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Case Report Details Use of Buprenorphine for Treatment of Kratom Dependence

 

Kratom is an herbal supplement that shares structural similarities with opioid analgesics

Kratom is an herbal supplement that shares structural similarities with opioid analgesics

Opioid-like dependence due to chronic kratom use can be successfully treated with buprenorphine, according to a recent case report published in the Journal of Addiction Medicine.

Kratom, an herbal supplement that shares structural similarities with opioid analgesics, has recently grown in popularity as an unapproved opioid replacement therapy. The drug is easily obtained via the Internet (as it does not require a prescription), but oftentimes contains higher than typical doses and may be mixed with adulterants, increasing the risk of toxicity.

In their article, the authors report on two patients who used kratom to self-treat their chronic pain after they could no longer receive opioid analgesics from healthcare providers. Both patients presented to the clinic with evidence of kratom dependence and withdrawal and underwent home initiation of sublingual buprenorphine-naloxone therapy. In each case, transitioning to buprenorphine-naloxone maintenance led to control of both their chronic pain and opioid withdrawal symptoms.

RELATED ARTICLES

“Although some debate whether kratom is a true opioid or not, this case series shows that opioid agonist treatment with buprenorphine-naloxone is effective for some patients with kratom dependence and demonstrates 2 safe home initiations of buprenorphine,” concluded the authors.

 

Treatment of Kratom Dependence With Buprenorphine

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Ketamine and Psychedelic Drugs Change Structure of Neurons

ummary: A new study reveals psychedelics increase dendrites, dendritic spines and synapses, while ketamine may promote neuroplasticity. The findings could help develop new treatments for anxiety, depression and other related disorders.

Source: UC Davis.

A team of scientists at the University of California, Davis is exploring how hallucinogenic drugs impact the structure and function of neurons — research that could lead to new treatments for depression, anxiety, and related disorders. In a paper published on June 12 in the journal Cell Reports, they demonstrate that a wide range of psychedelic drugs, including well-known compounds such as LSD and MDMA, increase the number of neuronal branches (dendrites), the density of small protrusions on these branches (dendritic spines), and the number of connections between neurons (synapses). These structural changes suggest that psychedelics are capable of repairing the circuits that are malfunctioning in mood and anxiety disorders.

“People have long assumed that psychedelics are capable of altering neuronal structure, but this is the first study that clearly and unambiguously supports that hypothesis. What is really exciting is that psychedelics seem to mirror the effects produced by ketamine,” said David Olson, assistant professor in the Departments of Chemistry and of Biochemistry and Molecular Medicine, who leads the research team.

Ketamine, an anesthetic, has been receiving a lot of attention lately because it produces rapid antidepressant effects in treatment-resistant populations, leading the U.S. Food and Drug Administration to fast-track clinical trials of two antidepressant drugs based on ketamine. The antidepressant properties of ketamine may stem from its tendency to promote neural plasticity — the ability of neurons to rewire their connections.

“The rapid effects of ketamine on mood and plasticity are truly astounding. The big question we were trying to answer was whether or not other compounds are capable of doing what ketamine does,” Olson said.

Psychedelics show similar effects to ketamine

Olson’s group has demonstrated that psychedelics mimic the effects of ketamine on neurons grown in a dish, and that these results extend to structural and electrical properties of neurons in animals. Rats treated with a single dose of DMT — a psychedelic compound found in the Amazonian herbal tea known as ayahuasca — showed an increase in the number of dendritic spines, similar to that seen with ketamine treatment. DMT itself is very short-lived in the rat: Most of the drug is eliminated within an hour. But the “rewiring” effects on the brain could be seen 24 hours later, demonstrating that these effects last for some time.

Fairfax | NOVA Ketamine IV Ketamine for depression | Fairfax, Va 22306 | 703-844-0184
Fairfax | NOVA Ketamine IV Ketamine for depression | Fairfax, Va 22306 | 703-844-0184

Ketamine and Psychedelic Drugs Change Structure of Neurons

Summary: A new study reveals psychedelics increase dendrites, dendritic spines and synapses, while ketamine may promote neuroplasticity. The findings could help develop new treatments for anxiety, depression and other related disorders.

Source: UC Davis.

A team of scientists at the University of California, Davis is exploring how hallucinogenic drugs impact the structure and function of neurons — research that could lead to new treatments for depression, anxiety, and related disorders. In a paper published on June 12 in the journal Cell Reports, they demonstrate that a wide range of psychedelic drugs, including well-known compounds such as LSD and MDMA, increase the number of neuronal branches (dendrites), the density of small protrusions on these branches (dendritic spines), and the number of connections between neurons (synapses). These structural changes suggest that psychedelics are capable of repairing the circuits that are malfunctioning in mood and anxiety disorders.

“People have long assumed that psychedelics are capable of altering neuronal structure, but this is the first study that clearly and unambiguously supports that hypothesis. What is really exciting is that psychedelics seem to mirror the effects produced by ketamine,” said David Olson, assistant professor in the Departments of Chemistry and of Biochemistry and Molecular Medicine, who leads the research team.

Ketamine, an anesthetic, has been receiving a lot of attention lately because it produces rapid antidepressant effects in treatment-resistant populations, leading the U.S. Food and Drug Administration to fast-track clinical trials of two antidepressant drugs based on ketamine. The antidepressant properties of ketamine may stem from its tendency to promote neural plasticity — the ability of neurons to rewire their connections.

“The rapid effects of ketamine on mood and plasticity are truly astounding. The big question we were trying to answer was whether or not other compounds are capable of doing what ketamine does,” Olson said.

Psychedelics show similar effects to ketamine

Olson’s group has demonstrated that psychedelics mimic the effects of ketamine on neurons grown in a dish, and that these results extend to structural and electrical properties of neurons in animals. Rats treated with a single dose of DMT — a psychedelic compound found in the Amazonian herbal tea known as ayahuasca — showed an increase in the number of dendritic spines, similar to that seen with ketamine treatment. DMT itself is very short-lived in the rat: Most of the drug is eliminated within an hour. But the “rewiring” effects on the brain could be seen 24 hours later, demonstrating that these effects last for some time.

image shows neurons under psychedelics and ketamine

Psychedelic drugs such as LSD and ayahuasca change the structure of nerve cells, causing them to sprout more branches and spines, UC Davis researchers have found. This could help in “rewiring” the brain to treat depression and other disorders. In this false-colored image, the rainbow-colored cell was treated with LSD compared to a control cell in blue. NeuroscienceNews.com image is credited to Calvin and Joanne Ly.

Behavioral studies also hint at the similarities between psychedelics and ketamine. In another recent paper published in ACS Chemical Neuroscience, Olson’s group showed that DMT treatment enabled rats to overcome a “fear response” to the memory of a mild electric shock. This test is considered to be a model of post-traumatic stress disorder (PTSD), and interestingly, ketamine produces the same effect. Recent clinical trials have shown that like ketamine, DMT-containing ayahuasca might have fast-acting effects in people with recurrent depression, Olson said.

These discoveries potentially open doors for the development of novel drugs to treat mood and anxiety disorders, Olson said. His team has proposed the term “psychoplastogen” to describe this new class of “plasticity-promoting” compounds.

“Ketamine is no longer our only option. Our work demonstrates that there are a number of distinct chemical scaffolds capable of promoting plasticity like ketamine, providing additional opportunities for medicinal chemists to develop safer and more effective alternatives,” Olson said.

 

Psychedelic drugs, ketamine change structure of neurons

Psychedelic drugs, ketamine change structure of neurons

Psychedelics as Possible Treatments for Depression and PTSD

A team of scientists at the University of California, Davis, is exploring how hallucinogenic drugs impact the structure and function of neurons — research that could lead to new treatments for depression, anxiety and related disorders.

In a paper published on June 12 in the journal Cell Reports, they demonstrate that a wide range of psychedelic drugs, including well-known compounds such as LSD and MDMA, increase the number of neuronal branches (dendrites), the density of small protrusions on these branches (dendritic spines) and the number of connections between neurons (synapses). These structural changes could suggest that psychedelics are capable of repairing the circuits that are malfunctioning in mood and anxiety disorders.

“People have long assumed that psychedelics are capable of altering neuronal structure, but this is the first study that clearly and unambiguously supports that hypothesis. What is really exciting is that psychedelics seem to mirror the effects produced by ketamine,” said David Olson, assistant professor in the departments of Chemistry and of Biochemistry and Molecular Medicine, who leads the research team.

Ketamine, an anesthetic, has been receiving a lot of attention lately because it produces rapid antidepressant effects in treatment-resistant populations, leading the U.S. Food and Drug Administration to fast-track clinical trials of two antidepressant drugs based on ketamine. The antidepressant properties of ketamine may stem from its tendency to promote neural plasticity — the ability of neurons to rewire their connections.

“The rapid effects of ketamine on mood and plasticity are truly astounding. The big question we were trying to answer was whether or not other compounds are capable of doing what ketamine does,” Olson said.

Psychedelics show similar effects to ketamine

Olson’s group has demonstrated that psychedelics mimic the effects of ketamine on neurons grown in a dish, and that these results extend to structural and electrical properties of neurons in animals. Rats treated with a single dose of DMT — a psychedelic compound found in the Amazonian herbal tea known as ayahuasca — showed an increase in the number of dendritic spines, similar to that seen with ketamine treatment. DMT itself is very short-lived in the rat: Most of the drug is eliminated within an hour. But the “rewiring” effects on the brain could be seen 24 hours later, demonstrating that these effects last for some time.

Behavioral studies also hint at the similarities between psychedelics and ketamine. In another recent paper published in ACS Chemical Neuroscience, Olson’s group showed that DMT treatment enabled rats to overcome a “fear response” to the memory of a mild electric shock. This test is considered to be a model of post-traumatic stress disorder, or PTSD, and interestingly, ketamine produces the same effect. Recent clinical trials have shown that like ketamine, DMT-containing ayahuasca might have fast-acting effects in people with recurrent depression, Olson said.

These discoveries potentially open doors for the development of novel drugs to treat mood and anxiety disorders, Olson said. His team has proposed the term “psychoplastogen” to describe this new class of “plasticity-promoting” compounds.

“Ketamine is no longer our only option. Our work demonstrates that there are a number of distinct chemical scaffolds capable of promoting plasticity like ketamine, providing additional opportunities for medicinal chemists to develop safer and more effective alternatives,” Olson said.

Additional co-authors on the Cell Reports “Psychedelics Promote Structural and Functional Neural Plasticity.” study are Calvin Ly, Alexandra Greb, Sina Soltanzadeh Zarandi, Lindsay Cameron, Jonathon Wong, Eden Barragan, Paige Wilson, Michael Paddy, Kassandra Ori-McKinney, Kyle Burbach, Megan Dennis, Alexander Sood, Whitney Duim, Kimberley McAllister and John Gray.

Olson and Cameron were co-authors on the ACS Chemical Neuroscience paper along with Charlie Benson and Lee Dunlap.

The work was partly supported by grants from the National Institutes of Health.

Psychedelics Promote Structural and Functional
Neural Plasticity

Below is the Intro and Discussion for the article:

Psychedelics Promote Structural and Functional neural Plasticity

Authors:

Calvin Ly, Alexandra C. Greb,
Lindsay P. Cameron, …,
Kassandra M. Ori-McKenney,
John A. Gray, David E. Olson
Correspondence
deolson@ucdavis.edu

In Brief
Ly et al. demonstrate that psychedelic
compounds such as LSD, DMT, and DOI
increase dendritic arbor complexity,
promote dendritic spine growth, and
stimulate synapse formation. These
cellular effects are similar to those
produced by the fast-acting
antidepressant ketamine and highlight
the potential of psychedelics for treating
depression and related disorders.

  • Highlights
     Serotonergic psychedelics increase neuritogenesis,
    spinogenesis, and synaptogenesis
  •  Psychedelics promote plasticity via an evolutionarily
    conserved mechanism
  •  TrkB, mTOR, and 5-HT2A signaling underlie psychedelicinduced
    plasticity
  •  Noribogaine, but not ibogaine, is capable of promoting
    structural neural plasticity

SUMMARY
Atrophy of neurons in the prefrontal cortex (PFC)
plays a key role in the pathophysiology of depression
and related disorders. The ability to promote
both structural and functional plasticity in the PFC
has been hypothesized to underlie the fast-acting
antidepressant properties of the dissociative anesthetic
ketamine. Here, we report that, like ketamine,
serotonergic psychedelics are capable of robustly
increasing neuritogenesis and/or spinogenesis both
in vitro and in vivo. These changes in neuronal structure
are accompanied by increased synapse number
and function, as measured by fluorescence microscopy
and electrophysiology. The structural changes
induced by psychedelics appear to result from stimulation
of the TrkB, mTOR, and 5-HT2A signaling
pathways and could possibly explain the clinical
effectiveness of these compounds. Our results underscore
the therapeutic potential of psychedelics
and, importantly, identify several lead scaffolds for
medicinal chemistry efforts focused on developing
plasticity-promoting compounds as safe, effective,
and fast-acting treatments for depression and
related disorders.

INTRODUCTION
Neuropsychiatric diseases, including mood and anxiety disorders,
are some of the leading causes of disability worldwide
and place an enormous economic burden on society (Gustavsson
et al., 2011; Whiteford et al., 2013). Approximately
one-third of patients will not respond to current antidepressant
drugs, and those who do will usually require at least 2–4 weeks
of treatment before they experience any beneficial effects
(Rush et al., 2006). Depression, post-traumatic stress disorder
(PTSD), and addiction share common neural circuitry (Arnsten,
2009; Russo et al., 2009; Peters et al., 2010; Russo and
Nestler, 2013) and have high comorbidity (Kelly and Daley,
2013). A preponderance of evidence from a combination of
human imaging, postmortem studies, and animal models suggests
that atrophy of neurons in the prefrontal cortex (PFC)
plays a key role in the pathophysiology of depression and
related disorders and is precipitated and/or exacerbated by
stress (Arnsten, 2009; Autry and Monteggia, 2012; Christoffel
et al., 2011; Duman and Aghajanian, 2012; Duman et al.,
2016; Izquierdo et al., 2006; Pittenger and Duman, 2008;
Qiao et al., 2016; Russo and Nestler, 2013). These structural
changes, such as the retraction of neurites, loss of dendritic
spines, and elimination of synapses, can potentially be counteracted
by compounds capable of promoting structural and
functional neural plasticity in the PFC (Castre´ n and Antila,
2017; Cramer et al., 2011; Duman, 2002; Hayley and Litteljohn,
2013; Kolb and Muhammad, 2014; Krystal et al., 2009;
Mathew et al., 2008), providing a general solution to treating
all of these related diseases. However, only a relatively small
number of compounds capable of promoting plasticity in the
PFC have been identified so far, each with significant drawbacks
(Castre´ n and Antila, 2017). Of these, the dissociative
anesthetic ketamine has shown the most promise, revitalizing
the field of molecular psychiatry in recent years.
Ketamine has demonstrated remarkable clinical potential as a
fast-acting antidepressant (Berman et al., 2000; Ionescu et al.,
2016; Zarate et al., 2012), even exhibiting efficacy in treatmentresistant
populations (DiazGranados et al., 2010; Murrough
et al., 2013; Zarate et al., 2006). Additionally, it has shown promise
for treating PTSD (Feder et al., 2014) and heroin addiction
(Krupitsky et al., 2002). Animal models suggest that its therapeutic
effects stem from its ability to promote the growth of dendritic
spines, increase the synthesis of synaptic proteins, and
strengthen synaptic responses (Autry et al., 2011; Browne and
Lucki, 2013; Li et al., 2010).

Like ketamine, serotonergic psychedelics and entactogens
have demonstrated rapid and long-lasting antidepressant and
anxiolytic effects in the clinic after a single dose (Bouso et al.,
2008; Carhart-Harris and Goodwin, 2017; Grob et al., 2011;
Mithoefer et al., 2013, 2016; Nichols et al., 2017; Sanches
et al., 2016; Oso´ rio et al., 2015), including in treatment-resistant
populations (Carhart-Harris et al., 2016, 2017; Mithoefer et al.,
2011; Oehen et al., 2013; Rucker et al., 2016). In fact, there
have been numerous clinical trials in the past 30 years examining
the therapeutic effects of these drugs (Dos Santos et al., 2016),
with 3,4-methylenedioxymethamphetamine (MDMA) recently
receiving the ‘‘breakthrough therapy’’ designation by the Food
and Drug Administration for treating PTSD. Furthermore, classical
psychedelics and entactogens produce antidepressant
and anxiolytic responses in rodent behavioral tests, such as
the forced swim test (Cameron et al., 2018) and fear extinction
learning (Cameron et al., 2018; Catlow et al., 2013; Young
et al., 2015), paradigms for which ketamine has also been shown
to be effective (Autry et al., 2011; Girgenti et al., 2017; Li et al.,
2010). Despite the promising antidepressant, anxiolytic, and
anti-addictive properties of serotonergic psychedelics, their
therapeutic mechanism of action remains poorly understood,
and concerns about safety have severely limited their clinical
usefulness.
Because of the similarities between classical serotonergic
psychedelics and ketamine in both preclinical models and clinical
studies, we reasoned that their therapeutic effects might
result from a shared ability to promote structural and functional
neural plasticity in cortical neurons. Here, we report that serotonergic
psychedelics and entactogens from a variety of chemical
classes (e.g., amphetamine, tryptamine, and ergoline) display
plasticity-promoting properties comparable to or greater than
ketamine. Like ketamine, these compounds stimulate structural
plasticity by activating the mammalian target of rapamycin
(mTOR). To classify the growing number of compounds capable
of rapidly promoting induced plasticity (Castre´ n and Antila,
2017), we introduce the term ‘‘psychoplastogen,’’ from the
Greek roots psych- (mind), -plast (molded), and -gen (producing).
Our work strengthens the growing body of literature indicating
that psychoplastogens capable of promoting plasticity
in the PFC might have value as fast-acting antidepressants
and anxiolytics with efficacy in treatment-resistant populations
and suggests that it may be possible to use classical psychedelics
as lead structures for identifying safer alternatives.

DISCUSSION
Classical serotonergic psychedelics are known to cause
changes in mood (Griffiths et al., 2006, 2008, 2011) and brain
function (Carhart-Harris et al., 2017) that persist long after the
acute effects of the drugs have subsided. Moreover, several
psychedelics elevate glutamate levels in the cortex (Nichols,
2004, 2016) and increase gene expression in vivo of the neurotrophin
BDNF as well as immediate-early genes associated with
plasticity (Martin et al., 2014; Nichols and Sanders-Bush, 2002;
Vaidya et al., 1997). This indirect evidence has led to the
reasonable hypothesis that psychedelics promote structural
and functional neural plasticity, although this assumption had
never been rigorously tested (Bogenschutz and Pommy,
2012; Vollenweider and Kometer, 2010). The data presented
here provide direct evidence for this hypothesis, demonstrating
that psychedelics cause both structural and functional changes
in cortical neurons.

Prior to this study, two reports suggested
that psychedelics might be able
to produce changes in neuronal structure.
Jones et al. (2009) demonstrated that DOI
was capable of transiently increasing the
size of dendritic spines on cortical neurons,
but no change in spine density was
observed. The second study showed
that DOI promoted neurite extension in a
cell line of neuronal lineage (Marinova
et al., 2017). Both of these reports utilized
DOI, a psychedelic of the amphetamine
class. Here we demonstrate that the ability
to change neuronal structure is not a
unique property of amphetamines like
DOI because psychedelics from the ergoline,
tryptamine, and iboga classes of compounds also promote
structural plasticity. Additionally, D-amphetamine does not increase
the complexity of cortical dendritic arbors in culture,
and therefore, these morphological changes cannot be simply
attributed to an increase in monoamine neurotransmission.
The identification of psychoplastogens belonging to distinct
chemical families is an important aspect of this work because
it suggests that ketamine is not unique in its ability to promote
structural and functional plasticity. In addition to ketamine, the
prototypical psychoplastogen, only a relatively small number of
plasticity-promoting small molecules have been identified previously.
Such compounds include the N-methyl-D-aspartate
(NMDA) receptor ligand GLYX-13 (i.e., rapastinel), the mGlu2/3
antagonist LY341495, the TrkB agonist 7,8-DHF, and the muscarinic
receptor antagonist scopolamine (Lepack et al., 2016; Castello
et al., 2014; Zeng et al., 2012; Voleti et al., 2013). We
observe that hallucinogens from four distinct structural classes
(i.e., tryptamine, amphetamine, ergoline, and iboga) are also
potent psychoplastogens, providing additional lead scaffolds
for medicinal chemistry efforts aimed at identifying neurotherapeutics.
Furthermore, our cellular assays revealed that several
of these compounds were more efficacious (e.g., MDMA) or more potent (e.g., LSD) than ketamine. In fact, the plasticity-promoting
properties of psychedelics and entactogens rivaled that
of BDNF (Figures 3A–3C and S3). The extreme potency of LSD
in particular might be due to slow off kinetics, as recently proposed
following the disclosure of the LSD-bound 5-HT2B crystal
structure (Wacker et al., 2017).
Importantly, the psychoplastogenic effects of psychedelics in
cortical cultures were also observed in vivo using both vertebrate
and invertebrate models, demonstrating that they act through an
evolutionarily conserved mechanism. Furthermore, the concentrations
of psychedelics utilized in our in vitro cell culture assays
were consistent with those reached in the brain following systemic
administration of therapeutic doses in rodents (Yang
et al., 2018; Cohen and Vogel, 1972). This suggests that neuritogenesis,
spinogenesis, and/or synaptogenesis assays performed
using cortical cultures might have value for identifying
psychoplastogens and fast-acting antidepressants. It should
be noted that our structural plasticity studies performed in vitro
utilized neurons exposed to psychedelics for extended periods
of time. Because brain exposure to these compounds is often
of short duration due to rapid metabolism, it will be interesting
to assess the kinetics of psychedelic-induced plasticity.
A key question in the field of psychedelic medicine has been
whether or not psychedelics promote changes in the density of
dendritic spines (Kyzar et al., 2017). Using super-resolution
SIM, we clearly demonstrate that psychedelics do, in fact, increase
the density of dendritic spines on cortical neurons, an effect
that is not restricted to a particular structural class of compounds.
Using DMT, we verified that cortical neuron spine
density increases in vivo and that these changes in structural
plasticity are accompanied by functional effects such as
increased amplitude and frequency of spontaneous EPSCs.

We specifically designed these experiments
to mimic previous studies of ketamine
(Li et al., 2010) so that we might
directly compare these two compounds,
and, to a first approximation, they appear
to be remarkably similar. Not only do they
both increase spine density and neuronal
excitability in the cortex, they seem to
have similar behavioral effects. We have
shown previously that, like ketamine,
DMT promotes fear extinction learning
and has antidepressant effects in the
forced swim test (Cameron et al., 2018). These results, coupled
with the fact that ayahuasca, a DMT-containing concoction, has
potent antidepressant effects in humans (Oso´ rio et al., 2015;
Sanches et al., 2016; Santos et al., 2007), suggests that classical
psychedelics and ketamine might share a related therapeutic
mechanism.
Although the molecular targets of ketamine and psychedelics
are different (NMDA and 5-HT2A receptors, respectively), they
appear to cause similar downstream effects on structural plasticity
by activating mTOR. This finding is significant because ketamine is
known to be addictive whereas many classical psychedelics are
not (Nutt et al., 2007, 2010). The exact mechanisms by which these
compounds stimulate mTOR is still not entirely understood, but
our data suggest that, at least for classical psychedelics, TrkB
and 5-HT2A receptors are involved. Although most classical psychedelics
are not considered to be addictive, there are still significant
safety concerns with their use in medicine because they
cause profound perceptual disturbances and still have the potential
to be abused. Therefore, the identification of non-hallucinogenic
analogs capable of promoting plasticity in the PFC could
facilitate a paradigm shift in our approach to treating neuropsychiatric
diseases. Moreover, such compounds could be critical to
resolving the long-standing debate in the field concerning whether
the subjective effects of psychedelics are necessary for their therapeutic
effects (Majic et al., 2015  ). Although our group is actively
investigating the psychoplastogenic properties of non-hallucinogenic
analogs of psychedelics, others have reported the therapeutic
potential of safer structural and functional analogs of ketamine
(Moskal et al., 2017; Yang et al., 2015; Zanos et al., 2016).
Our data demonstrate that classical psychedelics from several
distinct chemical classes are capable of robustly promoting the
growth of both neurites and dendritic spines in vitro, in vivo, and across species. Importantly, our studies highlight the similarities
between the effects of ketamine and those of classical serotonergic
psychedelics, supporting the hypothesis that the clinical
antidepressant and anxiolytic effects of these molecules might
result from their ability to promote structural and functional plasticity
in prefrontal cortical neurons. We have demonstrated that
the plasticity-promoting properties of psychedelics require
TrkB, mTOR, and 5-HT2A signaling, suggesting that these key
signaling hubs may serve as potential targets for the development
of psychoplastogens, fast-acting antidepressants, and anxiolytics.
Taken together, our results suggest that psychedelics
may be used as lead structures to identify next-generation neurotherapeutics
with improved efficacy and safety profiles.

Also below is a great article on DMT and neuroplasticity:

 

Dark Classics in Chemical Neuroscience N,N-Dimethyltryptamine DMT

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DRUG ADDICTION

There’s a lot of confusion about what drug addiction (also called substance use disorder, or SUD) actually means, even though it’s a problem that affects millions of Americans from all walks of life. The National Institute on Drug Abuse (NIDA) defines drug addiction as a chronic brain disease and one in which relapses are very common. It isn’t, though, a sign of weak moral character or lack of willpower. What might start as a choice to try a drug (as a legitimate prescription or recreationally) can result, over time, in someone losing the ability to choose and becoming addicted.

People with addiction cannot abstain, stop their drug-seeking behavior or control cravings without getting help. They compulsively need to use, regardless of the damage the addiction is causing in their lives – physically, mentally, emotionally, educationally, socially, spiritually, financially. Treatment is often necessary because the disease typically gets progressively worse and can even lead to disability or premature death. In fact, according to NIDA, using tobacco products is the number one preventable cause of disease, disability and death in the U.S.

Drugs of Addiction

To make matters more complicated, there are many types of drugs that people can become addicted to, and each has its own way of affecting the body, including its own unique withdrawal symptoms. Commonly abused substances include not just illicit drugs but also some prescription medications such as opioids (like oxycodone and hydrocodone), stimulants (such as cocaine and dextroamphetamine) and depressants (including benzodiazepines and barbiturates). These drugs may at first be prescribed for medical reasons and a person later takes the medication in a way that wasn’t prescribed by their healthcare provider, or illegally takes a medication without a prescription. Still others become addicted to over-the-counter medications like cough or cold syrups and sleeping pills that are readily available, legal drugs. Other commonly abused drugs include hallucinogens, inhalants, sedatives, hypnotics, cannabis (marijuana, for non-medical purposes), alcohol and, as mentioned above, tobacco.

Drugs Change the Brain

Part of the reason substance use disorders are so complex to understand and to treat is that over time drugs of abuse can actually change circuits in the brain – and those changes can persist even after stopping the drug and going through detoxification, or “detox.” Some drugs activate the brain’s reward system in such an intense way that a person can start to ignore activities they once enjoyed as they seek the intense pleasure or “high” the drug gives, driving them to keep using; cocaine and methamphetamine are good examples of this. When a drug user experiences this feeling of intoxication, it can affect their thinking, judgment, emotions and behavior and can lead to breathing problems, seizures, coma or even death. The brain can adapt to produce less dopamine (the neurotransmitter that controls the body’s reward and pleasure centers); the result is that the addict needs an ever-larger dose to experience the same high. Still other drugs, such as marijuana and heroin, work to dupe the brain into believing they’re brain chemical messengers known as neurotransmitters.

It’s important to understand that not everyone who tries a drug of abuse becomes addicted. Several factors are involved, including one’s biology (which includes family history and physiology), environment (whether friends and family use illicit drugs, for example) and developmental stage (adolescents are particularly vulnerable because their brains are still developing). All drugs have the potential to be addictive. But, in general, addiction to cocaine, methamphetamine and heroin can happen more quickly with fewer doses. (Alcohol is a very commonly abused drug, too; for more information on alcoholism, please visit the Alcoholism section.)

How Big is the Problem?

If you’re reading this because you’re concerned that you or a loved one may have a substance use problem, you’re not alone. Drug use is very common:

  • Nearly 25 million Americans were illicit drug users in 2013, according to the National Survey on Drug Use and Health (NSDUH), which came out in 2014.

  • That same report shows that an estimated 21.6 million Americans ages 12 and older had a substance use disorder in the previous year, meaning an addiction to drugs or alcohol.

Depression and other mental health issues play an important role in the prevalence of drug addiction; many people have both an SUD and a mental health issue (what’s known as co-occurring disorders). In other cases, people who become addicted to a drug of abuse may go on to experience one or more symptoms of a mental health problem such as an anxiety disorder, depression or psychosis – what’s known as a substance-induced mental disorder.

An SUD can be mild, moderate or severe, depending on how many symptoms a person has. The more symptoms, the greater the severity of the drug addiction. Many illicit drugs, but not all, produce withdrawal symptoms; those that do include opioids, sedatives, hypnotics (such as LSD) and anxiolytics (drugs to treat anxiety). Tobacco products, stimulants and marijuana have less apparent withdrawal symptoms, according to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, but they still cause withdrawal.

When people are addicted to a substance, it means in part that they’ve built up a tolerance to the drug; cravings make quitting extremely difficult – one of the reasons stopping a drug should be done under medical supervision. The first step, detoxification, is often done with the help of prescription medication to make the process more comfortable, but counseling is also needed to prevent the relapses that are common with this disease. Unfortunately, millions of addicts who could benefit from care at a specialty facility like a rehabilitation center don’t receive it, according to the NSDUH. For those who are addicted to two or more substances (what’s called a poly-drug addiction), treatment providers need to consider every substance a person is using when creating a treatment plan.

If you suspect that you or a loved one has a substance use problem, talk to a doctor, health care professional, addiction specialist or psychotherapist. These professionals can evaluate symptoms and make an accurate diagnosis that will help the recovery process begin.

People who abuse substances often say they take them to have fun or get high. It’s not that simple for addicts, though. An addicted person can no longer control whether or not he/she uses. Mentally and physically, the addict feels compelled to have the drug. Addiction is considered a chronic disease with the possibility of relapse an ever-present reality.

What you should know:

  • Addiction is a disease that is complex but treatable.

  • Prolonged drug use affects brain function.

  • Illegal drugs are defined as controlled substances under federal and state law. They are monitored and enforced by the Drug Enforcement Agency (DEA).

  • Marijuana is the most-used illicit drug, with 19.8 million U.S. users age 12 and over, according to the 2013 National Survey on Drug Use and Health (NSDUH), which is published by the Substance Abuse and Mental Health Services Administration (SAMHSA).

  • Six-and-a-half million Americans use prescription pain relievers non-medically, and 1.5 million are dependent on or abusing cocaine, according to SAMHSA’s 2013 NSDUH survey.

  • In 2013, 22.7 million people 12 and over who could have benefited from substance use treatment in a specialty facility did not receive that help. It’s a myth that someone must want to go into treatment for substance abuse for it to be effective, says the National Institute on Drug Abuse (NIDA).

Causes

For decades, researchers have been trying to figure out what leads people to become addicted to drugs. While there’s no single root cause of drug addiction, experts think a combination of the following are most likely to play a role:

  • Your role models. Your early years, including your mother’s and father’s parenting styles and whether one or both parents or even an older sibling abused substances can affect whether you experiment with drugs and go on to develop an addiction. Our early role models, for good or ill, influence our behavior. They can also teach us appropriate ways to handle problems, bounce back and persevere; these coping skills make it less likely someone will develop an addiction. A family history of substance abuse is also linked to an increased risk. For more on the role of genetics, go the Risk Factors section.

  • Your personal history. Stressful or traumatic events, living in poverty, the availability of illegal drugs, peer pressure and whether or not your friends and family use drugs – all are associated with a greater likelihood of developing a substance abuse problem.

  • Your psychological makeup. How you feel about yourself, especially your self-esteem during adolescence, your temperament, a tendency toward impulsive behavior and exhibiting aggressive or antisocial behavior early in life are thought to forecast later drug or alcohol problems as well as a tendency toward violence.

On the flip side, there are factors that can lower someone’s chances of having an addiction; these include developing good self-control, practicing religious beliefs, having healthy relationships with family and friends and being involved in social activities in the community, reports SAMSHA.

Symptoms of Drug Addiction

There are a number of signs that may indicate a substance abuse problem, including:

  • A change in friends and hangouts

  • An unexplained need for cash

  • Bloodshot eyes or enlarged pupils

  • Sudden weight changes (gain or loss)

  • Tremors in the hands

  • Slurred speech

  • Foul-smelling breath

  • Secretive behaviors

  • A drop in attendance at work or school

  • Lying

  • Belligerence

  • Changes in sleep, mood, motivation or attitude

Keep in mind that physical dependence on a drug or medication is not the same thing as having an addiction; a person may be dependent on a drug if he or she experiences withdrawal symptoms if the drug is stopped. Someone may also develop a tolerance to the substance so that he or she requires increasingly larger doses of a drug in order to achieve the same effect or high. And when a drug user comes off a substance, he or she may experience withdrawal symptoms that vary depending on the substance(s).  According to the American Psychiatric Association’s (APA) diagnostic manual, DSM-5, “Neither tolerance nor withdrawal is necessary for a diagnosis of a substance use disorder.”

Doctors, therapists and addiction counselors look at a variety of factors when deciding whether someone has a substance use disorder. If you or a loved one have two or three of the indicators below, it can point to a mild problem with drugs, while having four or five symptoms can underscore a moderate problem. Six or more of these symptoms may signal a severe substance use disorder. No matter how serious a drug problem is, recognizing the symptoms of drug addiction is the all-important first step to getting help – and recovering. So ask yourself these questions:

Are you or a loved one…

  • Using a substance over a longer time period of time than planned?

  • Making unsuccessful attempts to control or stop taking the drug(s)?

  • Spending a lot of time finding, using or recovering from using a substance(s)?

  • Experiencing cravings for a substance(s)?

  • Failing to show up or fulfill expectations at work, school or home?

  • Continuing to use an illegal substance(s) despite problems it’s causing in relationships?

  • Giving up activities once enjoyed in order to use a drug(s)?

  • Using a drug(s) regularly while in situations where it poses physical danger (such as driving, operating machinery or boating)?

  • Ignoring physical or psychological problems resulting from drug use?

  • Developing a tolerance for a drug’s effects?

  • Experiencing withdrawal symptoms or masking them with another substance(s)?

Risk Factors

The more you know about substance abuse, the better the chances of avoiding a drug addiction before it starts. Here are several red flags that raise the risk of becoming a substance abuser:

Source of article:  Addiction.com

  • Inheriting the genes
    As mentioned above, your biological makeup has a lot to do with whether you’ll develop an addiction. In fact, the APA goes so far as to say that 50% of your susceptibility to becoming addicted is related to genetic factors. And when it comes to tobacco, genetics account for 75% of a person’s tendency to try smoking and 60% of their chances of becoming hooked. But DNA alone isn’t destiny. Besides the genes you’re born with, environmental factors, like how you were raised; whether you were sexually or physically abused; and whether you grew up in poverty or witnessed violence can also influence a person’s vulnerability to addiction.

  • Dealing with a mental health issue
    If you or someone you love suffers from a mental disorder such as depression, anxiety, attention deficit disorder, post-traumatic stress disorder schizophrenia or an eating disorder, among other conditions, substance abuse is likelier to become a problem. In 2013, nearly eight million U.S. adults had both a substance use disorder and at least one mental issue. And 2.3 million of that group had a co-occurring SUD and a serious mental health issue, which the NSDUH defines as “a mental, behavioral or emotional disorder that substantially interferes with or limits one or more major life activities.”

  • Experimenting at an early age
    In 2013, nearly 9% of U.S. adolescents ages 12 to 17 were illicit drug users, and 1.3 million teens had a diagnosed SUD. While it’s possible to become an addict at any age, many teens are natural risk-takers, mostly because the parts of the brain in charge of self-control and good judgment are still developing in adolescence. That can make trying illicit drugs a lot more attractive. The trouble is, say experts at NIDA, “the earlier drug use begins, the more likely it will progress to more serious abuse.” And there’s some evidence to suggest that how a drug is taken – especially if it’s smoked or injected into a vein – may increase its risk of becoming addictive.

    There’s no single treatment that’s right for someone trying to overcome a substance addiction. Treatment for a substance use disorder (SUD) usually begins with detoxification or “detox” – a process during which the patient is medically supported while the substance(s) is removed from the person’s system. When someone enters treatment, one of the first things he/she may experience during the detox process is withdrawal, which can include physical symptoms such as nausea, diarrhea, shaking, fever, insomnia and sweating and/or psychological symptoms such as depression, anxiety, anger and upset. In some cases, a drug rehabilitation center will use FDA-approved medications to help counteract withdrawal symptoms with the goal of weaning the patient off the medication as soon as possible; although sometimes medication-assisted therapy is needed on a long-term basis to prevent cravings that can trigger drug-seeking behavior and relapse. While detox is the first step to any kind of treatment, counseling is also typically needed to achieve lasting results.

    Whether a substance use disorder is mild, moderate or severe, some kind of treatment is usually necessary, which makes it tragic that only a small number of those who need help actually get it. According to the Substance Abuse and Mental Health Services Administration’s National Survey on Drug Use and Health (2013), only 2.5 million people out of the 22.7 million people who needed treatment for drug or alcohol use actually received help at a specialty facility While there’s no cure for drug addiction, for most (though not all), abstinence or giving up the substance entirely is necessary.

    Below are some of the most common treatment options for substance use disorders. If you or a loved one seek treatment for drug addiction, it’s likely that a combination of several of these approaches will be recommended and used:

    Counseling

    Drug rehabilitation programs use a variety of counseling approaches to help people experience lasting recovery. Types of counseling include:

  • SMART Recovery® (Self-Management and Recovery Training): This community-support program has a four-point plan to teach self-reliance, and clients using SMART Recovery benefit from online support groups, message boards and chat rooms as well as in-person meetings to stay motivated in their recovery efforts.

  • BRENDA: BRENDA combines psychosocial counseling and pharmacotherapy (prescription drugs) to help patients deal with substance addiction. The acronym refers to the steps a counselor takes in treating a client using this method:

  • Biopsychosocial evaluation
    Report to the patient on evaluation findings
    Empathy
    Needs identified by both the patient and therapist
    Direct advice to the patient
    Assessing the patient’s reaction to advice; modifying the plan when needed

    This treatment model uses a type of psychotherapy called cognitive-behavioral therapy (CBT) in which a therapist will help clients examine their thinking and feelings in an effort to change negative and unproductive thoughts and beliefs that may lead to drug use.

    Other types of counseling:

  • Motivational incentives: For gains made in treatment, drug and alcohol counselors may offer a reward system to encourage patients to work hard in recovery. Rewards might be for a special privilege, outing or voucher.

  • Motivational Interviewing (MI): Therapists who use MI help clients feel inspired and empowered to make needed life changes and to reach recovery goals.

  • Multidimensional Family Therapy (MDFT): Sometimes the whole family needs to be willing to evaluate its dynamics in order to help one or more member(s) overcome an addiction and/or another mental health issue. MDFT involves the whole family in the healing process to improve relationships, end enabling behavior and create harmony.

  • Drug Rehabilitation

    Sometimes the right option for treating drug addiction may be going to an inpatient or residential treatment center to live for a period of time. How long depends on the severity of the addiction, the kind of addiction(s) and the patient’s progress. These specialized facilities offer medically-supervised detox, which is a process to get drugs out of the bloodstream and tissues. In rehab, patients also receive intensive counseling to cope with triggers, cravings and any co-occurring mental health disorders. It’s helpful to think of rehab as a kind of retreat where the addict lives and works on learning to overcome triggers of addiction and manage any underlying mental disorders that require treatment along with the substance use disorder.

    There are also outpatient rehab programs where patients live at home but attend a drug treatment (or partial hospitalization) program during the day, which may last for seven or eight hours. Or you or your loved one may attend an evening program that meets several times a week for several hours in the evenings only. With outpatient day or evening programs, patients sleep at home, which can be successful as long as drug networks, old haunts and triggers don’t interfere with the progress of treatment. While in treatment, patients in these programs, too, work on understanding their addiction and any mental health issues through counseling.

    When selecting a program, be aware that there are customized programs tailored to groups of people who are like-minded; by bringing together people from similar backgrounds who are grappling with the same or similar issue, members can effectively work together as a group. Program alumni may even meet up later for special weekends and offer one another ongoing support in recovery. Read on for several examples of custom-tailored programs now being offered by some treatment centers:

  • Christian programs address drug addiction with a Bible-based approach, so attendees can find strength through faith. Treatment may include counseling and 12-step or other community-support programs, yet the focus on scripture allows members of these programs to be guided to recovery in large part through their beliefs.

  • Women-only programs address both the substance use disorder as well as any past history of abuse or trauma or mental illness that may underpin a drug addiction.

  • Adolescent programs tend to be gender-specific and allow teens a safe place where they can work to overcome drug addiction while also attending classes, so they don’t fall behind in school during treatment.

  • Spanish-speaking programs make treatment more relatable for those who speak English as a second language. Counselors, too, speak Spanish, and all written materials are printed in Spanish.

  • Medication-Assisted Therapy (MAT)

    The Food and Drug Administration (FDA) has approved several prescription medications for the treatment of substance use disorders. Medication-assisted therapy proves most effective when used in conjunction with other approaches, such as counseling. Pharmacological approaches designed to help substance abusers detox and reduce the chances of relapse include these medications:

  • For opioids: The FDA has approved several prescription medications for opiate addiction to heroin, morphine or prescription painkillers like oxycodone and hydrocodone. There are a variety of prescription drugs that are used in treating opioid use disorders with active ingredients that either reduce withdrawal symptoms, like cravings, or block the effects of opiates altogether. These include:

    Buprenorphine – (brand name: Subutex):  An initial treatment to prevent or reduce withdrawal symptoms such as drug cravings

    Methadone – (brand names: Dolophine or Methadose): Used to prevent withdrawal symptoms and to block the high from taking illicit opiates. Only authorized, specially licensed facilities can administer methadone maintenance.

    Naltrexone – (brand names: Depade, Revia, and Vivitrol): All three block the effects of opioids; Vivitrol is an extended-release injection, given once a month.

    Naloxone – (brand name: Suboxone): Prescribed as a maintenance medication that contains buprenorphine as well, Suboxone blocks or reverses the effects of opioids. For opioid overdoses, Evzio, an auto-injector containing naloxone, is available for emergency home use.

  • While there are other prescription medications in the drug pipeline and now being tested, there are no drugs currently available for the treatment of cocaine, methamphetamine, cannabis (marijuana) or hallucinogen use disorders.

    12-Step Programs

    The original 12-step program is one you’ve undoubtedly heard of before: Alcoholics Anonymous (AA), which has been around since 1935. AA has been helping alcoholics get and stay sober for decades with meetings available in big cities and small towns across the globe. Over time, this community of support, in which alcoholics help each other, has inspired other, similar programs for a wide variety of drug addictions that people grapple with:

  • Cocaine Anonymous

  • Crystal Meth Anonymous

  • Heroin Anonymous

  • Marijuana Anonymous

  • Narcotics Anonymous

  • Nicotine Anonymous

  • Pills Anonymous

  • These 12-step programs borrow at least in part from the AA model, which is based on 12 consecutive processes (each step building on the one(s) preceding it). The steps include minimizing self-centeredness, providing support to others in the group and making amends to those whom the substance abuser has hurt, among others. For a full list of the 12 steps, go to the Get Help section.

    While some addicts rely solely on 12-step programs to treat and recover from their drug addiction, others use it in conjunction with counseling. And often 12-step programs are included as part of inpatient and outpatient drug rehabilitation.

    Suboxone | NOVA Addiction Specialists | 703-844-0184 | Heroin and drug abuse treatment
  • For tobacco/nicotine: For tobacco products containing highly addictive nicotine, several nicotine replacement therapies are available over-the-counter at drugstores. These include nicotine patches, sprays, gums and lozenges that alleviate drug cravings. Prescription drugs such as bupropion (brand names: Wellbutrin, Zyban) and varenicline (brand name: Chantix) are also FDA-approved.

  • If you find yourself asking the question, Am I addicted to drugs? you should take the answer to that question very seriously. Unless recognized and treated, an addiction to a medication or illicit/illegal drug can greatly diminish your chances of leading a functional life, maintaining a daily routine or experiencing an enduring sense of well-being. Fortunately, you can perform a fairly accurate self-assessment of your drug-using status if you know the signs that indicate active addiction.

    What Is Drug Addiction?

    The potential for drug (and alcohol) addiction arises when your brain starts to treat the chemical changes triggered by your habitual substance intake as a normal operating condition. Experts in the field refer to this state as physical dependence. Physical dependence transitions into active addiction when you lose control over your ability to limit the number of times you use a given substance and/or your ability to limit the amount of that substance you take on any given occasion.

    Signs to Look For

    In addition to losing control over the frequency and amount of your drug intake, you may also experience a range of other problems that point to the presence of an addiction. Specific things you may notice include:

  • An intense desire for the drug

  • The need to increase your intake of the drug in order to keep feeling its effects

  • Establishment of drug use as your daily priority

  • Devotion of money to purchasing drugs even if it means failing to meet important financial obligations

  • A drug-based inability to meet other important personal, social, school-related or work-related responsibilities

  • Repeated use of drugs in situations that pose a clear danger to yourself or others

  • Overlap With Substance Abuse

    When trying to figure out if you are addicted to drugs, it’s crucial to understand that doctors and public health officials don’t make a firm distinction between drug addiction and non-addicted drug abuse. Even if you don’t have problems with physical dependence, you can experience changes in your thoughts and behaviors that significantly interfere with your ability to function or maintain a feeling of wellness. In fact, the guidelines currently used by doctors in the U.S. include the symptoms of addiction and non-addicted substance abuse in a single illness category called substance use disorder. There are subtypes of this disorder for alcohol and every major addictive drug/medication.

    Resources

    Mayo Clinic: Drug Addiction – Symptoms
    http://www.mayoclinic.org/diseases-conditions/drug-addiction/basics/symptoms/con-20020970

    Substance Abuse and Mental Health Services Administration: Substance Use Disorders https://www.samhsa.gov/disorders/substance-use

  • An inability to stop using a drug for any substantial amount of time, and

  • The appearance of withdrawal symptoms if you halt your drug use even briefly

SUBOXONE| KETAMINE | 703-844-0184 | Sublocade for Opioid Use disorders | FAIRFAX | ALEXANDRIA | WOODBRIDGE | BUPRENORPHINE INJECTION | SUBLOCADE || SUBLOCADE IS NOW AVAILABLE || ADDICTION DOCTORS | TELEMEDICINE | BUPRENORPHINE INJECTABLE | SUBLOCADE : 22303 22307 22306 22309 22308 22311 22310 22312 22315 22003 20120 22015 22027 20121 22031 20124 22030 22033 22032 22035 22039 22041 22043 22042 22046 22044 22060 22066 20151 22079 20153 22101 22102 20171 20170 22124 22151 22150 22153 22152 20191 20190 22181 20192 22180 20194 22182

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I’m posting two totally unrelated items. One is a link to anti-inflammatory recipes I found to be pretty good. Then below is a link to Pharmacy Times article regarding Sublocade, the new once-a-month injectable version of Suboxone.

Anti-inflammatory Dinner Recipes

20 Easy Anti-Inflammatory Dinner Recipes That Will Make You Feel Great

 

Sublocade for Opioid Use disorder

Sublocade for Opioid Use Disorder: What Pharmacists Should Know

JANUARY 01, 2018

The United States is in the middle of an opioid abuse epidemic. Since 1999, the number of overdose deaths involving opioids has quadrupled and currently an estimated 91 Americans die every day from an opioid overdose.1 Over recent years, an emphasis has been placed on the role of medication-assisted treatment (MAT) combined with psychosocial support to combat the growing opioid epidemic.

In November 2017, the FDA approved Indivior’s Sublocade, an extended-release buprenorphine injection for the treatment of moderate-to-severe opioid use disorder (OUD) in adult patients who have initiated treatment with a transmucosal buprenorphine-containing product. With its approval, Sublocade became the first once-monthly buprenorphine injection for the treatment of OUD.

This article highlights several key therapeutics areas with Sublocade that every pharmacist should know.

Indication2
Sublocade contains buprenorphine, a partial opioid agonist, and is indicated for the treatment of moderate-to-severe OUD in patients who have initiated treatment with a transmucosal buprenorphine-containing product, followed by dose adjustment for a minimum of 7 days.

Sublocade should be used as part of a complete treatment program that includes counseling and psychosocial support.

Limitations of Use
The safety and effectiveness of Sublocade have not been established in pediatric patients.

Additionally, Sublocade is not appropriate for use in opioid naïve patients or for treatment where Sublocade would be the first buprenorphine product used.

Mechanism of Action
Sublocade contains an extended-release formulation of buprenorphine, which is a partial agonist at the mu opioid receptor and an antagonist at the kappa opioid receptor. Buprenorphine displays high affinity at these receptions and therefore is not easily replaced by other opioids.

Formulation and Storage
Sublocade is available as a sterile, clear solution in a single dose, prefilled syringe with safety needle. It is available in 2 formulations: 100 mg/0.5 mL and 300 mg/1.5 mL.

It should be stored in refrigeration at 2 to 8°C (35.6 to 46.4°F). Once outside the refrigerator it may be stored in its original packaging at room temperature for up to 7 days prior to administration. If left at room temperature for longer than 7 days Sublocade should be discarded.

Medication Availability
Only health care providers should prepare and administer Sublocade. Additionally, Sublocade is subject to a risk evaluation and mitigation strategy (REMS) program that includes a restricted distribution system to ensure that Sublocade is only administered by a healthcare provider. Therefore, this is not a medication that would typically be dispensed through retail pharmacy.

Dosing
The recommended dose of Sublocade following induction and dose adjustment with transmuscosal buprenorphine is 300 mg monthly by subcutaneous injection in the abdominal region for the first 2 months followed by a maintenance dose of 100 mg monthly.

The maintenance dose may be increased to 300 mg monthly for patients who tolerate the 100 mg dose, but do not demonstrate a satisfactory clinical response, as evidenced by self-reported illicit opioid use or urine drug screens positive for illicit opioid use.

A patient who misses a dose should receive the next dose as soon as possible, with the following dose given no less than 26 days later. Occasional delays in dosing up to 2 weeks are not expected to have a clinically significant impact on treatment effect.

Notably, Sublocade is only appropriate in adults who have initiated treatment on a transmucosal buprenorphine-containing product delivering the equivalent of 8 to 24 mg of buprenorphine daily. The patient may only be transitioned to this medication after a minimum of 7 days. Initiating treatment with Sublocade as the first buprenorphine product has not currently been studied.

Efficacy
The efficacy of Sublocade for the treatment of moderate to severe OUD was established in a phase 3 double-blind study and an opioid blockage study.

The phase 3 study was a 24-week, randomized, double-blind, placebo-controlled, multicenter trial in treatment-seeking patients who met the DSM5 criteria for moderate or severe OUD. Patients were randomly assigned to one of following dosing regimens: 6 once-monthly 300 mg doses, 2 once-monthly 300 mg doses followed by 4 once-monthly 100 mg doses, or 6 once-monthly SC injections of placebo. All patients received psychosocial support at least once a week. Prior to the first dose, treatment was initiated with Suboxone (buprenorphine/naloxone) sublingual film with doses adjusted from 8/2mg to 24/6 mg per day over a period of 7 to 14 days. Efficacy was evaluated over weeks 5 through 24 based on weekly urine drug screens combined with self?reported use of illicit opioid use.

A total of 504 patients were randomized into the study. Based on the cumulative distribution function (CDF) of the percentage of urine samples negative for illicit opioids combined with self-reports collected from week 5 through week 24, regardless of dose, Sublocade was statistically superior to the placebo group. Additionally, the proportion of patients achieving treatment success (defined as patients with ≥80% opioid?free weeks) was statistically significantly higher in both groups receiving Sublocade compared to the placebo group (28.4% [300 mg/100 mg], 29.1% [300 mg/300mg], 2% [placebo]).

The opioid blockage study evaluated the blockage of subjective opioid effects, pharmacokinetic, and safety of Sublocade in 39 patients with OUD. In the study, the average buprenorphine plasma concentrations of 2-3 ng/mL were associated with mu-opioid receptor occupancy ≥70%. Additionally, Sublocade was shown to be non-inferior to hydromorphone injections in terms of “drug liking.”

Safety
The most common adverse reactions of Sublocade reported in clinical trials include constipation, headache, nausea, injection site pruritus, vomiting, increased hepatic enzymes, fatigue, and injection site pain.

Sublocade has a boxed warning noting that serious harm or death could result if this medication is administered intravenously. Other warnings and precautions in the prescribing information include a risk of addiction, abuse, and misuse, respiratory depression, adrenal insufficiency, hepatic events, and opioid withdrawal with abrupt discontinuation.

Drug interactions
Benzodiazepines and other central nervous system (CNS) depressants should be used with caution due to an increased risk of respiratory depression. Patients taking CPY3A4 inhibitors and substrates should be closely monitored for potential over- or under-dosing.

Product Comparison3

Indication Administration Frequency Generic Available4
Sublocade (buprenorphine) Opioid dependence SQ Injection Monthly N
Probuphine (buprenorphine) Opioid dependence Intradermal implant 6 months x 1 dose N
Suboxone (buprenorphine and naloxone) Opioid dependence Sublingual tablet and film Daily Y (tablet), N (film)
Subutex (buprenorphine) Opioid dependence Sublingual tablet Daily Y
Zubsolv (buprenorphine and naloxone) Opioid dependence Sublingual tablet Daily N
Bunavail (buprenorphine and naloxone) Opioid dependence Buccal film Daily N
Buprenex (buprenorphine) Pain IM or IV injection Varies Y
Belbuca (buprenorphine) Pain Film Twice daily N
Butrans (buprenorphine) Pain Transdermal patch 7 days on, 3 weeks off N

Conclusion2
In clinical studies, Sublocade was shown to be effective in reducing illicit opioid use as compared to placebo and block ≥70% of mu-opioid receptors. Sublocade was relatively well-tolerated with most adverse effects attributed to injection site reactions and other effects common to all buprenorphine products. Sublocade is advantageous as a once monthly injection which can help remove the burden and decision of having to take another buprenorphine medication on a day-to-day basis. For some people, this may help improve adherence. Although Sublocade is the first once-monthly buprenorphine injection for the treatment of OUD another long-acting buprenorphine product, Probuphine, has been available on the market since 2016. Head to head studies would be beneficial to compare the efficacy of Sublocade versus other buprenorphine containing products.

References

  1. Understanding the Epidemic. CDC. https://www.cdc.gov/drugoverdose/epidemic/index.html. Accessed December 15, 2017
  2. Sublocade [Prescribing Information]. Indivior Inc. North Chesterfield, VA. November 2017.
  3. Lexicomp Online®, Lexi-Drugs®, Hudson, Ohio: Lexi-Comp, Inc.; December 15, 2017.
  4. Electronic Orange Book. Food and Drug Administration. Available at: http://www.fda.gov/cder/ob/default.htm/. Accessed December 20, 2017

 

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NOVA Addiction Specialists website – Suboxone and telemedicine treatment in Alexandria, Virginia 703-844-0184

Dr. Sendi – at NOVA Addiction Specialists can evaluate you to see if Sublocade will work for you.

NOVA Addiction facebook page

Suboxone treatment in Alexandria, Virginia 703-844-0184

Suboxone treatment in Fairfax, Virginia 703-844-0184

http://www.suboxonewoodbridge.com

Suboxone, buprenorphine telemedicine treatment in Alexandria  << Link here

http://addictiondomain.com/ Addiction Blog

https://www.facebook.com/novaddiction – Facebook page

http://www.suboxonealexandria.com

http://www.suboxonecenter.org/ Suboxone treatment – telemedicine also – 703-844-0184 24/7

 

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Blocking microglial pannexin-1 channels alleviates morphine withdrawal symptoms

Opiates are essential for treating pain, but termination of
opiate therapy can cause a debilitating withdrawal syndrome
in chronic users. To alleviate or avoid the aversive symptoms
of withdrawal, many of these individuals continue to use
opiates1–4. Withdrawal is therefore a key determinant of opiate
use in dependent individuals, yet its underlying mechanisms
are poorly understood and effective therapies are lacking. Here,
we identify the pannexin-1 (Panx1) channel as a therapeutic
target in opiate withdrawal. We show that withdrawal from
morphine induces long-term synaptic facilitation in lamina I
and II neurons within the rodent spinal dorsal horn, a principal
site of action for opiate analgesia. Genetic ablation of Panx1
in microglia abolished the spinal synaptic facilitation and
ameliorated the sequelae of morphine withdrawal. Panx1
is unique in its permeability to molecules up to 1 kDa in size
and its release of ATP5,6. We show that Panx1 activation
drives ATP release from microglia during morphine withdrawal
and that degrading endogenous spinal ATP by administering
apyrase produces a reduction in withdrawal behaviors.
Conversely, we found that pharmacological inhibition of
ATP breakdown exacerbates withdrawal. Treatment with
a Panx1-blocking peptide (10panx) or the clinically used
broad-spectrum Panx1 blockers, mefloquine or probenecid,
suppressed ATP release and reduced withdrawal severity.
Our results demonstrate that Panx1-mediated ATP release
from microglia is required for morphine withdrawal in rodents
and that blocking Panx1 alleviates the severity of withdrawal
without affecting opiate analgesia. 

Could This Inexpensive Medication Reduce Your Withdrawal Symptoms?

Could This Inexpensive Medication Reduce Your Withdrawal Symptoms?

Withdrawal. It’s a huge hurdle on the path to recovery.

Those struggling to leave opioids behind know they’ll eventually have to face the intimidating mental and physical effects of withdrawal. It’s a powerful and frightening thought.

Some of the most common withdrawal symptoms include:

  • Muscle aches and cramps
  • Nausea, vomiting, and diarrhea
  • Anxiety, profuse sweating, and restlessness
  • Blurry vision
  • High blood pressure

Help Where It’s Needed Most

Even though millions of Americans are in the midst of this battle, few medications are available to effectively manage their symptoms. This unavailability – and the onset of painful withdrawal symptoms – are often enough to make many people give up and return to opioids for relief.

But this could soon change…

According to the results of a recent study, help for intense withdrawal symptoms might be on the horizon, thanks to the discovery of a new drug.

“Opioid withdrawal is aversive, debilitating, and can compel individuals to continue using the drug in order to prevent these symptoms,” explains lead researcher Tuan Trang, PhD.

“In our study, we effectively alleviated withdrawal symptoms in rodents, which could have important implications for patients that may wish to decrease or stop their use of these medications.”

The Study

Researchers from the University of Calgary’s Faculty of Veterinary Medicine and Hotchkiss Brain Institute investigated the process of withdrawal and its’ possible causes. The study involved rats which had been given two potent opioids, morphine and fentanyl. The team identified the glycoprotein, pannexin-1, as the source of withdrawal symptoms in rodents. Pannexin-1 is also located throughout the human body, including the brain and spinal cord.

After identifying the cause of these symptoms, the team tested a drug already proven to block the effects of pannexin-1 called, Probenecid. It’s an anti-gout medication that’s fairly cheap and has few side effects.

The results showed this medicine was “effective in reducing the severity of withdrawal symptoms in opioid-dependent rodents.” Another encouraging aspect about their findings: the medication didn’t affect an opioids’ ability to relieve pain.

Previous research hadn’t explored this avenue, and this investigation has provided a better understanding of opioid withdrawal at the cellular level.

The Implications

Canadian pain researcher, Dr. Michael Salter, notes, “This is an exciting study which reveals a new mechanism and a potential therapeutic target for managing opioid withdrawal. The findings of Dr. Trang and his team could have important implications for people on opioid therapy and those attempting to stop opioid use.”

The team behind the study plan to continue their work and hope this new insight will lead to the creation of a more effective treatment method for the symptoms of withdrawal. Dr. Trang says their next steps will be to determine the drug effectiveness in humans and to ensure its’ safety. Their goal is to develop an effective method to treat the millions struggling with pain management and opioid dependency across the nation and around the world.

These results have already lead to the development of a clinical trial at the Calgary Pain Clinic.

 

FDA approves first medication to reduce opioid withdrawal symptoms

Announcement

May 16, 2018

LofexidineCourtesy of US WorldMeds, LLC.

The National Institute on Drug Abuse (NIDA), part of the National Institutes of Health, is pleased to announce that lofexidine, the first medication for use in reducing symptoms associated with opioid withdrawal in adults, has been approved by the U.S. Food and Drug Administration. Lofexidine, an oral tablet, is designed to manage the symptoms patients often experience during opioid discontinuation. Opioid withdrawal symptoms, which can begin as early as a few hours after the drug was last taken, may include aches and pains, muscle spasms/twitching, stomach cramps, muscular tension, heart pounding, insomnia/problems sleeping, feelings of coldness, runny eyes, yawning, and feeling sick, among others. The product will be marketed under the brand name LUCEMYRATM.

In 2016, more than 42,000 people died from an opioid overdose, or approximately 115 people per day. Although effective treatments exist for opioid addiction, painful and difficult withdrawal is one of the reasons treatment fails, and relapse occurs. By alleviating symptoms associated with opioid withdrawal, LUCEMYRA could help patients complete their discontinuation of opioids and facilitate successful treatment. To date, no other medications have been approved to treat opioid withdrawal symptoms.

LUCEMYRA will be marketed by US WorldMeds, a specialty pharmaceutical company that acquired a license for lofexidine from Britannia Pharmaceuticals in 2003. NIDA provided funding to US WorldMeds to support clinical trials to document the clinical pharmacokinetics of lofexidine and to test medical safety and efficacy of the medication, as compared to a placebo, among patients undergoing medically supervised opioid discontinuation. LUCEMYRA is expected to be commercially available in the United States in August 2018.

Read FDA press release: FDA approves the first non-opioid treatment for management of opioid withdrawal symptoms in adults

Read NIDA Director Dr. Nora Volkow’s blog: NIDA-Supported Science Leads to First FDA-Approved Medication for Opioid Withdrawal

For more information about opioids, go to the Opioids webpage. For information about treatment approaches for drug addiction, go to Treatment Approaches for Drug Addiction.

Medication for Opioid Withdrawal

 

May 16, 2018

Image of drug Lucemyra (Lofexidine)Courtesy of US WorldMeds, LLC

In 2016, 115 Americans died every day from an overdose involving prescription or illicit opioids. Addiction to any drug has multiple components—altered functioning of the reward system, learned associations with drug cues that promote preoccupation and craving, and changes to prefrontal circuits necessary for proper exertion of self-control. But physiological and psychological withdrawal symptoms play a major role in driving users repeatedly back to the drug, despite efforts to stop using.

Withdrawal is notoriously hard to endure for people addicted to opioids. Physical symptoms can start a few hours after last taking the drug and may include stomach cramps, aches and pains, coldness, muscle spasms or tension, pounding heart, insomnia, and many others. These symptoms, along with mood changes, like depression and anxiety, are a major reason people with opioid addiction may relapse. Yet until now, no medication has been approved to treat withdrawal.

This week, the Food and Drug Administration (FDA) approved lofexidine, the first medication targeted specifically to treat the physical symptoms associated with opioid withdrawal. NIDA’s medications development program helped fund the science leading to the drug’s approval. Lofexidine could benefit the thousands of Americans seeking medical help for their opioid addiction, by helping them stick to their detoxification or treatment regimens.

Two of the three FDA-approved medications to treat opioid use disorder, methadone and buprenorphine, can be initiated while a person is experiencing withdrawal symptoms, and can help curb craving. However, these medications are not always easy to access, and at this point are only received by a minority of people with opioid use disorder. The third FDA-approved drug, extended-release naltrexone, has also been found effective, but only after people have been fully detoxified.  The need to detox first—and endure those symptoms—prevents many patients from being treated with naltrexone. Lofexidine could make a big difference in making the latter treatment option more widely used.

New Nonopioid Med Blunts Drug Withdrawal Symptoms  < Medscape

Lofexidine is not an opioid. It acts to inhibit the release of norepinephrine in the brain and elsewhere in the nervous system. It was originally developed as a medication for hypertension, but has mainly been used for opioid withdrawal in the United Kingdom since the early 1990s. US WorldMeds acquired a license for lofexidine from Britannia Pharmaceuticals in 2003 and will market it in the US under the brand name LUCEMYRATM beginning this summer. NIDA helped fund the clinical trials to test lofexidine’s pharmacological properties, safety, and efficacy in patients who were discontinuing opioid use under medical supervision.

Lofexidine cannot address the psychological symptoms of opioid withdrawal; further research is needed to develop medications that could address mood problems during detoxification and after. But approval of the first medication to treat the physical symptoms of opioid withdrawal is a major milestone, one that could improve the lives and treatment success of thousands of people living with opioid addiction. And by helping prevent relapse, it could save lives. The approval of lofexidine is also a welcome example of the power of public-private collaborations in developing new treatments.

MIAMI — Lofexidine (Lucemyra, US Worldmeds), which has been in use in the United Kingdom for more than 20 years, is now
available in the United States. The drug is used in the management of symptoms of severe opioid withdrawal.
Dr Danesh Alam
In a double-blind, placebo-controlled, multicenter trial in opioid-dependent patients, lofexidine significantly improved opioid
withdrawal symptoms and significantly increased completion of a 7-day opioid discontinuation treatment program compared with
placebo.
“We desperately need something to address the opioid crisis, where we are losing about 100 Americans every day, with some
16 million on opioids,” Danesh Alam, MD, Northwestern Medicine Central Dupage Hospital, Winfield, Illinois, told Medscape
Medical News.
“Now we have a drug that actually enables us to achieve a rapid withdrawal from opioids. When we use lofexidine, we can
literally bring in someone using opioids, give them this drug, and they can immediately stop using opioids,” said Alam.
The study was presented at the American Society for Clinical Psychopharmacology (ASCP) 2018.
A Better Alternative
Currently, the standard of care for the treatment of opioid withdrawl is medication-assisted therapy with buprenorphine (multiple
brands), but many patients wish to stop using opioids completely, Alam said.
“Buprenorphine is essentially another opioid, albeit a designer opioid, but a number of patients object to clinicians saying that
the best evidence is to switch them over to buprenorphine and do buprenorphine for the rest of their life,” he said.
Lofexidine, a selective alpha-2-adrenergic agonist, acts on the central nervous system. Through its effect on the brain stem, it
reduces the symptoms of withdrawal to a point at which they become very tolerable.
“We found in our study that you could basically give patients the lofexidine and stop the opiate. In the majority of cases, the
withdrawal symptoms at that point were mild,” Alam said.
The researchers enrolled 602 men and women aged 18 years or older who sought treatment for dependence on short-acting
opioids. Most were men (71%); the mean age of the patients was 35 years (±11 years).
Most patients (83%) were dependent on heroin.
Participants were randomly assigned to receive placebo, lofexidine 0.6 mg qid (2.4 mg/day), or lofexidine 0.8 mg qid (3.2
mg/day) for 7 days after abrupt opioid discontinuation.
The study assessed the benefit of lofexidine with the Short Opiate Withdrawal Scale–Gossop (SOWS-G), a 10-item inventory of
common opioid withdrawal symptoms in which higher scores indicate worse symptoms; by the percentage of participants who
completed the study; and by use of the Clinical Opiate Withdrawal Scale (COWS), an 11-item inventory of opioid withdrawal
signs and symptoms in which higher scores indicate worse symptoms.

Scores on the SOWS-G were lower for patients treated with lofexidine at both doses compared to patients given placebo (-0.21
for lofexidine 2.4 mg, P = .02; and -0.26 for lofexidine 3.2 mg, P = .003). More patients in the lofexidine-treated group completed
the 7-day trial than in the placebo group (41.5% in the 2.4-mg group (odds ratio [OR], 1.85, P = .007), and 39.6% in the 3.2-mg
group (OR, 1.71; P = .02), vs 27.8% for placebo.
Mean COWS scores were significantly lower on days 1 to 5 for patients in the lofexidine groups than for patients who received
placebo (P < .01).
Good Timing
The most common side effects seen with lofexidine were hypotension, orthostatic hypotension, and bradycardia, but they
resulted in few study discontinuations.
The US debut of lofexidine comes at a crucial time. It was recently granted approval by the US Food and Drug Administration
(FDA), as reported by Medscape Medical News.
This approval came after 17 years of hard work on the part of the National Institute on Drug Abuse (NIDA).