Older People Seeking Care for Cannabis Use at Greater Risk for Dementia, Study Finds

 What an alarmist headline! I'm doing it after my next stroke to recover. Unless you have a stick in the mud doctor who still believes in 'Reefer Madness'.

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

 I consider most of this just self-medication, not marijuana causing the problem.

The latest here:

Older People Seeking Care for Cannabis Use at Greater Risk for Dementia, Study Finds

Users needing emergency care or hospitalization were more likely to later develop dementia, researchers reported. That does not prove cannabis was the cause.Roni Caryn Rabin April 14, 2025 Updated  4:11 p.m. ET Middle-aged and older adults who sought hospital or emergency room care because of cannabis use were almost twice as likely to develop dementia

 over the next five years, compared with similar people in the general population, a large Canadian study reported on Monday. When compared with adults who sought care for other reasons, the risk of developing dementia was still 23 percent higher among users of cannabis, the study also found. The study included the medical records of six million people in Ontario from 2008 to 2021. The authors accounted for health and sociodemographic differences between comparison groups, some of which play a role in cognitive decline. The data do not reveal how much cannabis the subjects had been using, and the study does not prove that regular or heavy cannabis use plays a causal role in dementia. But the finding does raise serious concerns that require further exploration, said Dr. Daniel T. Myran, the first author of the study, which was published in JAMA Neurology. “Figuring out whether or not cannabis use or heavy regular chronic use causes dementia is a challenging and complicated question that you don’t answer in one study,” said Dr. Myran, an assistant professor of family medicine at University of Ottawa. “This contributes to the literature and to a sign, or signal, of concern.” Dr. Myran’s previous research has found that patients with cannabis use disorder died at almost three times the rate of individuals without the disorder over a five-year period. He has also reported that more cases of schizophrenia and psychosis in Canada have been linked to cannabis use disorder since the drug was legalized. The latest study, focusing on dementia, adds to a growing body of literature on regular or heavy cannabis use and cognition. Researchers have reported impacts on verbal learning, memory and attention, while imaging studies have pointed to changes in the brain related to the use of cannabis and other substances Veterans with traumatic brain injuries in addition to cannabis use disorder may be at heightened risk for early-onset dementia, researchers reported last year. But many of the studies are relatively small. The new report’s strength was its large sample and the ability to track patients over time who did not have a diagnosis of dementia when they entered the study, said Madeline Meier, an associate professor of psychology at Arizona State University, who was not involved in the study. “They were able to rule out dementia at the time of the first cannabis visit, and were able to show the temporal order — the cannabis came first, and the dementia came second,” said Dr. Meier. Her research, whic has followed and periodically tested a cohort of over 1,000 individuals over a period of many years, has linked cannabis use and neuropsychological decline. “I think you want to combat this whole idea that cannabis is harmless and maybe even has some medical benefits,” Dr. Meier said. “This study is showing an association that I think people should take seriously and say, ‘Maybe this is putting me at risk.’” She noted that the work by Dr. Myran and his colleagues also found that people seeking care for alcohol use were even more likely to receive a dementia diagnosis than were cannabis users. “I’m worried about the substance abuse in that Baby Boomer age,” she said. More and more people, including seniors, are using cannabis. Medical visits related to cannabis increased more than fivefold among adults 45 and older between 2008 and 2021, the new study found. Among adults 65 and over, visits increased almost 27-fold. The study included more than 6 million people age 45 and over who did not have a diagnosis of dementia at the start of the research. Of them, 16,275 had an acute-care medical encounter because of cannabis. The patients with cannabis-related visits were compared to the matched general population, and in a separate comparison, to 140,824 matched patients who needed medical care for all other reasons. Within five years, 5 percent of those with acute care cannabis visits received a dementia diagnosis. The figure for individuals needing care for other reasons was 3.6 percent, and for similar individuals in the general population, 1.3 percent. But people who are heavy cannabis users differ from those who are not in a variety of ways, some of which may help explain the increased risk for dementia, Dr. Myran explained. While some of the factors can be accounted for, he said, “you can’t control for all of them.” Another unknown is self-medication,(THIS!) he said. Someone who has started experiencing symptoms of cognitive decline may be more likely to turn to cannabis. If so, then “it looks as if the cannabis is causing dementia, but it’s just on the pathway — they were already developing dementia,” Dr. Myran said. After making adjustments for age, sex, income and other factors, including other health conditions, he and his colleagues determined that patients who sought care for cannabis-related reasons were 1.23 times as likely as those who had gotten any kind of acute care to be diagnosed with dementia, and 1.72 times as likely as those in the healthier general population. A correction was made on April 14, 2025 Because of an editing error, an earlier version of this article referred incorrectly to the active ingredient in marijuana. It is tetrahydrocannabinol, not cannabis. When we learn of a mistake, we acknowledge it with a correction. If you spot an error, please let us know at

Mushroom bioactives—polysaccharides to psilocybin: a viewpoint on the therapeutic use of mushrooms for consumers and patients for health and neuroplasticity

Well, hasn't your doctor already prescribed various types of psychedelics to get you recovered? 

What about all these drugs for stroke recovery? Doesn't your doctor read the literature?

DMT (8 posts to November 2020)

ecstasy (19 posts to November 2012)

LSD (5 posts to September 2018)

CerAxon (5 posts to January 2012)

citicoline (15 posts to October 2011)

magic mushrooms (10 posts to October 2014) 

psilocybin (14 posts to May 2014)

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. 

The latest here:

Mushroom bioactives—polysaccharides to psilocybin: a viewpoint on the therapeutic use of mushrooms for consumers and patients for health and neuroplasticity

, ,

Translational Food Sciences, Volume 1, Issue 1, January 2025, vxaf001, https://doi.org/10.1093/trfood/vxaf001

Published:

02 April 2025

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Abstract

The use of mushrooms in health-promoting foods and substances is widely studied. There are compelling data to indicate that polysaccharides and phenolic compounds derived from mushroom sources have long-lasting metabolic effects when ingested. More recently, attention has returned to the traditional practices of using psychotropic bioactive ingredients obtained from mushrooms for the aid of the treatment of trauma and neuroplasticity therapeutic uses in alternative health practices. While this is heavily legislated and not universally accepted in all of the governments in the world, clinicians and psychotherapy professionals are reimagining the safe and controlled use of these substances (namely psilocybin-based compounds) for health management procedures. This short viewpoint article poses the question, aiming to create a debate of the potential use, as to whether these polysaccharides and psilocybin compounds could, or even should, have an alchemical role to play for consumers and patients in terms of health and neuroplasticity in therapeutic use as foods or medicines? What level of regulation would be required? And what safeguards should be implemented?

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Unraveling Berberine's Molecular Mechanisms in Neuroprotection against Neurodegeneration

 

 I started using berberine years ago because this: Berberine reduces triglycerides levels and systolic blood pressure.^123,124

Don't follow me, I'm not medically trained, is your doctor trained in this?

Novel Berberine Drug Cut HbA1c in Type 2 Diabetes

The latest here:

Unraveling Berberine's Molecular Mechanisms in Neuroprotection against Neurodegeneration

Md Zamshed Alam Begh  ¹ , Md Al Amin  ² , Mst Maharunnasa Shatu  ³ , Sherouk Hussein Sweilam  ⁴ , Sachin Puri  ⁵ , Bhagyashri Rathod  ⁵ , Uppuluri Varuna Naga Venkata Arjun  ⁶ , Thukani Sathanantham Shanmugarajan  ⁶ , Nagaveni Pommala  ⁷ , Akiladevi Durairaj  ⁶ , Susithra Ethiraj  ⁸ , Nagarajan Shenbakadurai  ⁹ , Irfan Ahmad  ¹⁰ , Talha Bin Emran  ¹¹

Affiliations

• PMID: 40128128
• DOI: 10.1002/cbdv.202500170

Abstract

Neurodegenerative diseases (NDs) exhibit significant global public health challenges due to the lack of effective treatments. Berberine (BBR), a natural alkaloid compound in various plants, has been recognized for its potential neuroprotective properties. This review explores the current understanding of BBR's mechanisms of action and its therapeutic potential in preventing and treating NDs such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. BBR's neuroprotective properties are attributed to its multifaceted actions, including anti-inflammatory, antioxidant, anti-apoptotic, and neurotrophic effects. Additionally, BBR can influence many signaling pathways involved in neurodegeneration, including AMP-activated protein kinase, nuclear factor erythroid 2-related factor 2, and brain-derived neurotrophic factor pathways. Furthermore, BBR targets vital signaling pathways, including AMPK, PI3K/Akt, and MAPK, essential for developing NDs. In addition, BBR's efficacy in reducing neurodegenerative pathology and improving cognitive function has been demonstrated through preclinical studies using cellular and animal models. Clinical trials demonstrating BBR's therapeutic potential in NDs have yielded promising results, but further research is needed to confirm its safety and efficacy in humans. BBR holds potential as a novel neuroprotective agent for preventing and treating NDs, providing a promising avenue for future therapeutic interventions.     

Cannabis Is Interfering With the Heart

 I look at this and see that smoking is the problem, not necessarily the cannabis.

 I'm doing it after my next stroke. Unless you have a stick in the mud doctor who still believes in 'Reefer Madness'.

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:

Cannabis Is Interfering With the Heart

New research suggests clinicians should warn patients about the potential of cannabis to harm cardiovascular health. But how big a risk cannabis presents depends on the amount used and how much stock should be placed in observational studies.

The link between cannabinoids and cardiovascular disease, which used to be limited to evidence from preclinical studies, case reports, and case series, is now evident in epidemiological studies, researchers from Stanford reported in a recent paper in Nature Reviews Cardiology.

A large-scale US study from 2024 relied on survey data from more than 430,000 respondents and found the 4% of respondents who reported using cannabis daily had a 49% increased risk for myocardial infarction and a twofold increased risk for stroke. The added risk from cannabis was similar among those who also smoked tobacco and those who never used tobacco.

The effect was also dose dependent. Among weekly users, cannabis was associated with a 3% increased likelihood of heart attack and a 5% increased risk for stroke.

Heart Attack and Stroke

The findings echo another Stanford University study from 2022, which analyzed UK Biobank data from 500,000 participants aged 40 years, and found those who reported smoking cannabis were significantly more likely to have a heart attack than compared with nonusers (53% vs 45%).

Several studies have found an association between arrhythmia, especially atrial fibrillation, and cannabis use. A study published last year in the European Heart Journal showed the risk for new onset arrhythmia in the first 180 days was 0.8% among more than 5000 patients who had filled a cannabis prescription vs 0.4% for control participants, matched according to age, sex, and the use of other pain medications.

Although cannabis contains 100t cannabinoids, research from cell culture and mouse models suggest tetrahydrocannabinol (THC) can cause inflammation and oxidative stress inside the vasculature, explained Mark Chandy, MD, PhD, a cardiologist scientist and assistant professor at Western University in London, Ontario, Canada. He is a co-author on the Stanford study as well as the Nature Reviews Cardiology paper.

THC binds to the CB1 receptor, found in the brain, but also in the myocardium, vascular endothelial, and smooth muscle cells. The CB1 receptor promotes atherosclerotic changes, Chandy explained, adding mouse models have found that cannabis increases atherosclerotic plaques. Scientists also theorize that cannabis might have a prothrombotic effect increasing the risk for heart attacks and strokes.

When it comes to arrhythmia, the activation of CB1 and CB2 receptors can also lead to enzyme inhibition that could ultimately affect the heart’s electrical conduction system.

Disturbing the Heart’s Electrical Conduction

Chip Lavie, MD, medical director at the John Ochsner Heart and Vascular Institute in New Orleans, Louisiana, said that “vasospasm and constriction of blood vessels combined with high platelet aggregation” is the most probable mechanism explaining the association between cannabis and cardiovascular disease. However, he also said that studies show that cannabis can increase the heart rate. “ Many studies show the benefits of a low resting heart rate,” he explained.

Lavie said that considering the evidence, he recommends patients avoid cannabis. If that is not possible, he advises patients to reduce their cannabis use and consume edible cannabis or oils, rather than smoking. Although there isn’t enough evidence to show that consuming cannabis by edibles or oils is safer for the heart, burning cannabis adds toxins.

Chandy suggested cardiologists inform patients who use cannabis about the potential long-term cardiovascular side effects. “I would advise them not to use cannabis. At least, they should be able to make an informed decision about it and know the potential consequences of it.” 

Despite the emerging association between cardiovascular disease and cannabis use, “there isn’t super strong evidence of causal effects,” said Anders Holt, MD, a cardiologist at Copenhagen University Hospital, Copenhagen, Denmark, who led the study that found higher rates of arrythmia among medical cannabis users. Mouse models frequently don’t translate to human physiology, he said.

Weighing the Evidence

As long-term randomized controlled trials studying cannabis and the heart are not feasible or ethical, evidence comes from observational studies, which are prone to confounders. For example, those who consume cannabis recreationally may be more likely to engage in other activities, like alcohol consumption or high-caloric diets, which can have an impact on cardiovascular results.

Much of the evidence linking cannabis use with coronary artery disease is based on studies of participants being asked about recent cannabis use. Patients may misremember previous use, focus only on their use in the last week, or hide their cannabis use from doctors.

Holt’s study was less prone to recall bias, as it relied on medical prescriptions, rather than self-reported data. Still, there could be important differences between patients who fill medical cannabis prescriptions and those who don’t.

Big picture, however, it may not matter whether the association between cannabis and an increased cardiovascular disease risk “is due to the lifestyle, or the selection of these patients, or the active components,” suggested Holt. “We know that people who use cannabis are at an elevated risk, so maybe they should be getting a more vigilant approach.” 

Talking to Patients

Holt said it would be reasonable “to bring up emerging evidence that puts into question whether medical cannabis is entirely safe for the heart” when talking to patients about lifestyle changes, they can make to reduce their risk for cardiovascular complications.

Despite the increased risk for arrhythmia, Holt said his study doesn’t imply that medical cannabis shouldn’t be used for chronic pain, however. For one, the overall absolute risk for arrhythmia remains low. For another, treating pain allows patients to engage in activities that are good for their overall health, and cannabis could be safer than alternatives. “There is very good evidence that nonsteroidal anti-inflammatory drugs (NSAIDs), antiepileptic drugs, and opioids are not ideal for the heart either.” 

In addition to discussing why patients use cannabis, Chandy suggested cardiologists discuss with their patients how much cannabis they consume and the route of administration. “One of the good things about legalization is that we now have labels to indicate approximately how much THC is inside,” said Chandy.

Chandy is especially concerned about synthetic cannabinoids, created in labs to bind more tightly to the CB1 receptor and create more intense psychedelic effects. “The data is more limited on the synthetic cannabis but given that it’s binding so tightly to the CB1 receptor, I would expect that it would cause more cardiovascular disease.” 

He also worries that the effects of cannabis will become more pronounced in the coming decades as research shows more young people are using cannabis. “Just like with cigarettes, it’s not just how much, but how long you’re exposed to it.”

Effects of psychedelics on neurogenesis and broader neuroplasticity: a systematic review

 

But this research says no neuroplasticity occurs. Ask your competent? doctor to clarify.

 ROBUST METHODS FOR QUANTIFYING NEURONAL
MORPHOLOGY AND MOLECULAR SIGNALING REVEAL THAT
PSYCHEDELICS DO NOT INDUCE NEUROPLASTICITY

  March 2024

Well, hasn't your doctor already prescribed various types of psychedelics to get you recovered? 

What about all these drugs for stroke recovery? Doesn't your doctor read the literature?

• DMT (8 posts to November 2020)

• ecstasy (19 posts to November 2012)

• LSD (5 posts to September 2018)

  • CerAxon (5 posts to January 2012)

  • citicoline (15 posts to October 2011)

   

• magic mushrooms (10 posts to October 2014) 

  psilocybin (14 posts to May 2014)

  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. 

The latest here:

Effects of psychedelics on neurogenesis and broader neuroplasticity: a systematic review

Abstract

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In the mammalian brain, new neurons continue to be generated throughout life in a process known as adult neurogenesis. The role of adult-generated neurons has been broadly studied across laboratories, and mounting evidence suggests a strong link to the HPA axis and concomitant dysregulations in patients diagnosed with mood disorders. Psychedelic compounds, such as phenethylamines, tryptamines, cannabinoids, and a variety of ever-growing chemical categories, have emerged as therapeutic options for neuropsychiatric disorders, while numerous reports link their effects to increased adult neurogenesis. In this systematic review, we examine studies assessing neurogenesis or other neurogenesis-associated brain plasticity after psychedelic interventions and aim to provide a comprehensive picture of how this vast category of compounds regulates the generation of new neurons. We conducted a literature search on PubMed and Science Direct databases, considering all articles published until January 31, 2023, and selected articles containing both the words “neurogenesis” and “psychedelics”. We analyzed experimental studies using either in vivo or in vitro models, employing classical or atypical psychedelics at all ontogenetic windows, as well as human studies referring to neurogenesis-associated plasticity. Our findings were divided into five main categories of psychedelics: CB1 agonists, NMDA antagonists, harmala alkaloids, tryptamines, and entactogens. We described the outcomes of neurogenesis assessments and investigated related results on the effects of psychedelics on brain plasticity and behavior within our sample. In summary, this review presents an extensive study into how different psychedelics may affect the birth of new neurons and other brain-related processes. Such knowledge may be valuable for future research on novel therapeutic strategies for neuropsychiatric disorders.

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Introduction

According to the Global Burden of Diseases study, used by the World Health Organization (WHO) for strategic planning, 264 million people, or about 4.5% of the world population, suffer from Major Depressive disorder (MDD). It is recognized as one of the most debilitating illnesses on a global scale, substantially significantly affecting daily activities, quality of life, cognitive abilities, and work productivity (James et al. 2018). MDD is characterized by persistent anhedonia, which can be continuous or episodic, and has a profound impact on self-esteem, as well as social, family, and professional life (Lépine and Briley 2011). Mood and anxiety disorders are the most prevalent mental illnesses and the third most prevalent cause of disability, contributing to the global burden of disease (WHO 2012). The majority of pharmacological interventions aiming to treat mood disorders such as MDD are benzodiazepines or selective serotonin reuptake inhibitors (SSRIs). However, these classes of drugs do not elicit positive outcomes for about 50 to 60% of patients, leading to a condition characterized as treatment-resistant depression (TRD) (Nestler et al. 2002). SSRIs, the most modern class of antidepressants, are taken daily, with an onset of the desired effects close to one month after the beginning of treatment. However, these medications can trigger adverse effects that appear early on and last for the duration of the therapy. These drugs also have a high risk of being misused, as individuals undergoing treatment tend to become physically dependent or addicted, even with the accompanying lethargy induced by them (Wong and Licinio 2001).

The pathophysiology of depression is not yet fully understood; however, empirical data from classical antidepressants have led to the widely accepted monoamine hypothesis, which predicts that this disorder arises from a deficiency or imbalance of monoamine neurotransmitters. It is worth noting that several studies support this theory. For instance, standard antidepressants primarily operate on the monoamine neurochemical route, aiming to re-establish dopamine (DA), noradrenaline (NA), and serotonin (5-HT) levels to homeostatic concentrations. The serotonin pathway is particularly important for the monoamine hypothesis, as it is the main target of many commonly used antidepressants. There are seven main classes of serotonin receptors (5-HT1 to 5-HT7), each with multiple subtypes. These receptors are involved in a wide range of physiological functions, including mood regulation, cognition, neuroplasticity, and responses to stress and anxiety (Hannon and Hoyer 2008; Savitz et al. 2009). Importantly, Psychedelics are believed to primarily activate the 5-HT2A serotonin receptors, which are G protein-coupled receptors abundant in the cerebral cortex and are responsible for the characteristic hallucinogenic effects (Geyer et al. 2009; Nichols 2016). Activation of these receptors by substances like LSD and psilocybin leads to altered sensory perception and cognition (Carhart-Harris and Nutt 2017). The 5-HT2C receptors also contribute to the effects of psychedelics by influencing mood and anxiety regulation, although to a lesser extent (Halberstadt et al. 2011). Additionally, psychedelics may act as partial agonists at 5-HT1A receptors, affecting anxiolytic and antidepressant responses, but these play a minor role compared to 5-HT2A receptors (Nichols 2016).

Moreover, monoamine antagonists like reserpine, typically used for arterial hypertension, can induce depressive symptoms when taken over extended periods (Baumeister et al. 2003; Freis 1954; De Freitas et al. 2016); Third, treatments for MDD and anxiety disorders usually require chronic, daily dosages for at least a month to produce meaningful effects (Kempermann 2002). The latter observation has also led to a reinterpretation of the long-standing monoamine hypothesis of depression to what is now termed the neurogenic hypothesis of depression. This revised theory suggests that depression correlates with a decrease in the formation of new neurons in the adult brain, a process that seems to be revived by prolonged antidepressant treatment (Jacobs et al. 2000).

Adult neurogenesis is the process by which new neurons are generated within specific brain niches throughout the life of an organism. Neurogenesis seems to be ubiquitous to all species with a central nervous system (CNS) (Barker et al. 2011), and for many of them, the process is confined to specific regions (Barnea and Pravosudov 2011; Drew et al. 2013). In rodents, it is restricted to two zones: the olfactory bulb (OB), driven by the neural stem cells (NSCs) located in the subventricular zone (SVZ), and the dentate gyrus sub-region of the hippocampus, driven by the radial glial-like cells (RGL) (Laplagne et al. 2006). The foundations of the neurogenic theory of depression are supported by empirical data from clinical and preclinical studies aimed at understanding how the neurogenesis process is reverted to homeostatic levels when SSRI chronic treatment is applied (Miller and Hen 2015). However promising, alternative pathways to the proposed hypothesis are under discussion (Data-Franco et al. 2017; N. X. Li et al. 2022; Raphael Mechoulam and Parker 2013; Sanches et al. 2021; Yuan et al. 2015) and new biochemical routes to treat depression are emerging, including the induction of neurogenesis independent of direct 5-HT modulation (Idell et al. 2017; Reiche et al. 2018). Among the chemical candidates for novel antidepressants, encouraging results have been found with the use of psychedelics (Aleksandrova and Phillips 2021; DeVos and Miller 2013; Muttoni et al. 2019).

Psychedelics are shown to induce a range of effects on brain plasticity by changing neuronal functionality at the molecular level and producing electrophysiological changes that stimulate neurotrophic signaling, including of Brain-Derived Neurotrophic Factor (BDNF), a key promoter of synaptic plasticity and neuronal survival (Browne and Lucki 2013; Castrén et al. 2007; Magaraggia et al. 2021; Muscat et al. 2021). Ultimately, neurotrophic factors induce neurite growth (Numakawa et al. 2010; Saengsawang and Rasenick 2016; Thompson et al. 2012), synaptic remodeling (Liu et al. 2013; Zhou and Song 2001), neurogenesis (García-Cabrerizo and García-Fuster 2016; Lima da Cruz et al. 2018; Liu et al. 2017), and oxidative stress reduction (Frecska et al. 2013, 2016; Szabo 2015). Thus, it is believed that psychedelics can create a window of opportunity for therapists to introduce cognitive-behavioral treatment strategies and produce long-lasting effects, which are independent of the classical pharmacological approaches to treat the hypothesized neurotransmitter imbalance (Keeler et al. 2021; Nichols 2016; Worrell and Gould 2021). Such a holistic and personalized approach can better integrate patients into the treatment process, reducing the current disconnection between popular beliefs on mental illnesses and scientific-guided psychiatric interventions (Healy 2004; Lacasse and Leo 2005).

Despite the encouraging perspectives on the applications of psychedelics, their safe employment requires a deeper understanding of their mechanisms, as the currently available compounds generally target multiple neurotransmitter systems and may lead to undesired effects (Belouin and Henningfield 2018; Brunton et al. 2011; Geyer et al. 2009). Moreover, the effects on brain physiology are shown to depend on ontogeny (Liu et al. 2006; Riga et al. 2016; Skaper and Di Marzo 2012), gender (Lee et al. 2014; Realini et al. 2011; Rubino et al. 2008), dose (Fortunato et al. 2009; Maeda et al. 2007; Marinova et al. 2017) and chemical interactions (Canales and Ferrer-Donato 2014; Zuo et al. 2018). For this reason, we sought to cover the effects of such compounds on the plasticity process associated with neurogenesis in the dentate gyrus (DG), rather than in the SVZ-OB system (Christie and Cameron 2006; Kempermann 2012). To categorize these compounds, we adapted a classification done elsewhere (Calvey and Howells 2018). Finally, we discuss findings encompassing any effect on the molecular, cellular, physiological and behavioural levels reported for in vivo or in vitro models related to neurogenesis.

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

Novel Berberine Drug Cut HbA1c in Type 2 Diabetes

 I started using berberine years ago because this: Berberine reduces triglycerides levels and systolic blood pressure.^123,124

Don't follow me, I'm not medically trained, is your doctor trained in this?

Novel Berberine Drug Cut HbA1c in Type 2 Diabetes

Higher-dose group also reported liver-related improvements

by Kristen Monaco, Senior Staff Writer, MedPage Today March 3, 2025

Key Takeaways

• Two strengths of berberine ursodeoxycholate improved HbA1c compared with placebo in a phase II trial.
• The higher-dose group also had improvements in other metabolic and liver markers.
• The treatment appeared to be safe and well-tolerated.

An investigational compound incorporating an herbal-based supplement improved blood glucose in adults with inadequately controlled type 2 diabetes in a Chinese phase II randomized clinical trial.

By week 12, HbA1c significantly improved among participants on twice-daily berberine ursodeoxycholate at 500 mg (-0.4%, 95% CI -0.79% to -0.03%, P=0.04) or 1,000 mg (-0.7%, 95% CI -1.10% to -0.35%, P<0.001) compared with placebo, Linong Ji, MD, of Peking University People's Hospital in Beijing, and colleagues wrote in JAMA Network Open.

More participants in the higher-dose group than placebo achieved an HbA1c under 7% (55.9% vs 15.2%) or under 6.5% (29.4% vs 6.1%). Significant drops in fasting plasma glucose levels were also reported in the 500 and 1,000 mg groups (-13.0 mg/dL and -18.4 mg/dL).

Though most participants had normal liver markers at baseline, the high-dose group had significant reductions in aspartate aminotransferase, alanine aminotransferase, and γ-glutamyltransferase levels from baseline. Other metabolic and inflammatory markers including LDL cholesterol, HDL cholesterol, non-HDL cholesterol, total cholesterol, fasting C-peptide, and HOMA-IR also improved in this group. Body weight didn't significantly change in any group.

Treatment was safe and well-tolerated, and nearly all participants completed the trial. The most common treatment-emergent adverse event was hyperlipidemia, occurring in three patients in each treatment group and in two placebo patients.

Berberine ursodeoxycholate, also known as HTD180, is a first-in-class orally administered gut-liver anti-inflammatory metabolic modulator. The compound "provides a unique dual mechanism of action (adenosine monophosphate [AMP] kinase activation and NLRP3 inflammasome inhibition) compared with the current therapeutic landscape," Ji and co-authors wrote. It represents "a new molecular entity that offers the possibility of combination therapy for chronic metabolic and nonviral liver diseases in a single treatment."

Berberine on its own has long been used in traditional Chinese and ayurvedic medicine and recently shot to popularity in the U.S., being touted on social media as "nature's Ozempic" for its potential metabolic benefits.

"Berberine shares several mechanisms of action with metformin, including activation of AMP-activated protein kinase, inhibition of gluconeogenesis, modulation of gut microbiota, and anti-inflammatory and antioxidant effects. These metabolic benefits may have led to its promotion as an alternative or adjunct to metformin, despite its lack of FDA approval for diabetes treatment," accompanying commentary author Nestoras Mathioudakis, MD, MHS, of Johns Hopkins University School of Medicine in Baltimore, pointed out.

Berberine's poor bioavailability is one of its drawbacks, said Mathioudakis, and "enhancing the absorption of berberine has been a key focus of research." Ji and co-authors said this prompted them to combine berberine with ursodeoxycholic acid, a key regulator of bile acid and inflammatory pathways that has been used to treat hepatobiliary disorders and cholestatic conditions, to boost pharmacological effects.

Putting berberine ursodeoxycholate's glucose-lowering effects into perspective, Mathioudakis said that equivalent doses of metformin tend to yield similar, but slightly more potent, results.

"[M]etformin at doses of 500 mg twice daily can reduce the HbA1c level by 1.0% to 1.5%, while 1,000 mg twice daily may achieve reductions of 1.5% to 2.0% over similar time frames [to the trial]," he wrote. But its glucose-lowering effects "align with other FDA approved antihyperglycemic medications," including SGLT2 inhibitors and DPP-4 inhibitors.

For certain patients, berberine ursodeoxycholate could "offer advantages over metformin," Mathioudakis added, which may include fewer adverse events, potential liver benefits, and a possible option for people who want natural alternatives. "By incorporating novel natural derivatives ... into our therapeutic armamentarium, we can address patient preferences and potentially improve adherence -- critical factors in achieving meaningful metabolic outcomes for individuals living with type 2 diabetes," he said.

The 14-site trial was conducted in China between March 2022 and January 2023 and enrolled 113 participants with type 2 diabetes. Average age was 54.3 years and 63.7% were male. At baseline, HbA1c was 8.2%, body mass index (BMI) was 25.5, and fasting plasma glucose was 160.7 mg/dL. Prior to the study, all participants underwent 8 or more weeks of diet and exercise and then were randomly assigned 1:1:1 in groups balanced for baseline disease severity.

The short 12-week follow-up and exclusively Han Chinese patient population were some of the study's limitations.

Ji's group said berberine ursodeoxycholate is being studied in more trials for type 2 diabetes and metabolic dysfunction-association steatohepatitis(MASH). The FDA previously granted it fast-track designation for both MASH and primary sclerosing cholangitis (PSC), and orphan drug designation for PSC.

• 

  Kristen Monaco is a senior staff writer, focusing on endocrinology, psychiatry, and nephrology news. Based out of the New York City office, she’s worked at the company since 2015.

Disclosures

The study was funded by Shenzhen HighTide Biopharmaceutical.

Ji reported relationships with Shenzhen HighTide Biopharmaceutical, Eli Lilly, Novo Nordisk, Merck, Bayer, Sanofi-Aventis, Roche, MSD, Metronics, AstraZeneca, Boehringer Ingelheim, Abbott, Fosun Pharma, Innovent Biologics, Gan & Lee Pharmaceuticals, Sinocare, Sibionics, and Shanghai Benemae Pharmaceutical Corp.

Co-authors reported relationships with Shenzhen HighTide Biopharmaceutical.

Mathioudakis reported no disclosures.

Primary Source

JAMA Network Open

Source Reference: opens in a new tab or windowJi L, et al "Berberine ursodeoxycholate for the treatment of type 2 diabetes: a randomized clinical trial" JAMA Netw Open 2025; DOI: 10.1001/jamanetworkopen.2024.62185.

Secondary Source

JAMA Network Open

Source Reference: opens in a new tab or windowMathioudakis N "A berberine derivative for treatment of type 2 diabetes" JAMA Netw Open 2025; DOI: 10.1001/jamanetworkopen.2024.62195.

Yes, physicians warn, cannabis is bad for the heart

But you don't tell us if this is smoked or gummies. What about the benefits for stroke recovery? Do the pros outrank the cons? 

Earlier research was positive on marijuana, did your competent? doctor take notice and prescribe it?

 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:

Yes, physicians warn, cannabis is bad for the heart

Cannabis use is on the rise throughout the United States, but it is not as harmless as some people may believe. In fact, according to a new in-depth analysis in Nature Reviews Cardiology, regular cannabis use increases a person’s risk of multiple adverse cardiovascular outcomes, including myocardial infarction, arrhythmias and cardiomyopathy.[1]

The study’s authors, a group of researchers with the Stanford Cardiovascular Institute, explored a wide variety of topics, including ongoing policy trends related to cannabis and the science behind why it appears to make such a significant impact on the cardiovascular system. The group also emphasized that it will be important to learn more about the long-term impact of cannabis use as time goes on. 

“Cannabis is emerging as a risk factor for adverse cardiovascular health,” wrote first author Mark Chandy, MD, PhD, who is now an assistant professor at Western University in Ontario, Canada, and colleagues. “With changing public perceptions and an overall decline in tobacco use, cannabis is poised to replace tobacco as a legal drug of choice. Previous restrictions are ending with the widespread decriminalization and legalization of cannabis, boosting use of the drug. A public perception that cannabis is harmless and therapeutically beneficial persists, despite mounting evidence from preclinical and clinical studies showing that cannabis use can harm the cardiovascular system and pose other serious health problems, not unlike tobacco.”

Exploring the link between cannabis use and cardiovascular disease

Chandy et al. noted that “robust evidence from basic science and clinical studies” has already linked cannabis use to an increased likelihood of developing cardiovascular disease. These risks appear to become more severe depending on how often the drug is used. 

Another key takeaway from the group’s assessment was the evidence that cannabis use can increase the risk of new-onset arrhythmias such as atrial fibrillation (AFib) and atrial flutter. 

“Cannabis use disorder, defined as an inability to stop using marijuana despite adverse health effects or social problems, is associated with increased occurrence of AFib, hospital admissions for uncontrolled AFib and thromboembolic events,” the authors wrote. “Moreover, cannabis use disorder and associated arrhythmias are more common in younger patients. After cannabis exposure, heart rate transiently increases due to increased sympathetic tone and decreased parasympathetic tone. The chronic use of cannabis results in bradycardia due to reversal of autonomic tone. Moreover, the burden of cannabis-related arrhythmic events is exacerbated in individuals with ischemic heart disease compared with those without.”

The regular use of cannabis also appears to increase a person’s risk of developing cardiomyopathy, and some studies have linked it to an increased heart failure risk. 

Synthetic cannabis: a cause for concern?

The authors also warned that there are now synthetic marijuana strands that “exert strong depressant effects when combined with alcohol” and are “far more potent” than traditional cannabis. 

“Clinical reports and case studies provide insight into the acute adverse effects and potential complications associated with the recreational use of synthetic cannabinoids, including respiratory depression, cardiovascular events, neuropsychiatric symptoms and death,” the authors wrote. “The use synthetic cannabinoids has also been linked to myocardial infarction, myocardial ischemia and other cardiovascular complications, particularly in pediatric patients.” 

Consuming tobacco and cannabis together could lead to even greater risks

The review also examined the fact that more and more people are now using cannabis and tobacco together, creating the potential for even worse patient outcomes. At this point, little is known about the long-term effects of combining these two substances, but the short-term evidence we have so far all points to “harmful health outcomes.”

Click here to read the full review, which covers decade of research and includes nearly 150 references.

Reference:

1. Mark Chandy, Nerea Jimenez-Tellez, Joseph C. Wu. The relationship between cannabis and cardiovascular disease: clearing the haze. Nature Reviews Cardiology. Jan. 23, 2025.