due to the DEA class I scheduling.


Nothing seems to be changing either. Just in the last two weeks, congress shot down an amendment that would have placed cannabis in a new category, still technically schedule I but the new class would have approved cannabis for clinical research. Why that didn’t pass I’ll never know.

While the rest of the first world research community is hog tied to a park bench, there remains a little gem full of great minds doing respectable research.


That would be the Israelis. This tiny country apparently has a better form of democracy than the US. They actually listen to the masses and respond appropriately. That means that cannabis research is full-bore in this desert nation.

Appropriately enough a very interesting publication came out earlier this year.

A new study published in the Journal of Bone and Mineral Research by Tel Aviv University and Hebrew University researchers explores another promising new medical application for marijuana. According to the research, the administration of the non-psychotropic component cannabinoid cannabidiol (CBD) significantly helps heal bone fractures. The study, conducted on rats with mid-femoral fractures, found that CBD — even when isolated from tetrahydrocannabinol (THC), the major psychoactive component of cannabis — markedly enhanced the healing process of the femora after just eight weeks.

The research was led jointly by Dr. Yankel Gabet of the Bone Research Laboratory at the Department of Anatomy and Anthropology at TAU’s Sackler Faculty of Medicine and the late Prof. Itai Bab of Hebrew University’s Bone Laboratory.[ref](http://www.sciencedaily.com/releases/2015/07/150716124359.htm) 07/23/2015 (original publication: Journal of Bone and Mineral Research, 2015; DOI: 10.1002/jbmr.2513.[/ref]

After the discovery of CB receptors within bone matrix, the road was paved for research into the effects of cannabinoids on bone mineralization and healing. They found that CBD makes bones harder while enhancing bone mineralization. After treatment with CBD the bone will be harder to break in the future said Dr Gabet.

The clinical potential of cannabinoid-related compounds is simply undeniable at this point, said Dr. Gabet. While there is still a lot of work to be done to develop appropriate therapies, it is clear that it is possible to detach a clinical therapy objective from the psychoactivity of cannabis. CBD, the principal agent in our study, is primarily anti-inflammatory and has no psychoactivity

…We found CBD alone to be sufficiently effective in enhancing fracture healing. Other studies have also shown CBD to be a safe agent, which leads us to believe we should continue this line of study in clinical trials to assess its usefulness in improving human fracture healing.[ref]IBID[/ref]

Is Cannabis a Gateway Drug?

Is Cannabis a Gateway Drug?

A 2014 NIDA study was written by acting director Dr Volkow. She had this to say among several other bullet points in her conclusions:

  1. Marijuana addiction increases the risk for using other illicit drugs.

Is cannabis a gateway drug? Number 4 (from her list) suggests that it opens the pathway for many hapless experimenters who eventually succumb to its charms like sirens luring you to a rocky shore.

What evidence do we have that supports the theory that cannabis smoking leads to the use of “harder” drugs such as heroin or cocaine? The so-called gateway theory. This idea has taken on a life of its own. Nearly anyone you talk to will chortle something on cannabis use as a gateway drug. What are the facts?

Time magazine published an article in 2010 entitled: Marijuana as a Gateway Drug: The Myth That Will Not Die. By Maia Szalavitz.

She quotes the Institute of Medicine’s publication from 1999 in a report commissioned by Congress to look at the possible dangers of medical marijuana.

Patterns in progression of drug use from adolescence to adulthood are strikingly regular. Because it is the most widely used illicit drug, marijuana is predictably the first illicit drug most people encounter. Not surprisingly, most users of other illicit drugs have used marijuana first. In fact, most drug users begin with alcohol and nicotine before marijuana — usually before they are of legal age.

In the sense that marijuana use typically precedes rather than follows initiation of other illicit drug use, it is indeed a “gateway” drug. But because underage smoking and alcohol use typically precede marijuana use, marijuana is not the most common, and is rarely the first, “gateway” to illicit drug use. There is no conclusive evidence that the drug effects of marijuana are causally linked to the subsequent abuse of other illicit drugs.

Statistically, there are many more people who have tried cannabis than cocaine or heroin. For example, the federal government’s survey on drug use showed that in 2009, 2.3 million people reported trying cannabis — compared with 617,000 who tried cocaine and 180,000 who tried heroin. [ref](http://healthland.time.com/2010/10/29/marijuna-as-a-gateway-drug-the-myth-that-will-not-die/) 07/15/2015[/ref] If marijuana was a true gateway you would expect to see far greater percentage of cannabis users going on to try heroin or cocaine.


One theory is that cannabis smokers who develop good relations with their dealer may be exposed to harder drugs from the trust that develops between them. Dealers are more apt to sell only to those they know especially when it comes to hard drugs like coke and heroin since the penalties are far greater. In this way, marijuana users can be exposed to harder drugs.

The Dutch coffeeshop experience was in part, based on abolishing the rapport consumers had with their dealers by eliminating dealers altogether. A 2010 Rand report verified that evidence existed to show a “weakened gateway” in the Netherlands. Pot smoking among their youth has decreased as well. They concluded that the data clearly challenge any claim that the Dutch have strengthened the gateway to hard drug use.[ref]IBID[/ref]

Another theory is taste. Those that like to alter their consciousness may prefer various platforms to try out. Not being satisfied with simply smoking cannabis they may experiment with harder drugs. This is analogous to fitness buffs who like to try many differing forms and styles of exercise. Or music aficionados who are not satisfied with only listening to Sonny and Cher’s Billboard top 10 smash hit “The Beat Goes On,” from their 1967 album In Case You’re In Love. However, it doesn’t mean a teen’s fondness for Sonny and Cher becomes a gateway to the Sex Pistols.

Just How Addictive is Cannabis? Dr. Rasmussen Investigates...

Just How Addictive is Cannabis? Dr. Rasmussen Investigates…

I always remind people when they say that cannabis is addictive, that it lowers IQ, and makes you amotivational, that Carl Sagan, one of the most prolific scientists of our era, was a noted user. One of the most gifted singer/songwriters of our era, the late Amy Winehouse, was also a big fan of marijuana. Which of course doesn’t prove anything but it’s a good counterargument showing the same associations that our experts love to make. Aside from my humble opinion, there exists plenty of new and old data that trumps much of the caterwauling on addiction.

From the website [ref]http://clinicalcannabisincontext.tumblr.com/[/ref] of Ian Mitchell, MD, a noted expert in marijuana matters. He reminds us of some of the cannabis benefits he pulled from the enlightened Vancouver city council:

  1. As a substitute for more harmful drugs (e.g. alcohol, tobacco, prescription opiates and some illegal drugs such as heroin or cocaine)
  2. As a means to reduce the rates of opioid overdose deaths and opioid-related morbidity
  3. To relieve withdrawal symptoms during detox and to increase retention rates during treatment [Emphasis mine]

These are all excellent points that clinicians need to be aware of when discussing the addiction potential of cannabis. It is safer than heroin. It is far superior to anything else in helping to relieve opiate withdrawal symptoms. Therefore, trading a major addiction for a minor one is good, ethical medicine.

Even if pot is addicting, many authorities are not impressed. Research shows that most patients could kick a cannabis addiction as easily as a heavy coffee drinker going cold turkey. Well, actually it’s probably easier than quitting coffee.

Part of the problem within the literature is that many of our trusted experts know surprisingly little in regards to the true nature of pot. For example, we have experts that apparently don’t know the difference between CBD and THC. An article entitled Cannabis and the maturing brain: Role in psychosis development, by Crocker and Tibbo, (no, they’re not from Miami Vice) mentions the peril involved when treating epilepsy:

In cases such as epilepsy, where medical cannabis may be used in children, we do not yet know all the implications on adult outcomes, though we have discussed a potentially severe problem in this article.

The authors lose credibility here. These “experts” display an amazing lack of clinical knowledge on what components of cannabis are used in treating epilepsy. Again Dr Mitchell:

While there are cases of children being treated for epilepsy with cannabis, the active ingredient that is sought after and used is an isolated extract of [marijuana called] cannabidiol, a non-psychoactive cannabinoid that has shown great promise. Cannabidiol has not been linked to psychosis and has actually shown anti-psychotic properties. The authors have no basis for suggesting that cannabidiol can lead to schizophrenia. Another aspect of treating adolescents has to do with the concept of risk vs benefit. Rather than focusing entirely on risk, clinicians have to weigh risk compared to benefit.

If the same experts can be this misinformed regarding THC and CBD, why should we trust their opinion regarding addiction?


An important concept was introduced above. It’s called risk versus benefit ratio. An astonishing lack of honesty is often employed when clinicians comment on marijuana use in treating diseases. For example, in treating seizure disorders many of the drugs used carry moderate to severe risks of harms which are titanic compared to marijuana’s side effects. I mentioned one such disfiguring risk previously in another publication: gingival hyperplasia from the use of phenytoin.

But that doesn’t stop one from prescribing it. It should be the same for marijuana. If it is addicting you still need weigh its beneficial role FIRST for the patient, then decide if habit forming is worse than the disease. Under these circumstances, cannabis usually prevails.

As America and the rest of the free world mobilize to completely legalize cannabis for medical and recreational use, the notion of addiction storms to the forefront.

Like a thunderhead looming in the distance, detractors will insist that marijuana is highly addictive and urge caution by not legalizing it. Others feel that cannabis, if it is addicting, is very mild, and probably better or at least no worse than food addictions, sex addictions, gambling or a 2 pot-a-day coffee habit.

In a Time magazine publication in 2010 the issues of addiction were raised in Is Marijuana Addictive? It Depends How You Define Addiction. By Maia Szalavitz.

By the book [DSM IV], addiction is the compulsive use of a substance despite ongoing negative consequences, which may lead to tolerance or withdrawal symptoms when the substance is stopped. By this definition, about 10% of people who smoke marijuana become addicted to it.

One of the unique aspects of cannabis addiction is that there are virtually no physical side effects from withdrawal, that it’s a psychological addiction, a craving for the high without many systemic manifestations. It’s quite unlike heroin withdrawal, the classic addiction, which can generate unbearable physical anguish. That’s indeed true but modern medicine no longer separates psychological from physical addiction (DSM V see below).

How addicting is it? Maia Szalavitz:

So the question is, how does marijuana compare to these classically addictive drugs? Estimates vary, but compared with tobacco, which hooks about 20% to 30% of smokers, marijuana is much less addictive, coming in at 9% to 10%. In contrast, 23% to 25% of heroin users get addicted, along with 15% of alcohol users and 15% to 20% of those who use cocaine.

Marijuana is the most heavily used drug in the country — by their 20s, 56% of Americans have tried it — but only 16% of people who are in addiction treatment report that marijuana is their primary drug. In contrast, just 2% of young adults have ever tried heroin, but heroin addicts make up 14% of treatment admissions.

The experts agree that cannabis is addicting in some ways. But is that necessarily bad?

Dr Carl Hart was interviewed for the above feature. He’s an associate professor of clinical neuroscience at Columbia University, who has studied marijuana withdrawal. His take on it:

You can actually die from alcohol withdrawal. Heroin withdrawal you can’t really die from; it’s more like the flu. Marijuana withdrawal is annoying, but it isn’t life threatening.

You might see anxiety, mood disturbances, irritability and a decrease in food intake in addition to other effects like insomnia. But they are clearly much milder than even tobacco withdrawal.

Furthermore, since marijuana has active metabolites that reside in the fatty compartment of your body they tend to leech out slowly over several weeks. This provides a smoothing out of any potential withdrawal effects.

Dr Peele makes a very important point regarding cannabis addiction. Even if it is addicting it makes little difference since its side effects are scant. According to Stanton Peele, author of the classic book Love and Addiction,[ref](http://healthland.time.com/2010/10/19/is-marijuana-addictive-it-depends-how-you-define-addiction/) 07/15/2015[/ref] he remarks:

Marijuana is addictive — so what? How harmful is this addiction compared to other addictions? It can be disruptive to people’s lives; I have a treatment center, and some people end up there because of marijuana. On the other hand, in terms of physical assaults to your body, it’s better than smoking and better than alcohol.

Perhaps it compares favorably to coffee addiction. Heavy coffee drinkers suffer intractable headaches and a craving for a steaming cup that rivals a lion’s bloodlust. But that’s about it.

The article finishes making the point that with the new DSM V manual many unconventional addictions are now listed including gambling, sex, food and shopping. So even these habits are considered addictive now along with cannabis.

The Greatest Harm for Cannabis Users: The U.S. Justice System

The Greatest Harm for Cannabis Users: The U.S. Justice System

Let me ask you a very important question. What do you consider worse, doing ten to twenty in a federal penitentiary like New York’s Big House (Sing Sing), or being sentenced to some sordid state facility where you can bone up on your gladiatorial skills? Or trading a miserable prison term for a decrease in your ability to recall someone’s phone number?

I’ve just listed two of the harms from marijuana. One of the harms is a decrease in short-term memory called cognitive dysfunction. The other is being busted and ending up in the judicial system. Yet everyone seems to be ignoring the latter, like the half-wit uncle living in the crawlspace. But it is clearly the greatest harm that can occur from the use of cannabis.

It’s called pot prohibition. And it’s just like alcohol prohibition only worse.

Let’s be honest here. A run in with the judicial system is likely to destroy your life more than ANY side effect from marijuana. We’ll talk about this highly detrimental process today.

Dr Mitchell (from http://clinicalcannabisincontext.tumblr.com/) makes his best point when he remarks that:

Young people increasingly recognize that while alcohol and tobacco are legal, they are far more injurious to health than cannabis. In greatest danger for adolescents due to cannabis use comes from legal consequences secondary to prohibition.

Most of the professional community take it off the table, the notion that prison time is not part of the harms incurred from using recreational cannabis. But it certainly is. Everyone seems to forget that while some states in the US have relaxed their medieval penalties for possession of marijuana, many states have done little to alter their draconian punishments. It’s still a felony to grow any cannabis, even one plant in nearly every state. Several states will get you 10-30 years or more if you have a half-dozen plants in your house.

In fact, hundreds of thousands of people are still being arrested and put into cages for simple possession. Living in a 10 x 10 cell for ten years is clearly worse than cognitive dysfunction is it not?

From the NORML website:

Enforcing marijuana prohibition costs taxpayers an estimated $10 billion annually and results in the arrest of more than 693,000 individuals per year — far more than the total number of arrestees for all violent crimes combined, including murder, rape, robbery and aggravated assault.

A high school student arrested for possession of cannabis will have his student loan privileges revoked. That person can’t enter college without the ability to pay for it. That same person may never reach his full potential because he will have a criminal record. With that he may not be able to secure any number of government jobs. The private sector is worse if you have a record. He may even become a burden on society if he cannot secure a productive job. With a felony conviction the risk for failure increases substantially. Why would any government want to take a young, otherwise normal, kid and transform him into an ex-con burden on society? This is absurd to any rational thinker. Yet, this is exactly what has happened year after year for the last 7 decades.

It gets better. In the US there are an estimated 6,899,000 persons under the supervision of adult correctional systems at yearend 2013. Folks that’s nearly 7 million people! The numbers of incarcerated and paroled in the US are far more than China and Russia combined. Let’s examine the attrition rates for illicit drug users snagged by the law.

(Number Of People Serving Time For Drug Offenses In US Prisons)
Federal: “Between 2001 and 2013, more than half of prisoners serving sentences of more than a year in federal facilities were convicted of drug offenses. On September 30, 2013 (the end of the most recent fiscal year for which federal offense data were available), 98,200 inmates (51% of the federal prison population) were imprisoned for possession, trafficking, or other drug crimes.”
State: “Drug offenders comprised 16% (210,200 inmates) of the total state prison population in 2012.

(People On Probation For Drug Offenses In The US, 2013) Of the 3,910,647 adults on probation in the US at the end of 2013, 25% (approximately 977,662 people) had a drug charge as their most serious offense.

(People On Parole For Drug Offenses In The US, 2013) Of the 853,215 people on parole at the end of 2013, 32% (approximately 273,029 people) had a drug charge as their most serious offense.[ref]http://www.drugwarfacts.org/cms/Prisons_and_Drugs[/ref]


Are you sitting down? You’ll need to after reading this: 98,200 plus 210,200 plus 977,662 plus 273,029 equals 1,559,091. That’s one and one-half million people either in prison, on parole, or on probation who are victims of the drug war.

(Estimated Number Of People In The US Sentenced To State and Federal Prison For Marijuana Offenses)

Total Federal Prisoners 2004 = 170,535
Total State Prisoners 2004 = 1,244,311

Percent of federal prisoners held for drug law violations = 55%
Percent of state prisoners held for drug law violations = 21%

Marijuana/hashish, Percent of federal drug offenders, 2004 = 12.4%
Marijuana/hashish, Percent of state drug offenders, 2004 = 12.7%

(Total prisoners x percent drug law) x percent marijuana = “marijuana prisoners”

Federal marijuana prisoners in 2004 = 11,630
State marijuana prisoners in 2004 = 33,186
Total federal and state marijuana prisoners in 2004 = 44,816

Note: These data only address people in prisons and thus exclude the 700,000+ offenders who may be in local jails because of a marijuana conviction.

As you can see there is a significant number of prisoners wasting away for simple possession/use/distribution of weed.

It’s revealing to note that of the estimated 196,574 people incarcerated into the US federal prison system in 2012, there were approximately nine times the number of drug offenses than there were of violent crimes: 11,688 were incarcerated for violent offenses including homicide and armed robbery, and an estimated 99,426 who were incarcerated for drug offenses. A ten to one ratio? I never would have anticipated that one.

(Local Jail Inmates) According to a federal survey of jail inmates, of the total 440,670 jail inmates in the US in 2002, 112,447 (25.5%) were drug offenders: 48,823 (11.1%) for possession and 56,574 (12.8%) for trafficking.[ref]IBID[/ref]

There is no question that we have an imbalanced system of justice in the US when it comes to drug use and possession. In a society where 56% of its adult population have tried marijuana, the laws do not reflect this new attitude.

My question to the reader is when marijuana becomes legal in the US what becomes of all those non-violent drug offenders caught in the system? Will they have to serve out their sentences while the rest of us enjoy our new freedoms? Or will those with a moral compass allow them an early release?