Cannabis compounds may boost metabolic health while supporting weight loss: Study

 Say it isn't so. 'Reefer Madness' was a documentary, wasn't it?

Cannabis compounds may boost metabolic health while supporting weight loss: Study

What Does the Reclassification of Marijuana Mean for Physicians?

 It means your competent? doctor should be able to prescribe marijuana for the benefits to stroke recovery. Unless you have a stick in the mud doctor who still believes in 'Reefer Madness'.

 I'm doing it after my next stroke.

My 13 reasons for marijuana use post-stroke.  

Don't follow me, I'm not medically trained and I don't have a Dr. in front of my name.

This: 

Pot Smoking Baby Boomers Are On The Rise, Why Are Scientists So Happy For Them? Hint: Benefits For The Aging Brain

And this:

The Experiments Revealing How Marijuana Could Treat Dementia

The latest here:

What Does the Reclassification of Marijuana Mean for Physicians?

Governmental figures have spent decades debating the laws and regulations regarding cannabis. The current political climate has reinvigorated a proposal to downgrade the drug class of marijuana from a Schedule I to Schedule III controlled substance.¹ It remains unclear, however, whether this proposal is solely political grandstanding, or if the change would have serious implications for medical practices and patients.

We spoke to Dr Mikhail Kogan, associate professor of medicine and medical director at the George Washington University (GWU) Center for Integrative Medicine,² as well as Griffen J Thorne, a partner at Lewis Brisbois and chair of the Lewis Brisbois Cannabis, Hemp, and Regulated Substances Practice,³ to help discern the possible effects of the reclassification of marijuana.

The Reclassification of Marijuana

Thorne believes reclassification will not affect the average person. Politicians claim no individual should be in jail for the use of marijuana; however, if political figures really wanted to ensure that was the reality, they would need to consider de-scheduling the substance and allowing the states or at least 1 federal agency to regulate it, as is the case with tobacco and alcohol, he explained.

Reclassifying marijuana from a Schedule I to Schedule III substance means that any individual found in possession of the substance could still face penalties or jail time from federal law enforcement or law enforcement in states that have not yet regulated marijuana. “The idea that no one will be arrested is inaccurate,” Thorne further clarified.

Rescheduling marijuana from Schedule 1 to Schedule III is unlikely to remedy any societal or legal ramifications of marijuana use. Nonetheless, this change could help advance research on this medicinal substance.

Although the reclassification of marijuana may not impact the average person in certain respects, Thorne believes it will likely reduce tax burdens for state-licensed cannabis businesses and enable more research opportunities, which may have downstream effects on clinical practices and social stigmas.

The Potential Impact of Rescheduling on Drug Research

According to Dr Kogan, the reclassification of marijuana will open new doors for research.

“Reclassifying marijuana from Schedule I to a lower schedule would significantly ease the regulatory burden on researchers. A lower classification would streamline the process for obtaining necessary federal licenses and funding,” Dr Kogan explained. This change would lead to more studies and a greater variety of research since researchers won’t need to obtain Schedule I licenses and follow required Schedule I procedures. 

Dr Kogan continued, “With fewer regulatory hurdles, studies could expand to explore the impacts of marijuana on conditions beyond pain management, such as neurologic disorders, mental health conditions, autoimmune diseases, and more.”

Current research demonstrates the promising effects of cannabis when it is used to treat seizure disorders, symptoms of multiple sclerosis (MS), and chronic pain. However, cannabis-based medications are already available for these conditions.⁴ Broadening research on marijuana could help better understand the risks vs benefits of its use in healthy populations and for specific mental or physical conditions.

Public Health Implications of Rescheduling Marijuana

As a Schedule 1 drug, cannabis is said to have “no accepted medical purpose” and a high risk for abuse.⁵ Although this may be debatable, clear criteria have been established for cannabis use disorder (CUD), which is defined as the continued use of cannabis and an inability to quit regardless of harmful consequences.⁴

Per the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), cannabis use and dependence can be defined as “a problematic pattern” that includes at least 2 of the following criteria over the span of 1 year:⁵

• Cannabis is usually consumed in more significant amounts or over a longer period than originally intended;      
• Efforts to cut down or control cannabis use are unsuccessful;      
• A lot of time is spent engaging in activities that are necessary to obtain or use cannabis, or recover from its effects;      
• A craving or a strong desire or urge to use cannabis persists;      
• Recurrent cannabis use results in failure to fulfill work or school obligations, or obligations at home;      
• Uninterrupted cannabis use, despite having continued social or interpersonal problems due to or exacerbated by the effects of cannabis;      
• Important social, occupational, or recreational activities are forfeited or reduced in number due to cannabis use;
• Recurrent use of cannabis even if in an environment in which cannabis is physically hazardous;      
• Cannabis use continues despite knowledge of having a persistent or recurrent physical or psychologic problem that is likely to have been attributable to or exacerbated by cannabis;
• Increased tolerance, defined by either a need for markedly increased cannabis to achieve intoxication or desired effect, or a markedly diminished effect with continued use of the same amount of the substance; or,      
• Experiencing a withdrawal, as manifested by either the characteristic withdrawal syndrome for cannabis, or cannabis is taken to relieve or avoid withdrawal symptoms.

“Reclassification should consider the potential for increased marijuana use and risk for CUD,” stated Dr Kogan. “Education and preventive measures must be in place to mitigate these risks. However, it is unlikely that recreational marijuana use and CUD risk will increase considering its widespread use, despite its current legal status,” continued Dr Kogan.

Health care providers should receive updated training on the risks and benefits of marijuana use, including the identification and management of CUD, Dr Kogan stated. “For example, there are currently no required standards in any health care training curriculum. Our GWU medical cannabis research team recently finished developing a national standard for medical schools and we are waiting to get it published before advocating for broad acceptance,” he shared.

The ways in which reclassification might affect different populations, particularly vulnerable groups who might be at higher risk for substance use disorders (SUDs), must also be considered. Research suggests that men in high-income countries have the greatest risk for CUD.⁴

Finally, evidence-based policies must be prioritized. “Policymaking should be guided by current scientific evidence and continuous research should inform adjustments to regulations and guidelines,” advised Dr Kogan.

Discussing Marijuana and Cannabis Use With Patients

Cannabis policy reform may further promote the common misbelief that marijuana and cannabis products are completely natural and risk-free. As a result, clinicians remain responsible for messaging on the potential risks, both short- and long-term, particularly for young adults and pregnant women. In addition, adults must stay vigilant about the dangers of accidental intoxication in children and safely store cannabis out of the reach of children.⁵

Physicians should approach marijuana use with an open and nonjudgmental attitude to encourage honest communication, warned Dr Kogan. When engaging with patients, Dr Kogan suggested utilizing the following process:

• Assess use: Ask patients about their marijuana use (ie, frequency, methods of use, reasons for use) in a routine and standard way. Discuss use in the context of symptom management, not “drug use.”
• Provide education: Provide evidence-based information about the potential benefits and risks of marijuana use. 
• Offer personalized advice: Tailor advice based on the patient’s medical history, current health status, and specific conditions being treated. For example, discuss potential interactions with other medications and the impact of marijuana on chronic conditions.
• Share safety precautions: Advocate for safe practices (ie, avoiding smoking) and the consideration of alternative methods (ie, topical, oral, sublingual, rectal). 

The Future of Marijuana Rescheduling

Rescheduling marijuana from a Schedule 1 to Schedule III drug is not likely to remedy any societal or legal ramifications of marijuana use. Nonetheless, this change could help advance research on the substance.

While certain populations may benefit from the use of marijuana and cannabis products, the potential dangers shouldn’t be overlooked, especially in young and healthy populations. Not only is marijuana associated with a risk for CUD, its use can also induce changes in brain development, reduced intelligence, driving impairments, the “unmasking of chronic psychotic disorders,” and negative effects on fertility and pregnancy outcomes.⁴

Physicians should better counsel patients on the potential health risks of using cannabis to treat self-treat chronic, neurologic, and psychiatric conditions.

The U.S. Drug Enforcement Administration (DEA) hearing on the proposed rescheduling of marijuana on January 21, 2025 has been postponed, which has delayed the process for approximately 3 months.⁶

The Long-Term Consequences of Marijuana Use For The Brain

Oh my, the propaganda is getting worse and worse.(Reefer Madness strikes again)  Never mind how helpful it might be to stroke survivors, including your parents and grandparents. Any use for stroke would likely be short term.
I'm not medically trained so I obviously don't know anything.  But I will do marijuana after my next stroke.

My 13 reasons for marijuana use post-stroke. 

Consuming Cannabis Could Slash Your Chances Of Blood Clots, Stroke: Study

The Long-Term Consequences of Marijuana Use For The Brain

Study reveals how long-term marijuana use affects the brain’s structure and function.

Regular marijuana users have increased connectivity in their brains, despite having some gray matter loss in areas related to addiction, a study finds.

The research, published in the Proceedings of the National Academy of Sciences, is the first to use multiple brain scanning techniques to examine both the structure and function of the brain.

Dr. Sina Aslan, one of the study’s authors, explained:

“What’s unique about this work is that it combines three different MRI techniques to evaluate different brain characteristics.

The results suggest increases in connectivity, both structural and functional that may be compensating for gray matter losses.

Eventually, however, the structural connectivity or ‘wiring’ of the brain starts degrading with prolonged marijuana use.”

The study involved 48 adult marijuana users who used the drug, on average, three times a day (Filbey et al., 2014).

They were compared to 62 matched non-users of marijuana.

The researchers found that the pattern of changes in both connectivity and structure of the brain depended on when and how often the drug was used.

Increases in connectivity were greatest when people began to use the drug and, the more they used it, the greater those increases.

Over time, though, an area of the brain called the orbitofrontal cortex is smaller in long-term marijuana users.

This area is crucial in how we make decisions and is central to how to brain processes rewards.

Taken together, this may explain why long-term marijuana users often seem to be doing reasonably well: structural losses in one area are being compensated for by connectivity gains.

It may also explain why the studies on marijuana’s effects on the brain have been so varied — some saying there is little damage, others more alarmist.

Dr. Francesca Filbey, who led the study, said:

“To date, existing studies on the long-term effects of marijuana on brain structures have been largely inconclusive due to limitations in methodologies.

While our study does not conclusively address whether any or all of the brain changes are a direct consequence of marijuana use, these effects do suggest that these changes are related to age of onset and duration of use.”

We still don’t know, though, the long-term effects of occasional marijuana use or whether the changes revert back to normal after drug-use is stopped.

Dr. Filbey concluded:

“We have seen a steady increase in the incidence of marijuana use since 2007.

However, research on its long-term effects remains scarce despite the changes in legislation surrounding marijuana and the continuing conversation surrounding this relevant public health topic.”

This study provides a fascinating insight into a controversial area.

Cannabinoids found to be suitable treatment for migraine attacks

You might want this treatment to reduce your stroke risk. But I bet your doctor won't even mention it, 'Reefer Madness' you know.

Migraine linked to increased stroke risk in women

Cannabinoids found to be suitable treatment for migraine attacks

• Download PDF Copy

June 24, 2017

A study presented at the Congress of the European Academy of Neurology in Amsterdam confirmed that cannabinoids are just as suitable as a prophylaxis for migraine attacks as other pharmaceutical treatments. Interestingly though, when it comes to treating acute cluster headaches they are only effective in patients that suffered from migraine in childhood.
Germany's recent decision to liberalize the use of cannabis for medical purposes has rekindled policy debate across Europe. While politics and health authorities continue to weigh up the pros and cons of this treatment method, researchers are constantly furthering scientific understanding of the use of cannabinoids.
Progress was reflected in the results of a current Italian study presented at the 3rd Congress of the European Academy of Neurology (EAN). A research team led by Dr. Maria Nicolodi investigated the suitability of cannabinoids as a prophylaxis for migraine and in the acute treatment of migraines and cluster headaches. To start with the researchers had to identify the dosage required to effectively treat headaches. A group of 48 chronic migraine volunteers were given a starting oral dose of 10mg of a combination of two compounds. One contained 19 percent tetrahydrocannabinol (THC), and while the other had virtually no THC it had a 9 percent cannabidiol (CBD) content. The outcome was that doses of less than 100mg produced no effects. It was not until an oral dose of 200mg was administered that acute pain dropped by 55 per cent.
In phase 2 of the study, 79 chronic migraine patients were given a daily dose of either 25mg of amitriptyline - a tricyclic antidepressant commonly used to treat migraine - or 200mg of the THC-CBD combination for a period of three months. 48 cluster headache patients also received either 200mg THC-CBD or a daily dose of 480mg of the calcium channel blocker verapamil. For acute pain, an additional 200mg TCH-CBD was administered for both types of headaches.

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The results after three months of treatment and follow-up after a further four weeks produced various insights. While the TCH-CBD combination yielded slightly better results than amitriptyline (40.1 percent) with a 40.4 percent reduction in attacks, the severity and number of cluster headache attacks only fell slightly. When analyzing use in the treatment of acute pain, the researchers came across an interesting phenomenon: cannabinoids reduced pain intensity among migraine patients by 43.5 percent. The same results were seen in cluster headache patients, but only in those that had experienced migraine in childhood. In patients without previous history, THC-CBD had no effect whatsoever as an acute treatment. "We were able to demonstrate that cannabinoids are an alternative to established treatments in migraine prevention. That said, they are only suited for use in the acute treatment of cluster headaches in patients with a history of migraine from childhood on," Dr Nicolodi summarized.
Drowsiness and difficulty concentrating aside, the side effects observed during the study were highly positive. The incidence of stomach ache, colitis and musculoskeletal pain - in female subjects - decreased.

Source:

http://www.bkkommunikation.com/en/

Cannabis use not associated with stroke risk in young adults

Well duh, this was so obvious that the smoking was the problem, not the cannabis. But the damage was done, our stupid federal legislators will not remember the corrected headlines. They prefer to remember 'Reefer Madness'. I will assume that over 45 years of age would have the same negative correlation.

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training.

Your Mom and Grandmother need to be screaming in their faces that marijuana is useful for stroke rehab, so get the fuck out of the way.
http://www.healio.com/cardiology/stroke/news/online/%7B791de373-10b4-44f9-bcf3-262bdf2ff051%7D/cannabis-use-not-associated-with-stroke-risk-in-young-adults?
Cannabis use in young adulthood was not associated with incidence of stroke in adults younger than 60 years, according to new data.

However, tobacco smoking had a significant dose-response relationship with stroke risk.
“Recently, a growing body of research has linked cannabis use to stroke, particularly to those occurring before 45 years of age,” Daniel Falkstedt, PhD, of the department of public health sciences at the Karolinska Institutet, and colleagues wrote. “It seems cannabis-associated strokes usually occur in chronic or current cannabis users who also smoke tobacco, either in combination with or immediately after cannabis use.”
Falkstedt and colleagues studied Swedish men (n = 49,321) who were conscripted into military services in 1969-1970 at age 18 to 20 years. Cannabis, tobacco and alcohol use were assessed at baseline. Stroke incidence was obtained from national databases until age 59 years.
During the follow-up period, 1,037 strokes occurred, 192 of which happened at age 45 years or younger.
Factors that were significantly more common in men with stroke before age 60 years included: parental history of CVD, being overweight, low cardiorespiratory fitness, low socioeconomic position in childhood, short schooling, heavy smoking and high alcohol consumption.
According to data, heavy cannabis use (> 50 times) in young adulthood showed no association with stroke incidence at age 45 years or younger (HR = 0.93; 95% CI, 0.34-2.57) or up to age 60 years (HR = 0.95; 95% CI, 0.59-1.53) in multivariable models.
In crude models, the risk for ischemic stroke during the follow-up period for participants with heavy cannabis use was almost two times higher compared with nonusers. However, a dose-response shaped association with ischemic stroke was seen only with tobacco use and not alcohol or cannabis use, and the risk for ischemic stroke with heavy cannabis use was attenuated after adjustment for tobacco use (HR = 1.47; 95% CI, 0.83-2.56).
Smoking 20 or more cigarettes per day was associated with stroke at age 45 years or younger (HR = 5.04; 95% CI, 2.8-9.06) and with stroke up to age 60 years (HR = 2.15; 95% CI, 1.61-2.88), according to the researchers.
“We have expanded current knowledge by examining cannabis use in young adulthood in relation to the subsequent risk of stroke in a large population-based cohort,” Falkstedt and colleagues wrote. “We found no evident association between cannabis use and stroke, including stroke before 45 years of age. Tobacco smoking, however, showed a clear, dose-response shaped association with stroke across multivariable models.” – by Cassie Homer

Cannabinoid Type-2 Receptor Drives Neurogenesis and Improves Functional Outcome After Stroke

We will never get this in the United States until all our stupid federal legislators are replaced with intelligent persons that aren't scared of 'Reefer Madness'. You better plan on traveling to more enlightened countries for research and recovery.
http://stroke.ahajournals.org/content/48/1/204?etoc=

Isabel Bravo-Ferrer, María I. Cuartero, Juan G. Zarruk, Jesús M. Pradillo, Olivia Hurtado, Víctor G. Romera, Javier Díaz-Alonso, Juan M. García-Segura, Manuel Guzmán, Ignacio Lizasoain, Ismael Galve-Roperh, María A. Moro

https://doi.org/10.1161/STROKEAHA.116.014793

Stroke. 2017;48:204-212

Originally published November 29, 2016

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Abstract

Background and Purpose—Stroke is a leading cause of adult disability characterized by physical, cognitive, and emotional disturbances. Unfortunately, pharmacological options are scarce. The cannabinoid type-2 receptor (CB2R) is neuroprotective in acute experimental stroke by anti-inflammatory mechanisms. However, its role in chronic stroke is still unknown.

Methods—Stroke was induced by permanent middle cerebral artery occlusion in mice; CB2R modulation was assessed by administering the CB2R agonist JWH133 ((6aR,10aR)-3-(1,1-dimethylbutyl)-6a,7,10,10a-tetrahydro-6,6,9-trimethyl-6H-dibenzo[b,d]pyran) or the CB2R antagonist SR144528 (N-[(1S)-endo-1,3,3-trimethylbicyclo-[2.2.1]-heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide) once daily from day 3 to the end of the experiment or by CB2R genetic deletion. Analysis of immunofluorescence-labeled brain sections, 5-bromo-2´-deoxyuridine (BrdU) staining, fluorescence-activated cell sorter analysis of brain cell suspensions, and behavioral tests were performed.

Results—SR144528 decreased neuroblast migration toward the boundary of the infarct area when compared with vehicle-treated mice 14 days after middle cerebral artery occlusion. Consistently, mice on this pharmacological treatment, like mice with CB2R genetic deletion, displayed a lower number of new neurons (NeuN⁺/BrdU⁺ cells) in peri-infarct cortex 28 days after stroke when compared with vehicle-treated group, an effect accompanied by a worse sensorimotor performance in behavioral tests. The CB2R agonist did not affect neurogenesis or outcome in vivo, but increased the migration of neural progenitor cells in vitro; the CB2R antagonist alone did not affect in vitro migration.

Conclusions—Our data support that CB2R is fundamental for driving neuroblast migration and suggest that an endocannabinoid tone is required for poststroke neurogenesis by promoting neuroblast migration toward the injured brain tissue, increasing the number of new cortical neurons and, conceivably, enhancing motor functional recovery after stroke.

CB1 and CB2 Cannabinoid Receptor Antagonists Prevent Minocycline-Induced Neuroprotection Following Traumatic Brain Injury in Mice

It should not be called neuroprotection, it is stopping the neuronal cascade of death. Bet this never gets approved for stroke survivors in the USA. It is better to let survivors stay disabled rather than allow 'Reefer Madness' to take place in our elderly population. 

CB1 and CB2 Cannabinoid Receptor Antagonists Prevent Minocycline-Induced Neuroprotection Following Traumatic Brain Injury in Mice

1. Ana Belen Lopez-Rodriguez1,5,
2. Eleni Siopi2,
3. David P. Finn4,
4. Catherine Marchand-Leroux2,
5. Luis M. Garcia-Segura5,
6. Mehrnaz Jafarian-Tehrani2,3 and
7. Maria-Paz Viveros1⇑

+ Author Affiliations

1. ¹Faculty of Biology, Department of Animal Physiology (Animal Physiology II), Complutense University of Madrid—Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain,
2. ²Faculté des Sciences Pharmaceutiques et Biologiques, Laboratoire de Pharmacologie de la Circulation Cérébrale (EA4475),
3. ³CNRS UMR 8194, UFR Biomédicale des Saints-Pères, Université Paris Descartes, Sorbonne Paris Cité, Paris, France,
4. ⁴Pharmacology and Therapeutics, School of Medicine, NCBES Neuroscience Cluster and Centre for Pain Research, National University of Ireland Galway, Galway, Ireland
5. ⁵Instituto Cajal, Consejo Superior de Investigaciones Cientificas (CSIC), Madrid, Spain

1. Address correspondence to Maria-Paz Viveros, Department of Animal Physiology (Animal Physiology II), Faculty of Biology, Complutense University of Madrid, Calle Jose Antonio Novais 2, Madrid 28040, Spain. Email: pazviver@bio.ucm.es

Abstract

Traumatic brain injury (TBI) and its consequences represent one of the leading causes of death in young adults. This lesion mediates glial activation and the release of harmful molecules and causes brain edema, axonal injury, and functional impairment. Since glial activation plays a key role in the development of this damage, it seems that controlling it could be beneficial and could lead to neuroprotective effects. Recent studies show that minocycline suppresses microglial activation, reduces the lesion volume, and decreases TBI-induced locomotor hyperactivity up to 3 months. The endocannabinoid system (ECS) plays an important role in reparative mechanisms and inflammation under pathological situations by controlling some mechanisms that are shared with minocycline pathways. We hypothesized that the ECS could be involved in the neuroprotective effects of minocycline. To address this hypothesis, we used a murine TBI model in combination with selective CB1 and CB2 receptor antagonists (AM251 and AM630, respectively). The results provided the first evidence for the involvement of ECS in the neuroprotective action of minocycline on brain edema, neurological impairment, diffuse axonal injury, and microglial activation, since all these effects were prevented by the CB1 and CB2 receptor antagonists.

Three FDA-approved THC drugs are Marinol, Cesamet and Syndros.

If there is any protocol using these drugs to address uses for stroke I can't find it.
The three FDA-approved drugs are Marinol, Cesamet and Syndros. 
This article below is basically an extended version of reefer madness, you can't trust people to use marijuana responsibly. FUD (Fear, Uncertainty, Doubt). That will prevent us ever getting marijuana legalized unless you get your elderly mom and grandma to start screaming in our federal legislators faces. And we need it completely legalized before we will ever get open research on it.
My 13 reasons for marijuana use post-stroke. I would have to self treat my stroke rehab needs because we have NO stroke leadership or strategy to figure out how to create THC or marijuana protocols. I can't self treat using any form of medical marijuana including this THC because it would require getting a prescription and with no protocol doctors are not going to write prescriptions. Our fucking failures of stroke associations are doing nothing to actually help survivors by creating stroke protocols and solving all the fucking problems in stroke.

Pot Pushers’ Dirty Little Secret: Legal THC Pills

How Does Marijuana Affect the Brain and Behavior? Here's What Recent Studies Say

My God, anything to put a negative spin on marijuana. We already know that young brains aren't fully developed until 26-28, so unless we know the age of the participants this may not be a valid conclusion. We'll never know because we have NO stroke strategy or stroke leadership in any part of stroke. But Reefer Madness strikes again.
The sky is falling article here:

How Does Marijuana Affect the Brain and Behavior? Here's What Recent Studies Say

Actual research article here: It references young adults. Can't tell who sponsored the research.

Effects of marijuana use on impulsivity and hostility in daily life

Cannabis Use: Signal of Increasing Risk of Serious Cardiovascular Disorders

Oh my god, reefer madness strikes again. Only by reading well into this report do you find that tobacco use was also involved, but they blamed the addition of cannabis for the problems. So rather than analyzing the tipping point of smoke inhalation as to the cause of these problems they seemed to go after their pre-identified bogeyman.
http://jaha.ahajournals.org/content/3/2/e000638.full
Don't follow anything I suggest:
My 13 reasons to use it post-stroke.