SweetSue's Class Notes

I have this sneaking suspicion that a lot of the people talking about “adverse effects” haven’t ever been high, and have no real idea that being buzzed is really just feeling really, really good. I think of it as “normal.” :rofl:
 
Went back and re-read the editorial, now that it’s been busted apart. It’s so much easier to read and understand when you give the words some space to breathe. :cool:
 
Physiologically, this phenomenon is easily explained on the basis that CB1 receptors are densely represented in the limbic system areas that are responsible for the affective elements of pain perception.

What he’s saying here is that cannabis breaks the memory loop pain establishes. Chronic pain is its own beast, and you develop expectations of future pain that will change your response to life, even before you feel the pain.

Because your limbic system stored all the memories of how bad it hurts, and how hopeless you feel in the face of that pain. Cannabis breaks the spell of pain.

I explain it as sitting pain in the corner of the farthest room in your mind and giving it a puppy. :laughtwo:
 
The ECS vs pain

The ECS vs pain

Materials by Green Flower Media

Your brain and pain

Your brain and pain

Materials by Green Flower Media

Your brain and body and the eCBRs

Your brain and body and the eCBRs

Materials by Green Flower Media

Choosing your cannabinoids

Choosing your cannabinoids

Materials by Aunt Zelda’s, by way of Green Flower Media

Dosing guidelines

Dosing guidelines

Materials by Aunt Zelda’s, by way of Green Flower Media

Dosing guidelines

Dosing guidelines

Materials by Aunt Zelda’s, by way of Green Flower Media

Dosing guidelines

Dosing guidelines

Materials by Aunt Zelda’s, by way of Green Flower Media

Back pain

Back pain

Materials by Green Flower Media

The Nervous System

The Nervous System

Materials from Green Flower Media

Cannabis use reduces polypharmacy of dangerous pharmaceutical and OTC drugs

Cannabis use reduces polypharmacy of dangerous pharmaceutical and OTC drugs

Materials from Green Flower Media
 
Source


October 30, 2017
4 Chemicals That Activate Happiness, and How to Gamify Them

Written by
CLARK BUCKNER

Nicole Lazzaro is a world-renowned game designer. And if you’re thinking, what does game design have to do with a website that covers workplace software, you haven’t been paying attention.
Gamification is changing how companies build software and how consumers interact with it, not just at home, but at work as well.

To get an insider’s perspective on this revolution, we spoke with Nicole about her theories on the science of fun. Listen to our short interview then read on for more about why gamification works so well (hint: you’ll use brain power).

If you’re interested in hearing more from Nicole, check out her website, 4k2f.com.

Gamification isn’t silly, it’s science.

There are four major chemicals in the brain that influence our happiness (DOSE):
  1. Dopamine
  2. Oxytocin
  3. Serotonin
  4. Endorphins.

As Nicole explains, each plays a different role in happiness. And guess what? They are all triggered by gamified experiences. Let’s dig a little deeper.

Dopamine is what we normally think of as the happiness drug. However, that’s a big misconception. Dopamine is actually involved more with anticipation than the actual “happiness” feeling. Nicole describes it as a striving emotion.

Oxytocin is the neurochemical that has allowed us to become social creatures. It makes us feel empathy which helps us feel close and bonded to others when it’s released.

If you’re in a good mood, you’ve got serotonin to thank. And if you’re in a bad mood, you’ve got serotonin to blame. It’s a regulator. Interestingly, Nicole explains, 80 percent of serotonin exists in the gut, and is governed by your state of hunger (yes, this is why you’re hangry).

Endorphins are responsible for masking pain or discomfort, which explains their association with the “fight or flight” response. When it comes to designing happiness, endorphins help you “power through.” Nicole, for example, is an avid runner. Endorphins allow her to push farther and harder as she works towards distance goals.

Together these chemicals create desirable brain states (and keep people coming back).

Experiences that release the DOSE neurochemicals make us happy, which makes us want more of the same. Does a desire to return to the same experience sound like a desire you probably have for your customers? Yes, it certainly does: customer loyalty. Gamified user experiences created with neuroscience in mind keep consumers coming back for more.

Whether those experiences are created to keep employees returning to your LMS for more gamified training, or to keep readers revisiting your site for more gamified content, this scientifically-backed approach works. It’s the reason gamification is expected to grow to a $5.5 billion industry by the end of 2018, and the reason you should be thinking about how to include gamified experiences into your technology.

The Takeaways:
  • There are four primary chemicals in the brain that effect happiness: dopamine, oxytocin, serotonin, and endorphins
  • By designing gamified experiences that activate these chemicals, you can increase your users’ happiness and loyalty
 
From Wikipedia:

Biochemically, the indoleamine molecule derives from the amino acid tryptophan, via the (rate-limiting) hydroxylation of the 5 position on the ring (forming the intermediate 5-hydroxytryptophan), and then decarboxylationto produce serotonin.[10] Serotonin is primarily found in the enteric nervous system located in the gastrointestinal tract (GI tract). However, it is also produced in the central nervous system(CNS), specifically in the Raphe nuclei located in the brainstem. Additionally, serotonin is stored in blood platelets and is released during agitation and vasoconstriction, where it then acts as an agonist to other platelets.[11]

Approximately 90% of the human body's total serotonin is located in the enterochromaffin cells in the GI tract, where it regulates intestinal movements.[12][13] The serotonin is secreted luminally and basolaterally, which leads to increased serotonin uptake by circulating platelets and activation after stimulation, which gives increased stimulation of myenteric neurons and gastrointestinal motility.[14] The remainder is synthesized in serotonergic neurons of the CNS, where it has various functions. These include the regulation of mood, appetite, and sleep. Serotonin also has some cognitive functions, including memory and learning.

Several classes of antidepressants, such as the SSRIs and the SNRIs among others, interfere with the normal reabsorption of serotonin after it is done with the transmission of the signal, therefore augmenting the neurotransmitter levels in the synapses.

Serotonin secreted from the enterochromaffin cells eventually finds its way out of tissues into the blood. There, it is actively taken up by blood platelets, which store it. When the platelets bind to a clot, they release serotonin, where it can serve as a vasoconstrictor or a vasodilator while regulating hemostasis and blood clotting. In high concentrations, serotonin acts as a vasoconstrictor by contracting endothelial smooth muscle directly or by potentiating the effects of other vasoconstrictors (e.g. angiotensin II, norepinephrine). The vasoconstrictive property is mostly seen in pathologic states affecting the endothelium – such as atherosclerosis or chronic hypertension. In physiologic states, vasodilation occurs through the serotonin mediated release of nitric oxide from endothelial cells. Additionally, it inhibits the release of norepinephrine from adrenergic nerves.[15] Serotonin is also a growth factor for some types of cells, which may give it a role in wound healing. There are various serotonin receptors.

Serotonin is metabolized mainly to 5-HIAA, chiefly by the liver. Metabolism involves first oxidation by monoamine oxidase to the corresponding aldehyde. There follows oxidation by aldehyde dehydrogenase to 5-HIAA, the indole acetic-acid derivative. The latter is then excreted by the kidneys.

Besides mammals, serotonin is found in all bilateral animals including worms and insects,[16] as well as in fungi and in plants. Serotonin's presence in insect venoms and plant spines serves to cause pain, which is a side-effect of serotonin injection.[17] Serotonin is produced by pathogenic amoebae, and its effect in the human gut is diarrhea.[18] Its widespread presence in many seeds and fruits may serve to stimulate the digestive tract into expelling the seeds.[19]

Serotonin is also present in plants as phytoserotonin.[20]



Perception of resource availabilityEdit

Serotonin mediates the animal's perceptions of resources; In less complex animals, such as some invertebrates, resources simply mean food availability.[21] In plants serotonin synthesis seems to be associated with stress signals.[20] In more complex animals, such as arthropods and vertebrates, resources also can mean social dominance.[22] In response to the perceived abundance or scarcity of resources, an animal's growth, reproduction or mood may be elevated or lowered. This may somewhat depend on how much serotonin the organism has at its disposal.[citation needed]

Cellular effectsEdit
In humans, serotonin is a neurotransmitter used throughout the body having action of 14 variants of the serotonin receptor

to have diverse effects on mood, anxiety, sleep, appetite, temperature, eating behaviour, sexual behaviour, movements and gastrointestinal motility.

These are the same functions attributed to the ECS, and it’s cannabinoids that turn off the flow of serotonin.


[23] Serotonin is not administered clinically as a drug itself as it is not specific enough. However, drugs that selectively target specific serotonin receptor subtypes are used therapeutically for antidepressant effects; these are called selective serotonin re-uptake inhibitors. They are dependent on serotonin availability in the synapse.[24]

ReceptorsEdit
The 5-HT receptors, the receptors for serotonin, are located on the cell membrane of nerve cells and other cell types in animals, and mediate the effects of serotonin as the endogenous ligand and of a broad range of pharmaceutical and hallucinogenic drugs. Except for the 5-HT3 receptor, a ligand-gated ion channel, all other 5-HT receptors are G-protein-coupled receptors (also called seven-transmembrane, or heptahelical receptors) that activate an intracellular second messengercascade.[25]

TerminationEdit
Serotonergic action is terminated primarily via uptake of 5-HT from the synapse. This is accomplished through the specific monoamine transporter for 5-HT, SERT, on the presynaptic neuron. Various agents can inhibit 5-HT reuptake, including cocaine, dextromethorphan(an antitussive), tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs). A 2006 study conducted by the University of Washington suggested that a newly discovered monoamine transporter, known as PMAT, may account for "a significant percentage of 5-HT clearance".[26]

Contrasting with the high-affinity SERT, the PMAT has been identified as a low-affinity transporter, with an apparent Km of 114 micromoles/l for serotonin; approximately 230 times higher than that of SERT. However, the PMAT, despite its relatively low serotonergic affinity, has a considerably higher transport 'capacity' than SERT, "resulting in roughly comparable uptake efficiencies to SERT in heterologous expression systems.”[26] The study also suggests some SSRIs, such as fluoxetine and sertraline anti-depressants, inhibit PMAT but at IC50 values which surpass the therapeutic plasma concentrations by up to four orders of magnitude. Therefore, SSRI monotherapy is "ineffective" in PMAT inhibition. At present, no known pharmaceuticals are known to appreciably inhibit PMAT at normal therapeutic doses. The PMAT also suggestively transports dopamine and norepinephrine, albeit at Km values even higher than that of 5-HT (330–15,000 μmoles/L).[26]

SerotonylationEdit
Serotonin can also signal through a nonreceptor mechanism called serotonylation, in which serotonin modifies proteins.[27] This process underlies serotonin's effects upon platelet-forming cells (thrombocytes) in which it links to the modification of signaling enzymes called GTPases that then trigger the release of vesicle contents by exocytosis.[28] A similar process underlies the pancreatic release of insulin.[27]

The effects of serotonin upon vascular smooth muscle tone (this is the biological function from which serotonin originally got its name) depend upon the serotonylation of proteins involved in the contractile apparatus of muscle cells.[29]
 
I wanted an official take.


Cannabis is a synergistic with opioids, meaning that a lower than threshold dose of each will get you greater results than either will alone.
- That makes it a good choice for tapering back opioids.

Legal states consistently find that active and operating dispensaries and access to cannabis leads to
  • Lower opioid deaths
  • Lower numbers of opioid prescriptions written

Numerous patient studies in the U.S., Canada and Israel have had respondents consistently reply that they choose to include cannabis in their regimen because
  • They feel better
  • They have fewer negative side effects

So we have this quandary of
  • Continuance of the Schedule 1 lie and all its inherent restrictions
  • Absolutely no clinical guidance from the governments
  • Widespread access to cannabis

It’s to our collective benefit to look at:
  • The supporting data for using cannabis for pain.
  • How we can use this data to best effect.
  • How to communicate that cannabis isn’t the cure-all or a poison. It’s one more pain medicine available to the patients, and this is how to use it. :love:

View media item 1754290

The ECS:
  • receptors
  • ligands
  • enzymes for control This is an interesting way to put this, and the first I’ve heard it expressed this way. :hmmmm:
The ECS is widespread through the cellular community, regulating
  • Memory
  • analgesia
  • appetite
  • stress
  • sleep
“Relax, eat, sleep, forget, protect.“

Tetrahydrocannabinol (THC) is analgesic, mood-altering, appetite stimulating.
- partial agonist to CB1 and CB2

  • Cannabidiol (CBD) doesn’t bind to any ECS receptors we know of.
    non-intoxicating
  • May be protective against the intoxicating effects of THC
  • anti-inflammatory
  • anti-convulsant
  • peripheral pain effects
I’ll finish later.The sheer number of varied cannabinoids in cannabis is causing some of the problem. Pharmaceutical companies like to isolate the effective molecule and market that. Cannabis has the infamous “Entourage Effect.”

Clinicians and researchers are frustrated about the rush of CBD products. You can buy the, anywhere, but to research effects to nail down therapeutic applications you must have a Schedule 1 permit. :straightface:
 
I get so exasperated when the systems don’t work well with my manic pace. I can’t edit properly today.

I’ll finish later.
 

Whew! She talks like a doctor. A translation will be a handy tool. What she shares is profound and energetic, but over most people’s heads.

She gives an impassioned retelling of how we came to be spaces of the medical community and how doctors became pill-pushers.

I may do a full transcript and then translate.
 
“....how we came to be spaces....”.

Gosh.... I don’t remember what I really meant to say there. :rofl:
 
SweetSue said:
I wanted an official take.


Cannabis is a synergistic with opioids, meaning that a lower than threshold dose of each will get you greater results than either will alone.
- That makes it a good choice for tapering back opioids.

Legal states consistently find that active and operating dispensaries and access to cannabis leads to
  • Lower opioid deaths
  • Lower numbers of opioid prescriptions written

Numerous patient studies in the U.S., Canada and Israel have had respondents consistently reply that they choose to include cannabis in their regimen because
  • They feel better
  • They have fewer negative side effects

So we have this quandary of
  • Continuance of the Schedule 1 lie and all its inherent restrictions
  • Absolutely no clinical guidance from the governments
  • Widespread access to cannabis

It’s to our collective benefit to look at:
  • The supporting data for using cannabis for pain.
  • How we can use this data to best effect.
  • How to communicate that cannabis isn’t the cure-all or a poison. It’s one more pain medicine available to the patients, and this is how to use it. :love:

View media item 1754290

The ECS:
  • receptors
  • ligands
  • enzymes for control This is an interesting way to put this, and the first I’ve heard it expressed this way. :hmmmm:
The ECS is widespread through the cellular community, regulating
  • Memory
  • analgesia
  • appetite
  • stress
  • sleep
“Relax, eat, sleep, forget, protect.“

Tetrahydrocannabinol (THC) is analgesic, mood-altering, appetite stimulating.
- partial agonist to CB1 and CB2

  • Cannabidiol (CBD) doesn’t bind to any ECS receptors we know of.
    non-intoxicating
  • May be protective against the intoxicating effects of THC
  • anti-inflammatory
  • anti-convulsant
  • peripheral pain effects
I’ll finish later.The sheer number of varied cannabinoids in cannabis is causing some of the problem. Pharmaceutical companies like to isolate the effective molecule and market that. Cannabis has the infamous “Entourage Effect.”

Clinicians and researchers are frustrated about the rush of CBD products. You can buy the, anywhere, but to research effects to nail down therapeutic applications you must have a Schedule 1 permit. :straightface:
Click to expand...

I listened to the rest of this, and the man falls into the official line of addiction and dependence concerns that I think are a bogus smokescreen to keep us from being courageous enough to return to the idea that we don’t need clinicians to heal. :straightface:

I get so tired of hearing about the dangers of cannabis when there is no real danger. I have no patience for perpetuating the erroneous science that was pursued with the sole intent to vilify cannabis.

The report by the National Academy Of Sciences has so little validity in my world where facts rule over propaganda and bad science that I turn off as soon as a speaker mentions that the data they’re going to present was gained by that report.

And that was where I lost interest with this young man, who speaks of the value of cannabis to save us from the opioid crisis out of one side of his mouth, then speaks of the addictive quality of a plant that one can’t get addicted to.

How can we be seen as credible when we hold to the lies?
 
SweetSue said:
I listened to the rest of this, and the man falls into the official line of addiction and dependence concerns that I think are a bogus smokescreen to keep us from being courageous enough to return to the idea that we don’t need clinicians to heal. :straightface:

I get so tired of hearing about the dangers of cannabis when there is no real danger. I have no patience for perpetuating the erroneous science that was pursued with the sole intent to vilify cannabis.

The report by the National Academy Of Sciences has so little validity in my world where facts rule over propaganda and bad science that I turn off as soon as a speaker mentions that the data they’re going to present was gained by that report.

And that was where I lost interest with this young man, who speaks of the value of cannabis to save us from the opioid crisis out of one side of his mouth, then speaks of the addictive quality of a plant that one can’t get addicted to.

How can we be seen as credible when we hold to the lies?
Click to expand...

It's an interesting thing: Let's look at the criteria for substance abuse.

Exhibit 2-6, DSM-IV-TR Criteria for Substance Abuse and Substance Dependence - Managing Chronic Pain in Adults With or in Recovery From Substance Use Disorders - NCBI Bookshelf

Exhibit 2-6DSM-IV-TR Criteria for Substance Abuse and Substance Dependence
CategoryCriteria
Substance AbuseA maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by one (or more) of the following, occurring within a 12-month period:
  • Recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences or poor work performance related to substance use; substance-related absences, suspensions, or expulsions from school; neglect of children or household)
  • Recurrent substance use in situations in which it is physically hazardous (e.g., driving an automobile or operating machinery when impaired by substance use)
  • Recurrent substance-related legal problems (e.g., arrests for substance-related disorderly conduct)
  • Continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance (e.g., arguments with spouse about consequences of intoxication, physical fights)
Click to expand...

There are problems with each area of how substance abuse is even defined. Here's the circular argument:

Cannabis is not universally accepted or legal. If you have substance-related legal problems, are suspended or expelled (or fired) from work or school, or have arguments with your family about those consequences of cannabis not being legal or accepted then you fit the diagnostic criteria for substance abuse. Because it is not always legal or accepted you will have at least one of these troubles potentially, even if the plants benefits you. So because you continue to use it for its benefits you are an abuser by definition.

That's how this is set up and it's a wrong way to look at it. There is a difference between the substance causing you to be violent and the system causing violence upon you, but the definition accepts both as "proof" of your abuse. It is BS.

Of course it's BS because the substance that finally allows you to live triggers the system to oppress you and it is that very oppression that is the proof you supposedly have a substance abuse problem, not your actual relationship with the substance.

Substance DependenceA maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more)of the following, occurring any time in a 12-month period:
  • Tolerance, as defined by either of the following: (a) a need for markedly increased amounts of the substance to achieve intoxication or desired effect, or (b) markedly diminished effect with continued use of the same amount of the substance
  • Withdrawal, as manifested by either of the following: (a) the characteristic withdrawal syndrome for the substance, or (b) the same (or closely related) substance is taken to relieve or avoid withdrawal symptoms
  • The substance is often taken in larger amounts or over a longer period than intended
  • There is a persistent desire or unsuccessful efforts to cut down or control substance use
  • A great deal of time is spent in activities necessary to obtain the substance, use the substance, or recover from its effects
  • Important social, occupational, or recreational activities are given up or reduced because of substance use
  • The substance use is continued despite knowledge of having a persistent physical or psychological problem that is likely to have been caused or exacerbated by the substance (e.g., current cocaine use despite recognition of cocaine-induced depression, continued drinking despite recognition that an ulcer was made worse by alcohol consumption)
Click to expand...

Again there are problems with the definition of dependence. If something helps you function then of course you will spend a great deal of time in activities to obtain it (like cultivating it). When society makes you choose between the substance that helps you and other activities due to its illicit status how is that a problem with the substance itself (for instance, the local dance is tonight but your pain is bad and you can't use in public so you stay home and medicate like a normal person)? And because of those social problems and legal problems you want to cut down and out but if you do the pain returns. This is further evidence of dependence. By the definition of tolerance some have tolerance to tylenol and ibuprofen as their pain may require increasing amounts to achieve the desired relief.

These definitions are problematic, but they are used when speaking about cannabis abuse and dependence.

Oh, on cannabis withdrawal for the definition above: CWS is new in DSM V. Here we go:


They were followed by the announcement of cannabis dependence criteria in the DSM-5 under the chapter on diagnosis of “Substance-Related and Addictive Disorders” (18). The specific diagnostic criteria are: Inclusion: Requires at least three of the following symptoms, developing within one week of ceasing (or reducing) cannabis use that has been heavy and prolonged.

i. Irritability; anger or aggression
ii. Nervousness or anxiety
iii. Sleep difficulty
iv. Decreased appetite or weight loss
v. Restlessness
vi. Depressed mood
vii. Somatic symptoms causing significant discomfort

Exclusion: If the symptoms are attributable to another medical condition or better explained by another mental disorder, including intoxication with or withdrawal from another substance, do not make diagnosis.
Click to expand...

Now, here again is where prohibition and the fact that cannabis is not accepted as medical treatment by the system cause problems.

If cannabis is not accepted to treat depression, anxiety, PTSD, and others then when you stop using cannabis and your symptoms appears again then instead of being seen as a natural consequence of stopping your medicine it is seen as proof of "withdrawal". This is a major blind spot in clinicians who do not understand the benefits of cannabis so those symptoms will not be attributed to the underlying disease but will be blamed on withdrawal from the substance used to treat the underlying disease.

The problem is that few are questioning the very definitions and those are the very things that need to be questioned and changed regarding substance abuse and dependence.

I mean, being arrested for simple possession is treated the same as having hallucinations while going on a rampage and biting off someone's face. It's ridiculous on its face.

I offer some grace to those stating the official facts, but those speaking on this subject have a responsibility to further educate themselves, to question the status quo, and to really get to know the people using this as medicine.

Hope that wasn't too long or intrusive.
 
A few notes from Anna Wilcox’s article “11 Facts About Cannabis And Pain You May Not Know” over at Green Flower Media. (3/7/2019)

Cannabis is effective against both pathological and inflammatory pain
  • Pathological pain = damage to the nervous system (i.e. injury, disease, surgery)
  • Inflammatory pain = caused by immune response (I.e. MS, fibromyalgia, arthritis)
Fear of euphoria keeps Cannabis from being studied as a pain medicine.

How have we allowed ourselves to become so brainwashed that feeling good is a criminal action? :hmmmm:

Pharmaceutical companies are looking into combining low-dose THC with opioids to create new medicines.

How ironic. Cannabis works well on its own and best as FECO, so let’s take a low dose of a synthetic THC and combine it with our poison. People will be fooled into overlooking the fact that we could have done it the other way around with low-dose opioids combined with higher-dose FECO.

Yeah...... that’s what keeps us doing what we do, educating. :battingeyelashes:

The biphasic nature of cannabis means high levels of THC may make some types of pain worse.
  • There appears to be a sweet spot for each individual.
  • Cannabis may be effective up to this spot.
  • Step past the sweet spot and you may cause some types of pain to worsen
Track it down Susan. Dose-dependent study on volunteers

Dose-dependent Effects of Smoked Cannabis on Capsaicin-induced Pain and Hyperalgesia in Healthy Volunteers (2007)

How sad.... over a decade and nothing to really follow this up? :oops:

Start low. Go slow.​

Proper dosage has many variables, the chief ones being
  • the type of pain being treated
  • the method of administration (the pathway into the body)
  • how the patient’s body processes cannabis (everyone’s different)

Both THC and CBD engage capsaicin receptors in the body, enhancing the inflammatory relief.
  • CBD isn’t intoxicating, making it attractive to those trying to avoid euphoria. Given how easy it’s proving to be to balance the cannabinoid values to tone down the wonderful euphoric effects of THC why is this still a concern?
Combining THC and CBD potentials both.

Russo’s Taming THC

  • The major cannabinoids work synergistically to relieve pain.
  • Add in the entourage effect of terpenes and the rest of the components in the essential oil of cannabis and you have more potential for enhanced pain relief.
  • Variety in strain/chemovar choice coupled with different pathways of treatment may be the best route.



 
Hebrew University did a study of chronic pain patients in 2016. Four years ago, and we’ still debating the issue. :oops:

Clin J Pain. 2016 Dec;32(12):1036-1043.
The Effect of Medicinal Cannabis on Pain and Quality-of-Life Outcomes in Chronic Pain: A Prospective Open-label Study.
Haroutounian S1, Ratz Y, Ginosar Y, Furmanov K, Saifi F, Meidan R, Davidson E.
Author information

Abstract
OBJECTIVES:
The objective of this prospective, open-label study was to determine the long-term effect of medicinal cannabis treatment on pain and functional outcomes in participants with treatment-resistant chronic pain.

PATIENTS AND METHODS:
The primary outcome was the change in the pain symptom score on the S-TOPS (Treatment Outcomes in Pain Survey-Short Form) questionnaire at the 6-month follow-up in an intent-to-treat population.

Secondary outcomes included
  • the change in S-TOPS physical,
  • social, and
  • emotional disability scales,
  • the pain severity, and
  • pain interference on the Brief Pain Inventory,
  • sleep problems, and
  • the change in opioid consumption.

RESULTS:
A total of 274 participants were approved for treatment;
  • complete baseline data were available for 206 (intent-to-treat),
  • and complete follow-up data for 176 participants.

At follow-up,
  • the pain symptom score improved from median 83.3 (95% confidence interval [CI], 79.2-87.5) to 75.0 (95% CI, 70.8-79.2) (P<0.001).
    The pain severity score (7.50 [95% CI, 6.75-7.75] to 6.25 [95% CI, 5.75-6.75]) and
  • the pain interference score (8.14 [95% CI, 7.28-8.43] to 6.71 [95% CI, 6.14-7.14]) improved (both P<0.001),
  • together with most social and emotional disability scores.
  • Opioid consumption at follow-up decreased by 44% (P<0.001).
  • Serious adverse effects led to treatment discontinuation in 2 participants.
DISCUSSION:

The treatment of chronic pain with medicinal cannabis in this open-label, prospective cohort resulted in
  • improved pain and
  • functional outcomes, and
  • a significant reduction in opioid use.

Results suggest long-term benefit of cannabis treatment in this group of patients,

but the study's noncontrolled nature should be considered when extrapolating the results.
 
Medical marijuana reduces use of opioid pain meds, decreases risk for some with chronic pain

DateMarch 22, 2016ContactContact: Laurel Thomas
ANN ARBOR—Patients using medical marijuana to control chronic pain reported a 64 percent reduction in their use of more traditional prescription pain medications known as opioids, a University of Michigan study finds.

The 185 patients from a medical marijuana dispensary in Ann Arbor also reported
  • fewer side effects from their medications and a
  • 45-percent improvement in quality of life since using cannabis to manage pain.

Researchers from the U-M School of Public Health and Medical School said their results suggest that for some people, medical marijuana may be an alternative to more common prescription painkillers at a time when national health leaders are asking the medical community to cut back on prescribing drugs like Vicodin and OxyContin.

A 65% reduction in ingested opioids and a 45% increase in quality of life, and they think it might be worth investigating. :oops:

“We’re in the midst of an opioid epidemic and we need to figure out what to do about it,” said Kevin Boehnke, lead author of the study and doctoral student in the School of Public Health’s Department of Environmental Health Sciences. “I’m hoping our research continues a conversation of cannabis as a potential alternative for opioids.”

Just last week, the Centers for Disease Control and Prevention issued 12 recommended guidelines for prescribing opioids, saying prescriptions for them have quadrupled since 1999, and that 40 people die every day from an overdose of these drugs.

“We are learning that the higher the dose of opioids people are taking, the higher the risk of death from overdose. This magnitude of reduction in our study is significant enough to affect an individual’s risk of accidental death from overdose,” said study senior author Dr. Daniel Clauw, professor of pain management anesthesiology at the U-M Medical School.

Surveys were conducted from November 2013 to February 2015.

The researchers originally set out to find out if cannabis use was more effective for sufferers with severe centralized chronic pain, for whom the opioids have not always worked well.

“We hypothesized that cannabis might be particularly effective for the type of pain seen in conditions such as fibromyalgia, since there are many studies suggesting that synthetic cannabinoids work in these conditions,” Clauw said. “We did not see this because the patients in this study rated cannabis to be equally effective for those with different pain severity.”

It was the patients with less severe chronic pain who reported better quality of life and less use of opioids.

“We would caution against rushing to change current clinical practice towards cannabis, but note that this study suggests that cannabis is an effective pain medication and agent to prevent opioid overuse,” Boehnke said.

At present, 23 states and the District of Columbia have legalized cannabis for medical purposes and four states allow it for recreational use.

The numbers are now up to 33 states with medical and 11 with full access. And we still lack a cohesive look at what cannabis can do to counter what doctors did by writing all those damned prescriptions.

I sure find solace in the profit margins everyone’s collecting. :straightface:

The researchers said population level research has shown a reduction in opioid use in states where medical cannabis is legal, but the U-M study is one of the first to look at individual patterns of use. A study also released this month from Israel followed people for six months and found a 44-percent reduction in opioid use.

The researchers said one limitation of their study, however, is that it was conducted with people at a dispensary who are presumed to be believers in the medical benefits of marijuana. These participants were surveyed after they had been using marijuana, which may decrease the accuracy of their recollections. Say what? :hmmmm:

The team plans to continue research with this population but also conduct studies with patients who have not yet tried marijuana for pain management.

I wonder if they’ve done this additional research yet? Time to go looking,...... after I take a break.

Dr. Evangelos Litinas of Ann Arbor also was a member of the research team.
 
Source
Cannabis and Pain: A Clinical Review
Kevin P. Hill, Matthew D. Palastro, [...], and Joseph W. Ditre

Abstract

Introduction: Cannabis has been used for medical purposes across the world for centuries. As states and countries implement medical and recreational cannabis policies, increasing numbers of people are using cannabis pharmacotherapy for pain. There is a theoretical rationale for cannabis' efficacy for pain management, although the subjective pain relief from cannabis may not match objective measurements of analgesia. As more patients turn to cannabis for pain relief, there is a need for additional scientific evidence to evaluate this increase.

Materials and Methods: Research for this review was performed in the PubMed/National Library of Medicine database.

Discussion: Preclinical studies demonstrate a narrow therapeutic window for cannabis as pharmacotherapy for pain; the body of clinical evidence for this indication is not as extensive. A recent meta-analysis of clinical trials of cannabis and cannabinoids for pain found modest evidence supporting the use of cannabinoid pharmacotherapy for pain. Recent epidemiological studies have provided initial evidence for a possible reduction in opioid pharmacotherapy for pain as a result of increased implementation of medical cannabis regimens.

Conclusion: With increased use of medical cannabis as pharmacotherapy for pain comes a need for comprehensive risk-benefit discussions that take into account cannabis' significant possible side effects. As cannabis use increases in the context of medical and recreational cannabis policies, additional research to support or refute the current evidence base is essential to attempt to answer the questions that so many healthcare professionals and patients are asking.

Keywords: : anandamide, cannabidiol, cannabinoids, endocannabinoid, pain, THC
 
SweetSue said:
These participants were surveyed after they had been using marijuana, which may decrease the accuracy of their recollections. Say what? :hmmmm:
Click to expand...

Their concern is confirmation bias on the part of participants. If they believe it will work it is more likely to work, i.e. the placebo effect.

Double blind studies with controls are the gold standard. Even they have limitations (what population was studied, etc;...). Self report surveys are vulnerable to a number of biases including not just confirmation but also related to social acceptance and to perceived bias of researchers per the study participants (IOW, how do those taking the survey perceive what the researchers' aims are in doing the study) among other biases.
 

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