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Ketamine has much support in the use of hard-to-treat depression and suicidal behaviors. Below are studies and their links, including a meta-analysis, which demonstrate the effect of Ketamine. Also a recent trial by Carlos Zarate shows the heterogenous nature of response to Ketamine . It is difficult to say who is going to be lifted from their depression completely or partially respond, but in the study, Dr. Zarate showed that patients with a long history of suicidal thinking and self-harm will have less of a response in some cases.

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Intravenous ketamine may rapidly reduce suicidal thinking in depressed patients << Article link 

Intravenous ketamine may rapidly reduce suicidal thinking in depressed patients

Repeat intravenous treatment with low doses of the anesthetic drug ketamine quickly reduced suicidal thoughts in a small group of patients with treatment-resistant depression. In their report receiving Online First publication in the Journal of Clinical Psychiatry, a team of Massachusetts General Hospital (MGH) investigators report the results of their study in depressed outpatients who had been experiencing suicidal thought for three months or longer.

“Our finding that low doses of ketamine, when added on to current antidepressant medications, quickly decreased suicidal thinking in depressed patients is critically important because we don’t have many safe, effective, and easily available treatments for these patients,” says Dawn Ionescu, MD, of the Depression Clinical and Research Program in the MGH Department of Psychiatry, lead and corresponding author of the paper. “While several previous studies have shown that ketamine quickly decreases symptoms of depression in patients with treatment-resistant depression, many of them excluded patients with current suicidal thinking.”

It is well known that having suicidal thoughts increases the risk that patients will attempt suicide, and the risk for suicide attempts is 20 times higher in patients with depression than the general population. The medications currently used to treat patients with suicidal thinking — including lithium and clozapine — can have serious side effects, requiring careful monitoring of blood levels; and while electroconvulsive therapy also can reduce suicidal thinking, its availability is limited and it can have significant side effects, including memory loss.

Primarily used as a general anesthetic, ketamine has been shown in several studies to provide rapid relief of symptoms of depression. In addition to excluding patients who reported current suicidal thinking, many of those studies involved only a single ketamine dose. The current study was designed not only to examine the antidepressant and antisuicidal effects of repeat, low-dose ketamine infusions in depressed outpatients with suicidal thinking that persisted in spite of antidepressant treatment, but also to examine the safety of increased ketamine dosage.

The study enrolled 14 patients with moderate to severe treatment-resistant depression who had suicidal thoughts for three months or longer. After meeting with the research team three times to insure that they met study criteria and were receiving stable antidepressant treatment, participants received two weekly ketamine infusions over a three-week period. The initial dosage administered was 0.5 mg/kg over a 45 minute period — about five times less than a typical anesthetic dose — and after the first three doses, it was increased to 0.75 mg/kg. During the three-month follow-up phase after the ketamine infusions, participants were assessed every other week.

The same assessment tools were used at each visit before, during and after the active treatment phase. At the treatment visits they were administered about 4 hours after the infusions were completed. The assessments included validated measures of suicidal thinking, in which patients were directly asked to rank whether they had specific suicide-related thoughts, their frequency and intensity.

While only 12 of the 14 enrolled participants completed all treatment visits — one dropped out because of ketamine side effects and one had a scheduling conflict — most of them experienced a decrease in suicidal thinking, and seven achieved complete remission of suicidal thoughts at the end of the treatment period. Of those seven participants, two maintained remission from both suicidal thinking and depression symptoms throughout the follow-up period. While there were no serious adverse events at either dose and no major differences in side effects between the two dosage levels, additional studies in larger groups of patients are required before any conclusions can be drawn.

“In order to qualify for this study, patients had to have suicidal thinking for at least three months, along with persistent depression, so the fact that they experienced any reduction in suicidal thinking, let alone remission, is very exciting,” says Ionescu, who is an instructor in Psychiatry at Harvard Medical School. “We only studied intravenous ketamine, but this result opens the possibility for studying oral and intranasal doses, which may ease administration for patients in suicidal crises.”

She adds, “One main limitation of our study was that all participants knew they were receiving ketamine. We are now finishing up a placebo-controlled study that we hope to have results for soon. Looking towards the future, studies that aim to understand the mechanism by which ketamine and its metabolites work for people with suicidal thinking and depression may help us discover areas of the brain to target with new, even better therapeutic drugs.”

 

Rapid and Sustained Reductions in Current Suicidal Ideation Following Repeated Doses of Intravenous Ketamine: Secondary Analysis of an Open-Label Study  << Article in Clinical Psychiatry

Ketamine for Rapid Reduction of Suicidal Thoughts in Major Depression: A Midazolam-Controlled Randomized Clinical Trial Article link for below:

Ketamine was significantly more effective than a commonly used sedative in reducing suicidal thoughts in depressed patients, according to researchers at Columbia University Medical Center (CUMC). They also found that ketamine’s anti-suicidal effects occurred within hours after its administration.

The findings were published online last week in the American Journal of Psychiatry.

According to the Centers for Disease Control and Prevention, suicide rates in the U.S. increased by 26.5 percent between 1999 and 2015.

“There is a critical window in which depressed patients who are suicidal need rapid relief to prevent self-harm,” said Michael Grunebaum, MD, a research psychiatrist at CUMC, who led the study. “Currently available antidepressants can be effective in reducing suicidal thoughts in patients with depression, but they can take weeks to have an effect. Suicidal, depressed patients need treatments that are rapidly effective in reducing suicidal thoughts when they are at highest risk. Currently, there is no such treatment for rapid relief of suicidal thoughts in depressed patients.”

Most antidepressant trials have excluded patients with suicidal thoughts and behavior, limiting data on the effectiveness of antidepressants in this population. However, previous studies have shown that low doses of ketamine, an anesthetic drug, causes a rapid reduction in depression symptoms and may be accompanied by a decrease in suicidal thoughts.

The 80 depressed adults with clinically significant suicidal thoughts who enrolled in this study were randomly assigned to receive an infusion of low-dose ketamine or midazolam, a sedative. Within 24 hours, the ketamine group had a clinically significant reduction in suicidal thoughts that was greater than with the midazolam group. The improvement in suicidal thoughts and depression in the ketamine group appeared to persist for up to six weeks.

Those in the ketamine group also had greater improvement in overall mood, depression, and fatigue compared with the midazolam group. Ketamine’s effect on depression accounted for approximately one-third of its effect on suicidal thoughts, suggesting the treatment has a specific anti-suicidal effect.

Side effects, mainly dissociation (feeling spacey) and an increase in blood pressure during the infusion, were mild to moderate and typically resolved within minutes to hours after receiving ketamine.

“This study shows that ketamine offers promise as a rapidly acting treatment for reducing suicidal thoughts in patients with depression,” said Dr. Grunebaum. “Additional research to evaluate ketamine’s antidepressant and anti-suicidal effects may pave the way for the development of new antidepressant medications that are faster acting and have the potential to help individuals who do not respond to currently available treatments.”

Ketamine for Rapid Reduction of Suicidal Thoughts in major depression – A midazolam controlled trial PDF article

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Ketamine as a Potential Treatment for Suicidal Ideation A Systematic Review of the Literature 2015

Abstract
Objective To review the published literature on the efficacy
of ketamine for the treatment of suicidal ideation (SI).
Methods The PubMed and Cochrane databases were
searched up to January 2015 for clinical trials and case
reports describing therapeutic ketamine administration to
patients presenting with SI/suicidality. Searches were also
conducted for relevant background material regarding the
pharmacological function of ketamine.
Results Nine publications (six studies and three case
reports) met the search criteria for assessing SI after
administration of subanesthetic ketamine. There were no
studies examining the effect on suicide attempts or death
by suicide. Each study demonstrated a rapid and clinically
significant reduction in SI, with results similar to previously
described data on ketamine and treatment-resistant
depression. A total of 137 patients with SI have been
reported in the literature as receiving therapeutic ketamine.
Seven studies delivered a dose of 0.5 mg/kg intravenously
over 40 min, while one study administered a 0.2 mg/kg
intravenous bolus and another study administered a liquid
suspension. The earliest significant results were seen after
40 min, and the longest results were observed up to
10 days postinfusion.
Conclusion Consistent with clinical research on ketamine
as a rapid and effective treatment for depression, ketamine
has shown early preliminary evidence of a reduction in
depressive symptoms, as well as reducing SI, with minimal
short-term side effects. Additional studies are needed to
further investigate its mechanism of action, long-term
outcomes, and long-term adverse effects (including abuse)
and benefits. In addition, ketamine could potentially be
used as a prototype for further development of rapid-acting
antisuicidal medication with a practical route of administration
and the most favorable risk/benefit ratio.
Key Points
Preliminary data from randomized controlled trials
have demonstrated that ketamine may rapidly and
effectively control treatment-resistant depression,
though the effects are transient.
A small subset of studies has demonstrated similar
results in the effects of ketamine on suicidal ideation.
Ketamine has potential as a rapid treatment for
suicidal ideation and/or a possible model compound
for future drug development.

4 Discussion
With an estimated prevalence of mood disorders ranging
from 3.3 to 21.4 % and the substantially increased risk of
suicide among patients with mood disorders, treatment is
certainly warranted [19]. Current treatment options for
suicidality are limited. They include brain stimulation
therapeutics, such as ECT, and pharmacological intervention
(lithium, clozapine). The efficacy of lithium in treating
suicidality has been documented [20, 21] and has recently been reviewed and pooled in a recent meta-analysis of 48
studies [22]. Clozapine has also been shown to reduce
suicide risk in patients with schizophrenia [23, 24]. The
limitations of both lithium and clozapine include a longer
time to efficacy in this psychiatric emergency/urgency,
compared with the early response to ketamine [25]. Ketamine
seems to be gaining substantial evidence as a pharmacological
option for depression with a fast onset of
action, but its long-term effects need further investigation.
In addition, ketamine probably offers a faster onset of
action in terms of SI, but further work is certainly needed
in this area. Given the risk of suicide and even the
increasing rates of suicide in certain subgroups, such as
soldiers and veterans [26, 27], there is an urgent need for
faster therapeutics for SI and TRD. Importantly, suicidality
and suicide pose a high global burden of patient suffering
to families and society. Although several small-to-moderate
sized studies, in addition to several reviews, have been
published that have examined the efficacy of ketamine in
TRD, there are considerably fewer published data
specifically examining ketamine in patients presenting with
SI. Notably, only three studies have directly examined SI
as the primary outcome [11, 16, 17], while the rest
examined SI as the secondary outcome [4, 15, 18], not
including case reports. This review summarizes the current
published literature regarding ketamine as a treatment for
SI. The data so far show promising trends of ketamine
being an effective and rapid treatment with minimal side
effects.
Pharmacologically, ketamine is an N-methyl-D-aspartate
(NMDA) receptor antagonist. It has been used for anesthesia
in the USA since the 1970s. At subanesthetic doses,
ketamine has been shown to increase glutamate levels [3].
This mechanism is relevant, as glutamate regulation and
expression are altered in patients with major depressive
disorder (MDD). Studies have also demonstrated an
abnormal glutamate–glutamine–gamma-aminobutyric acid
cycle in patients with suicidality [28]. Furthermore, ketamine
has also been shown to work on nicotinic and opioid
receptors [29]. No other class of antidepressant medication
works to modulate the glutamatergic system, and research
continues into this, with the goal of characterizing the full
mechanism of action of ketamine and perhaps developing
other compounds that would have similar effects. Thus,
even if the approval and marketing of ketamine as a rapidacting
antisuicidal and antidepressant medication is not
realized, it could well be a prototype for development of
other medication(s) that retain the mechanism of action
with more favorable qualities and a lesser adverse effect
profile (such as a longer duration of action or less or no
addictive potential). Although the mechanisms explaining
the antisuicidal effect and the NMDA receptor antagonism
of ketamine are still unclear, some of the initial evidence
points to an anti-inflammatory action via the kynurenic
acid pathway. Strong suggestions as to the causal relationship
between inflammation and depression/suicidality
has come from studies demonstrating that cytokines [30,
31] and interferon-b [32] induce depression and suicidality.
Other recent studies have added to the notion of implicating
brain immune activation in the pathogenesis of suicidality.
For instance, one study showed microglial
activation of postmortem brain tissue in suicide victims
[33]. Another study found increased levels of the cytokine
interleukin-6 in cerebrospinal fluid from patients who had
attempted suicide [34]. Higher levels of inflammatory
markers have been shown in suicidal patients than in nonsuicidal
depressed patients [33, 35]. Inflammation leads to
production of both quinolinic acid (an NMDA agonist) and
kynurenic acid (a NMDA antagonist). An increased
quinolinic acid to kynurenic acid ratio leads to NMDA
receptor stimulation. The correlation between quinolinic
acid and Suicide Intent Scale scores indicates that changes
in glutamatergic neurotransmission could be specifically
linked to suicidality [36].
Small randomized controlled trials have demonstrated
the efficacy of ketamine in rapidly treating patients with
both TRD and/or bipolar depression [4, 8, 9, 11, 16–18].
Some studies have also examined suicide items as a secondary
measure in their depression rating scales [4, 7]. In
total, the studies examining ketamine and TRD have nearly
consistently demonstrated that ketamine provides relief
from depressive and suicidal symptoms, starting at 40 min
and lasting for as long as 5 days. Questions still remain as
to the long-term effects of this treatment, how much should
be administered and how often, any serious adverse effects,
and the mechanism of action.
Pharmacologically, ketamine has poor bioavailability
and is best administered via injection [37]. In their landmark
study, Berman et al. [4] found that a subanesthetic
dose (0.5 mg/kg) rapidly improved depressive symptoms.
Most of the subsequent studies have delivered ketamine as
a constant infusion for 40 min at a rate of 0.5 mg/kg.
Others have examined its efficacy after multiple infusions
and observed similar results [8, 13, 16, 38]. Currently, it is
recommended that ketamine be administered in a hospital
setting [39].

______________________________________

Characterizing the course of suicidal ideation response to ketamine

Characterizing the course of suicidal ideation response to ketamine PDF

2018 article from Carlos Zarate discussing the variable course outcomes with Ketamine for suicidality and correlations to serum markers and behavior and longevity of self-harm prior to treatment:

 

Background: : No pharmacological treatments exist for active suicidal ideation (SI), but the glutamatergic
modulator ketamine elicits rapid changes in SI. We developed data-driven subgroups of SI trajectories after
ketamine administration, then evaluated clinical, demographic, and neurobiological factors that might predict SI
response to ketamine.
Methods: : Data were pooled from five clinical ketamine trials. Treatment-resistant inpatients (n = 128) with
DSM-IV-TR-diagnosed major depressive disorder (MDD) or bipolar depression received one subanesthetic
(0.5 mg/kg) ketamine infusion over 40 min. Composite SI variable scores were analyzed using growth mixture
modeling to generate SI response classes, and class membership predictors were evaluated using multinomial
logistic regressions. Putative predictors included demographic variables and various peripheral plasma markers.
Results: : The best-fitting growth mixture model comprised three classes: Non-Responders (29%), Responders
(44%), and Remitters (27%). For Responders and Remitters, maximal improvements were achieved by Day 1.
Improvements in SI occurred independently of improvements in a composite Depressed Mood variable for
Responders, and partially independently for Remitters. Indicators of chronic SI and self-injury were associated
with belonging to the Non-Responder group. Higher levels of baseline plasma interleukin-5 (IL-5) were linked to
Remitters rather than Responders.
Limitations: : Subjects were not selected for active suicidal thoughts; findings only extend to Day 3; and plasma,
rather than CSF, markers were used.
Conclusion: : The results underscore the heterogeneity of SI response to ketamine and its potential independence
from changes in Depressed Mood. Individuals reporting symptoms suggesting a longstanding history of chronic
SI were less likely to respond or remit post-ketamine.

1. Introduction
Suicide poses a serious threat to public health. Worldwide, suicide
accounts for approximately 1 million deaths, and 10 million suicide
attempts are reported annually (World Health Organization, 2014). In
the United States, the national suicide rate has increased by approximately
28% over the last 15 years (Curtin et al., 2016). At the same
time, relatively few interventions for suicide risk exist. While treatments
such as clozapine and lithium have demonstrated effects on
suicidal behavior over weeks to months, these effects may be limited to
specific diagnoses (Cipriani et al., 2005; Griffiths et al., 2014). Currently,
no FDA-approved medications exist to treat suicidal ideation
(SI), leaving those who experience a suicidal crisis with limited options
for a reprieve of symptoms. Consequently, a critical need exists for
rapid-acting treatments that can be used in emergency settings.
A promising off-label agent for this purpose is the rapid-acting antidepressant
ketamine, which past studies have suggested reduces suicidal
thoughts (Diazgranados et al., 2010a; Murrough et al., 2015; Price
et al., 2009). A recent meta-analysis of 167 patients with a range of
mood disorder diagnoses found that ketamine reduced suicidal
thoughts compared to placebo as rapidly as within a few hours, with
effects lasting as long as seven days (Wilkinson et al., 2017). These
results are reinforced by newer findings of reduced active suicidal
ideation post-ketamine compared to a midazolam control(Grunebaum et al., 2018). As the efficacy literature develops in the era
of personalized medicine, two important issues must be addressed.
First, little is known about the acute course of SI following ketamine.
The speed with which antidepressant response occurs, and how much
improvement can be expected on average, has been documented for
single administrations of ketamine (Mathew et al., 2012; Sanacora
et al., 2017); in the limited available literature, researchers have
emulated previous studies examining antidepressant effect, where a
cutoff of 50% improvement demarcated response (Nierenberg and
DeCecco, 2001). Nevertheless, it remains unknown whether this categorization
accurately reflects the phenomenon of suicidal thoughts.
Empirically-derived approaches to the description of SI trajectory after
ketamine may be useful in operationalizing “response” in future clinical
trials.
Second, identifying demographic, clinical, or biological predictors
of SI response to ketamine would allow researchers and clinicians to
determine who is most likely to exhibit an SI response to ketamine. A
broad literature describes clinical and demographic predictors for suicide
risk (Franklin et al., 2017), and a smaller literature connects suicidal
thoughts and behaviors to plasma markers such as brain-derived
neurotrophic factor (BDNF) and cytokines (Bay-Richter et al., 2015;
Falcone et al., 2010; Isung et al., 2012; Serafini et al., 2017; Serafini
et al., 2013). However, no biomarkers have been shown to predict SI/
behavior response to intervention, a finding reinforced by the National
Action Alliance for Suicide Prevention’s Research Prioritization Task
Force’s Portfolio Analysis (National Action Alliance for Suicide
Prevention: Research Prioritization Task Force, 2015). Notably, predictor
analyses have the potential to reveal insights into personalized
treatments for suicidal individuals, as well as the neurobiology of SI
response. With respect to antidepressant response, for example, this
approach yielded the observation that individuals with a family history
of alcohol dependence may be more likely to exhibit an antidepressant
response to ketamine (Krystal et al., 2003; Niciu et al., 2014; PermodaOsip
et al., 2014).
The goals of this study were to elucidate trajectories of SI response
and identify predictors of that response, with the ultimate goal of
adding to the growing literature surrounding ketamine’s specific effects
on SI. In particular, we sought to determine whether the heterogeneous
patterns of change in SI after ketamine administration were better explained
by a model with two or more latent groups of trajectories rather
than a single average trajectory, using secondary analyses from previously
published clinical trials. These classes were then used to evaluate
potential clinical, demographic, and plasma biomarker predictors
of SI response to ketamine in order to generate hypotheses.. Discussion
This analysis used a data-driven approach to characterize SI response
to ketamine. The data were best explained by three trajectory
classes: one with severe average baseline SI and little to no response to
ketamine (Non-Responders), one with moderate average baseline levels
of SI and significant response to ketamine (Responders), and a third
with moderate average baseline levels of SI and complete remission of
SI by two days post-ketamine (Remitters). These findings suggest a
diversity of post-ketamine changes in SI that may not be captured under
traditional methods of categorizing response to treatment.
Furthermore, we found evidence that SI response and antidepressant
response could be distinguished from each other; one subset of participants
experienced improvement in SI that was partially explained by
improvements in Depressed Mood, while the other group’s improvements
in SI occurred independently of antidepressant response. With
regard to predictors of SI response trajectory, preliminary results suggest
the individuals least likely to experience improvement in SI postketamine
were those with the most severe SI and a history of self-injury.
Few plasma markers emerged as predictors of SI response in this study,
highlighting the limitations of connecting SI ratings of response with
biological markers.
The growth mixture modeling approach used here underscored the
heterogeneity of SI response to ketamine, which would not have been
captured by simply calculating the average trajectory. The class assignment
from this approach also differed from the definition of response
(50% reduction in symptoms) traditionally used in the antidepressant
literature, which often focuses on a specific timepoint rather
than the entire symptom trajectory. In comparing classification using a
50% response at Day 1 and Day 3 with the latent trajectory classes, we
found representation of almost every SI class across each responder
group, highlighting the potential limitations of the 50% response approach.
Further study is needed to determine which of these approaches
will prove more fruitful. Complete remission of SI has previously been
used as an outcome measure in clinical trials and in a meta-analysis of
ketamine’s efficacy (Grunebaum et al., 2017; Grunebaum et al., 2018;
Wilkinson et al., 2017), as well as in a study examining the relationship
between SI response to ketamine and changes in nocturnal wakefulness
(Vande Voort et al., 2017). One strength of the present study is that this
data-driven approach provides classifications that directly reflect the
phenomena under study as they are, as opposed to what they should be.
Especially when used in larger samples than the current study, this
approach is particularly promising in its ability to provide a more
nuanced understanding of the nature of SI response to ketamine.
Our results also support the idea that SI response in particular can target. First, it should be noted here that SI classes were not distinguishable
by baseline Depressed Mood scores; patients with the most
severe SI did not differ meaningfully in Depressed Mood scores from
those with the mildest SI. Second, while previous analyses of these data
documented that BMI and family history of alcohol dependence predicted
antidepressant response (Niciu et al., 2014), SI response was not
associated with these variables in the current analysis. Third, the antidepressant
response profiles of the SI classes suggest that SI response
and antidepressant response are not wholly redundant. This aligns with
previous clinical trials and meta-analytic reviews of the literature suggesting
that SI response to ketamine occurs partially independently of
antidepressant response (Grunebaum et al., 2018; Wilkinson et al.,
2017). Nevertheless, this independence did not hold true across both SI
response groups. Specifically, antidepressant and SI response were
clearly linked in Remitters, with depression accounting for half of the
changes in SI; however, in Responders, improvements in SI occurred
independently from improvements in Depressed Mood. These discrepancies
could be related to ketamine’s complex neurobiological
mechanisms or to the potentially low levels of clinical severity observed
in the Remitters.
Interestingly, the current analyses found no baseline demographic
variables that reliably distinguished Responders from Remitters. Some
phenotypic characteristics were uniquely associated with belonging to
the Non-Responder group, suggesting that a long-standing history of
self-injury or SI may indicate resistance to rapid changes in SI.
Relatedly, a recent, randomized clinical trial of repeat-dose ketamine
compared to placebo found that ketamine had no effect on SI in a
sample of patients selected for their longstanding, chronic history of SI
(Ionescu, 2017). These results highlight the importance of patient selection,
particularly for suicide risk. It should be stressed, however, that
SI does not necessarily translate to suicidal attempts or deaths; to our
knowledge, no study has yet linked ketamine with reduced risk of
suicidal behavior. Indeed, in the present study the SI Non-Responders
experienced limited antidepressant effects in response to ketamine, but
may nevertheless have improved on other, unmeasured symptoms that
could provide important benefit and relief. As the ketamine literature
develops, it will be important to identify which clinical symptom profiles
are most likely to have a robust anti-SI and anti-suicidal behavior
response to ketamine and which ones may benefit from other interventions.
While we evaluated a range of potential plasma markers previously
linked to suicidal ideation and behavior, in the present analysis only IL5
was associated with the SI Responder subgroup. Ketamine is known to
have anti-inflammatory effects (Zunszain et al., 2013), but the relationship
between antidepressant response and change in cytokine
levels remains unclear (Park et al., 2017). Cytokines have been linked
to suicidal behavior in the past; a recent meta-analysis found that lower
levels of IL-2 and IL-4, and higher levels of TGFbeta, were associated
with suicidal thoughts and behaviors (Serafini et al., 2013); however, toour knowledge IL-5 has not previously been linked to SI. Given the large
number of comparisons and lack of precedent in the literature, this
result may have been spurious and should be interpreted with caution.
A number of other results may reflect meaningful relationships, but the
high degree of variability—and the associated wide confidence intervals—suggests
that larger sample sizes are needed to better elucidate
the nature of any such relationships (e.g. baseline VEGF: χ2 = 6.13,
p = .05, but OR (95% CI) 13.33 (0.93–200.00)). Somewhat surprisingly,
plasma BDNF levels were not associated with responder class.
Previous studies of bipolar, but not MDD, samples found that plasma
BDNF levels were associated with SI response after ketamine
(Grunebaum, 2017; Grunebaum et al., 2017), suggesting that the mixed
diagnostic composition of this study may explain differences from
previous work. Studies exploring the relationship between BDNF and
antidepressant response to ketamine have also yielded mixed findings
(Haile et al., 2014; Machado-Vieira et al., 2009). Other data-driven
approaches have considered both biological and behavioral variables in
characterizing depression (Drysdale et al., 2017); a similar approach
might prove useful for predicting SI response.
The present study is associated with several strengths as well as
limitations. Strengths include the relatively large sample size of participants
who received ketamine, the use of composite SI scores from
previous exploratory factor analyses as opposed to individual items,
and the combination of clinical and biological markers as potential
predictors of class membership. Limitations include patient selection
methods, as these patients were part of an antidepressant trial and were
not selected for active suicidal thoughts, as well as the exploratory
nature of the analysis. As stated above, suicidal thoughts do not necessarily
equate to suicidal behavior, and class membership would thus
not necessarily correspond with an overall reduction in suicide risk.
Another limitation is that results were collapsed across several clinical
trials with slight variations in study design, and findings were thus only
extended to Day 3 rather than a week after ketamine administration. As
a result, only a subset of the sample could be used for predictive analyses.
In addition, plasma—rather than CSF—markers were used, and
the latter might better indicate underlying biology due to proximity to
the brain, though certain markers such as plasma BDNF may be related
to platelet storage, rather than the brain (Chacón-Fernández et al.,
2016). Comparison of results to trajectories of suicide-specific measures,
such as the Scale for Suicide Ideation (Beck et al., 1979), may also
give further insight into specific SI content. Finally, many clinical
predictors were collected upon hospital admission; future analyses
could use formal assessments, such as the Childhood Traumatic Questionnaire
(Bernstein et al., 1994), assessment of personality disorders,
or diagnoses such as post-traumatic stress disorder (PTSD) as potential
indicators of response.
Despite these limitations, the study demonstrates the utility of a
data-driven approach for characterizing the heterogeneity of SI response
to a rapid-acting intervention. This allows for a more finegrained
analysis of symptoms than would be permitted by traditionalapproaches, such as overall average response or dichotomization at
50% reduction in symptoms. This study identified several findings of
note. These included distinguishing at least three patterns of SI response
to ketamine and finding that subjects who exhibited more severe SI at
baseline were not likely to experience an SI response to ketamine.

 

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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
Woodbridge - 22191 - 22192 -22193 -22194 - 22195 
Springfield - 22150 - 22151 -22152-22153-22154-22155 -22156 - 22157 -22158 -22159 -22160 - 22161 
Front Royal 22630
Warren County 22610 22630 22642 22649
Fredericksburg Va 22401 22402 - 22403 - 22404 -22405 -22406 -22407 -22408 - 22412

MONKEY DUST | 703-844-0184 | SUBOXONE| KETAMINE | 703-844-0184 | FAIRFAX | ALEXANDRIA | HARRISONBURG | BUPRENORPHINE INJECTION | SUBLOCADE || MDPV – methylenedioxypyrovalerone – Ccrazy juice and its new rise || ADDICTION DOCTORS | TELEMEDICINE | BUPRENORPHINE INJECTABLE | SUBLOCADE

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Monkey Dust   <Article Link

'Epidemic' of psychotic patients hooked on monkey dust
Suboxone Treatment | Addiction Treatment | Fairfax, Va |22304 | 703-844-0184
A man high on monkey dust jumped from a building in the UK, landed on a car, and proceeded to grapple with police officers.
 Sky News / YouTube
  • A drug known as “monkey dust” is sweeping across the north of the UK.
  • It’s also known as “bath salts,” and has been linked to violent face-eating attacks in the US.
  • The substance makes people feel strong, and can cause them to act dangerously.
  • Paramedics and police have been called to scenes where people have scaled buildings and jumped from great heights.
  • Side effects of the drug include a paranoia, hallucinations, chest pain, and high blood pressure.

People sometimes take recreational drugs to escape, or to feel good. But a substance that is currently becoming an “epidemic” in the UK, according to police in the north of England, is causing psychotic, violent behaviour.

The drug, known as “monkey dust,” is sweeping across the northern UK, and is said to make users feel as though they have incredible strength akin to the Hulk, and can make them act dangerously — scaling buildings and jumping from great heights.

It’s the same drug as “bath salts” which have been linked to reports of “face-eating attacks” in the US in recent years. Bath salts used to be readily available to buy in the US in American petrol stations and convenience stores, but were outlawed by Obama in 2012.

The substance is methylenedioxypyrovalerone, or MDPV, and gives a similar feeling to that of Mcat or mephedrone, according to Why Not Find Out— an online source of information about drugs.

sad teenage boySabphoto/Shutterstock

It’s a class B drug in the UK to possess or sell, meaning if you’re caught with it you face an unlimited fine and up to five years in prison. Selling or producing it can mean being locked away for 14 years.

MDPV looks like a fine white or brownish powder, and usually sells for about £10 to £15 for a gram, which is significantly cheaper than other recreational drugs like MDMA and cocaine. Sky News reportsin Stoke-on-Trent it can be bought for as little as £2.

&mdash;Stoke Police (@Policingstoke) August 5, 2018 ” data-e2e-name=”embed-container” data-media-container=”embed” style=”box-sizing: border-box; margin: 20px 0px;”>

Stoke Police@Policingstoke

Neighbourhood Support Team Officers detained a male for in Town Centre yesterday.
Monkey Dust and Heroin recovered, male arrested! -TW

“It gives great energy and euphoria but can cause depression the following day,” according to Why Not Find Out. “It is addictive. It also makes people who take it smell of urine, as does their clothes and sheets.”

Other side effects include a paranoia, hallucinations, chest pain, and high blood pressure.

MDPV has risen in popularity this summer in the UK, according to Sky News, with police and paramedics responding to a series of violent attacks and psychotic episodes, including people leaping from buildings and trying to fight with officers. Apparently, MDPV makes people fearless.

“When you are trying to restrain them it’s like you are dealing with someone who thinks they are the Incredible Hulk,” PC Rich Frost told Sky News. “The strength is unbelievable.”

In June, there were reports of a “bad batch” of monkey dust being sold in Telford, which was linked to deaths in the area.

“If anyone has taken the drug and falls ill then they should seek medical attention immediately,” said Detective Inspector Lee Holehouse, from Telford CID.

“The dangers of taking drugs are well known and all drugs pose a risk to those who take them but I would like to reiterate this additional danger.”

_________________________________

MDPV

Why not find out More website

THE DRUG

MDPV is a stimulant powder with effects similar to that of Mcat or mephedrone. Its chemical name is methylenedioxypyrovalerone. It is a Class B drug illegal to possess or sell. It appears as a very fine white or brownish powder, sells for about £10-15 a gram so much cheaper than cocaine.

It is commonly called Monkey Dust or Dust. It is generally snorted or bombed. Its effects last a few hours perhaps 5-6.

It gives great energy and euphoria but can cause depression the following day. It is addictive. It also makes people who take it smell of urine, as does their clothes and sheets.

2-mk
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Documentary On The Effects Of Bath Salts And Legal Highs

Bath Salts MDPV

 

 

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Researchers at Yale published a new study titled “Acute and Longer-Term Outcomes Using Ketamine as a Clinical Treatment at the Yale Psychiatric Hospital” in Clinical Psychiatry.  In late 2014, Yale began providing ketamine as an off-label therapy on a case-by-case basis for patients who could not participate in research protocols.  The authors observed 54 patients that received IV ketamine infusion for the treatment of severe and treatment-resistant mood disorders such as depression.

“Ketamine is being used as an off-label treatment for depression by an increasing number of providers, yet there is very little long-term data on patients who have received ketamine for more than just a few weeks,” Samuel T. Wilkinson, MD,from the department of psychiatry, Yale School of Medicine and Yale Psychiatric Hospital, told Healio Psychiatry.

The Yale researchers studied the acute and longer-term outcomes in this patient population. Importantly, a subset of patients (n=14) received ketamine on a long-term basis, ranging from 12 to 45 total treatments, over a course of 14 to 126 weeks.  The researchers found no evidence of cognitive decline, increased proclivity to delusions, or emergence of symptoms consistent with cystitis in this subset of long-term ketamine patients.  They also reported that the infusions were generally well-tolerated.

Although this study population was relatively small, limiting the conclusions that can be drawn, this is still an important first step in establishing the long-term safety of ketamine for the treatment of a myriad of diseases that it’s being used to treat.

Acute and Longer-Term Outcomes Using Ketamine as a Clinical Treatment at the Yale Psychiatric Hospital

Samuel T. Wilkinson, MD; Rachel B. Katz, MD; Mesut Toprak, MD; Ryan Webler, BA; Robert B. Ostroff, MD; and Gerard Sanacora, MD, PhD

J Clin Psychiatry 2018;79(4):17m11731
10.4088/JCP.17m11731

Objective: Ketamine has emerged as a rapid-acting antidepressant, though controversy remains whether sufficient data exist to justify its use outside of research protocols. In October 2014, the authors’ institution began providing ketamine as an off-label therapy on a case-by-case basis for patients unable to participate in research protocols. Here, the participant experience during 29 months of providing ketamine as a clinical treatment for severe and treatment-resistant mood disorders through February 2017 is described.

Methods: Patients were initially treated with a single- or double-infusion protocol (0.5 mg/kg for 40 minutes intravenously) and were later transitioned to a 4-infusion protocol over 2 weeks.

Results: Fifty-four patients received ketamine, with 518 total infusions performed. A subset of 44 patients with mood disorders initiated the 4-infusion protocol, of whom 45.5% responded and 27.3% remitted by the fourth infusion. A subsample (n = 14) received ketamine on a long-term basis, ranging from 12 to 45 total treatments, over a course of 14 to 126 weeks. No evidence was found of cognitive decline, increased proclivity to delusions, or emergence of symptoms consistent with cystitis in this subsample.

Conclusions: In general, ketamine infusions were tolerated well. The response and remission rates in this clinical sample were lower than those observed in some research protocols. The small number of patients who were treated on a maintenance schedule limits the conclusions that can be drawn regarding the long-term safety of ketamine; however, no long-term adverse effects were observed in this sample.

If you are interested in Ketamine therapies for depression, PTSD, pain, anxiety, fibromyalgia…….call 703-844-0184.

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Zip CODES Served by NOVA Health Recovery:

Maryland (MD):
Bethesda 20814 – Bethesda 20816 – Bethesda 20817 – Chevy Chase 20815 – Colesville 20904 – Cabin John 20815 – Glen Echo 20812 – Gaithersburg 20855 – Gaithersburg 20877- Gaithersburg 20878 – Gaithersburg 20879 – Garrett Park 20896 – Kensington 20895 – Montgomery Village 20886 – Olney 20830 – Olney 20832 – Potomac 20854 – Potomac 20859 – Rockville 20850 – Rockville 20852 – Rockville 20853 – Silver Spring 20903 – Silver Spring 20905 – Silver Spring 20906 – Silver Spring 20910 – Takoma Park 20912 – Wheaton 20902
Washington DC:
Crestwood 20011- North Capitol Hill 20002 – Cathedral Heights 20016 – American University Park 20016 – Columbia Heights 20010 – Mount Pleasant 20010 – Downtown 20036 – Dupont Circle 20009 – Logan Circle 20005- Adams Morgan 20009 – Chevy Chase 20015 – Georgetown 20007 – Cleveland Park 20008 – Foggy Bottom 20037 – Rock Creek Park – Woodley Park 20008 – Tenleytown 20016
Northern Virginia:
McLean 22101- McLean 22102 – McLean 22106 – Great Falls 22066 – Arlington 22201 – Arlington 22202 – Arlington 22203 – Arlington 22205 – Falls Church 22041 – Vienna 22181 – Alexandria 22314 – 22308 -22306 -22305 -22304 Fairfax – 20191 – Reston – 22009 – Springfield – 22152 22015 Lorton 22199
Fairfax, Va
2303 – 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
Woodbridge – 22191 – 22192 -22193 -22194 – 22195
Springfield – 22150 – 22151 -22152-22153-22154-22155 -22156 – 22157 -22158 -22159 -22160 – 22161
Front Royal 22630

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Ketamine for Depression: A Q&A with Psychiatrist Alexander Papp, MD  << Article link

 

Ketamine for Depression: A Q&A with Psychiatrist Alexander Papp, MD

By Gabrielle Johnston, MPH   |   December 21, 2017

Every year, 15 to 20 million persons are diagnosed and treated for depression, making it the most common type of mental illness in the United States, according to the Centers for Disease Control. For roughly 30 percent of these patients, however, standard treatment options, such as antidepressants and talk therapy, are not effective. But for some, there may be a new option: ketamine, a medication originally developed as an anesthetic drug, but now being used to address treatment-resistant depression. Alexander Papp, MD, psychiatrist at UC San Diego Health, discusses the potential of ketamine as a remedy for depression when other treatments fail.

Alexander Papp

Question: How does ketamine work to reduce depression?

Answer: Ketamine works by quickly increasing the activity of the neurotransmitter glutamate in the frontal cortex of the brain, while also allowing new synapses to form in the same area. The speediness of ketamine in producing an antidepressant effect occurs because this drug bypasses the traditional serotonin route and goes directly to activating glutamate. This is very different from traditional antidepressants, which first increase the activity of serotonin in multiple different areas of the brain, and then ultimately affect glutamate. This process usually takes two to four weeks to take effect, while ketamine yields an almost immediate effect.

Q: What is treatment-resistant depression?

A: Treatment-refractory depression, better known as treatment-resistant depression, is a term used to describe cases of major depressive disorder that do not adequately respond to appropriate courses of at least two antidepressants. In this situation, “responding” to an antidepressant means not only improvement in mood, but experiencing a full disappearance of the majority of the depressive symptoms and a return to normal functioning.

Q: What is ketamine and how is it traditionally used in medicine?

A: Ketamine was originally developed as an anesthetic and an analgesic or pain reliever. Currently, ketamine is approved and labeled by the U.S. Food & Drug Administration (FDA) for both of these uses in the United States.

Q: Are there any adverse effects of ketamine as a treatment? Is this why some consider it to be an “experiential” treatment for depression?

A: As a treatment for depression, ketamine has a few mild adverse effects. These can include a dream-like feeling, blurred or double vision, dizziness, nausea or vomiting and short anxiety reactions after receiving a dose. This treatment is not experimental because this is an FDA-approved drug that is being used for “off-label” or a less common use.  An “off-label” use means that it is administered as a treatment that the FDA did not originally approve. The FDA approves medications only for a certain number of uses, but most medications eventually develop off-label uses due to the clinical experience that develops over time. As an example, the drug Prazosin was approved for the treatment of high blood pressure in 1976 but it is now mostly used for the treatment of nightmares in patients with post-traumatic stress disorder, a use that was not originally approved.

Q: When should a patient ask their doctor about trying ketamine as a treatment for depression?

depression

A: You should speak to your doctor when you have tried several antidepressant medications or combinations of medications, taken at the highest dose levels for at least two months, without a return to normal functioning. In these cases, it is also important to have other medical reasons for depression, such as a hormonal imbalance, ruled out as well.

Q: Apart from ketamine, are there any other treatments for this treatment-resistant depression on the horizon?

A: New studies have been published about administering Botox injections into the frown muscles on the forehead to treat depression. Botox is an FDA-approved drug to treat a variety of conditions, ranging from excessive sweating to muscle spasms to cosmetic uses, but its use to treat depression is another example of off-label use.

There are also a variety of other treatments available for this type of depression. Two of the more common options are repetitive transcranial magnetic stimulation and deep brain stimulation. Both of these are FDA-approved and are covered by some insurance plans.

___________________________________

If you are interested in Ketamine therapies for depression, PTSD, pain, anxiety, fibromyalgia…….call 703-844-0184.

Zip CODES Served by NOVA Health Recovery:

Maryland (MD):
Bethesda 20814 – Bethesda 20816 – Bethesda 20817 – Chevy Chase 20815 – Colesville 20904 – Cabin John 20815 – Glen Echo 20812 – Gaithersburg 20855 – Gaithersburg 20877- Gaithersburg 20878 – Gaithersburg 20879 – Garrett Park 20896 – Kensington 20895 – Montgomery Village 20886 – Olney 20830 – Olney 20832 – Potomac 20854 – Potomac 20859 – Rockville 20850 – Rockville 20852 – Rockville 20853 – Silver Spring 20903 – Silver Spring 20905 – Silver Spring 20906 – Silver Spring 20910 – Takoma Park 20912 – Wheaton 20902

Washington DC:
Crestwood 20011- North Capitol Hill 20002 – Cathedral Heights 20016 – American University Park 20016 – Columbia Heights 20010 – Mount Pleasant 20010 – Downtown 20036 – Dupont Circle 20009 – Logan Circle 20005- Adams Morgan 20009 – Chevy Chase 20015 – Georgetown 20007 – Cleveland Park 20008 – Foggy Bottom 20037 – Rock Creek Park – Woodley Park 20008 – Tenleytown 20016

Northern Virginia:
McLean 22101- McLean 22102 – McLean 22106 – Great Falls 22066 – Arlington 22201 – Arlington 22202 – Arlington 22203 – Arlington 22205 – Falls Church 22041 – Vienna 22181 – Alexandria 22314 – 22308 -22306 -22305 -22304 Fairfax – 20191 – Reston – 22009 – Springfield – 22152 22015 Lorton 22199
Fairfax, Va
2303 – 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
Woodbridge – 22191 – 22192 -22193 -22194 – 22195
Springfield – 22150 – 22151 -22152-22153-22154-22155 -22156 – 22157 -22158 -22159 -22160 – 22161
Front Royal 22630

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Science Article on how Ketamine may work rapidly

703-844-0184 | Ketamine 22306 | Ketamine for depression |

 

In contrast to most antidepressant medications, which can take several weeks to reduce depressive symptoms, ketamine — a commonly used veterinary anesthetic — can lift a person out of a deep depression within minutes of its administration, and its effects can last several weeks. Researchers have long-wondered how ketamine can both act quickly and be so long-lasting.

Now, researchers led by Mark Rasenick, distinguished professor of physiology and psychiatry in the University of Illinois at Chicago College of Medicine, describe the molecular mechanisms behind ketamine’s ability to squash depression and keep it at bay. They report their findings in the journal Molecular Psychiatry.

Two-thirds of participants in clinical studies who did not respond to traditional antidepressants experienced fast and lasting resolution of their depressive symptoms after being given ketamine intravenously, Rasenick explained. The effects of ketamine typically lasted about a week — much longer than would be expected with ketamine’s six-hour half-life in the body.

Rasenick and his colleagues used a cellular model system to investigate how ketamine acted.

In previous research, Rasenick and his colleagues showed that SSRIs — the most commonly prescribed class of antidepressants, which includes Prozac and Zoloft — work in the brain by moving molecules called G proteins off of “lipid rafts” on the cell membrane, where the G proteins are held inactive. G proteins produce cyclic AMP, which nerve cells need to signal properly. People with depression, Rasenick found, tend to have a greater proportion of their G proteins packed into these membrane patches, along with dampened brain cell signaling, which may contribute to symptoms of depression, including a feeling of overall numbness.

In the earlier research, when Rasenick exposed rat brain cells to SSRIs, the drug accumulated in the lipid rafts, and G proteins moved out of the rafts. The movement was gradual, over the span of several days, which Rasenick thinks is the reason why SSRIs and most other antidepressants can take a long time to begin working.

In his current research, Rasenick and his colleagues performed a similar experiment with ketamine and noticed that the G proteins left the rafts much faster. G proteins began migrating out of the lipid rafts within 15 minutes. And the long-lasting effects of ketamine may be due to the fact that the G proteins were very slow to move back into the lipid rafts, Rasenick explained.

The finding contradicts the long-held idea that ketamine works solely by blocking a cellular receptor called the NMDA receptor, which sits on the surface of nerve cells and helps transmit signals.

In fact, when the researchers knocked out the NMDA receptor, ketamine still had the same effect on the cells — quickly moving G proteins out of lipid rafts on the cell membrane.

“When G proteins move out of the lipid rafts, it allows for better communication among brain cells, which is known to help alleviate some of the symptoms of depression,” Rasenick said. “Whether they are moved out by traditional antidepressants or ketamine, it doesn’t matter, although with ketamine, the G proteins are very slow to move back into the lipid rafts, which would explain the drugs long-term effects on depressive symptoms.”

“This further illustrates that the movement of G proteins out of lipid rafts is a true biomarker of the efficacy of antidepressants, regardless of how they work,” Rasenick explained. “It confirms that our cell model is a useful tool for showing the effect of potential new antidepressant drug candidates on the movement of G proteins and the possible efficacy of these drugs in treating depression.”

Story Source:

Materials provided by University of Illinois at ChicagoNote: Content may be edited for style and length.


Journal Reference:

  1. Nathan H. Wray, Jeffrey M. Schappi, Harinder Singh, Nicolas B. Senese, Mark M. Rasenick. NMDAR-independent, cAMP-dependent antidepressant actions of ketamineMolecular Psychiatry, 2018; DOI: 10.1038/s41380-018-0083-8

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____________________________________________________

Psychology Today Article: Ketamine: Old Drug, New Tricks

 

Ketamine has been used as an anesthetic for 50 years, and for decades the clinicians prescribing it have noticed sudden, appreciable anti-suicide and antidepressant effects in their patients. Case reports of desperate suicidal depressionrelieved within half an hour were discussed in the waning years of the 20th century, but actual research papers with small trials have only started trickling in within the last two decades.

Even after all this time, the research done thus far has not led to ketamine being mainstream FDA-approved as standard therapy for depression or suicidal ideation. For one thing, the kind of ketamine used in the US for most of the last 50 years is an IV drip requiring nursing and vital sign monitoring. In my neck of the woods, IV ketamine treatment is $3,000 (not covered by insurance or Medicare), usually completed in six treatments over two weeks. Not exactly within reach for many of my patients with resistant depression (who tend to decline in socioeconomic status over time).

In the case studies, folks’ depression rather notoriously rebounded back from ketamine therapy and then became resistant, though that didn’t happen to everyone. But how could we study how effective ketamine is? It’s generic, so there’s no pharmaceutical company with the millions to blow on state-of-the-art, beautiful randomized controlled trials to bring before the FDA. The patient population for ketamine is also a difficult one. Suicidal folks and depressed people with illness resistant to standard therapy or meds are more likely to give a drug company an expensive and public failure rather than profit, no matter that this is a population desperately in need of new ideas and new thinking. However, new formulations and the slow grind of publicly funded studies means new life for this elderly drug.

Before we talk about how ketamine works, let’s talk about how mental illness arises in terms of the actual pathology in the brain. (Note: This will necessarily be an oversimplification.) In short, most mental illness develops at the intersection of too much emotional or physical stress and genetic vulnerability leading to limitations in efficient brain functioning. This happens when brain becomes overwhelmed with excitatory signals: too much stress, too much activation of the fight-or-flight nervous system leading to specific over-activation of certain brain areas (like the left prefrontal cortex, the hippocampus, or the amygdala) without compensatory time or resources for recovery and repair.

The emotional and physical stressors could be, for example, a death in the family, extended work stress, viral illness that affects the brain, medications that affect the brain, or traumatic brain injury. The genetic vulnerability could be an increased inefficiency in being able to make specific neurotransmitters or brain fertilizers that help in recovery and repair, or an increased genetic ability to send excitatory ions through cell membranes, or many more complex issues we haven’t yet figured out.

Under this theory, almost any intervention could decrease symptoms of mental illness if it increases general neuron recovery and repair—or the efficiency of neurotransmitter use in the recovery and repair pathway—or reduces neurotoxic activation of the excitatory pathway (or “excitotoxicity“). Interventions such as regular exercise, meditationpsychotherapy, selective serotonin reuptake inhibitors (SSRIs), antipsychotics, lithium, magnesium, anti-seizure meds and many other treatment paradigms can be at least partially effective to decrease symptoms. Keep in mind, sometimes the disease is a tank, and the spear in your arsenal (regular exercise, for example) is never going to be enough to take out that tank. Sometimes you need anti-tank missiles (such as low dose antipsychotics for severe resistant depression).

Ketamine is, among many other things, an NMDA receptor antagonist(though even this characterization is complicated). This means that ketamine blocks the action at the NMDA receptor, normally turned on by the major excitatory neurotransmitter in the nervous system, glutamate. NMDA receptor over-activation is ground zero for excitotoxiticy, kind of like a gas pedal that is stuck in the downward position. So far, though, not a single FDA-approved psychiatric medication in general practice specifically unsticks that gas pedal. But ketamine does. (So will, to a much lesser extent, magnesium* and the supplement NAC, which decreases glutamate concentrations). This gas pedal unsticking is how ketamine can seemingly do the impossible: take a dangerously suicidal patient and make them feel much, much better in less than an hour.

Wikimedia Commons
Source: Wikimedia Commons

In 2016, a new formulation of ketamine, esketamine, was granted FDA “breakthrough therapy” designation for major depressive disorder with imminent risk of suicide. It’s a nasal spray used in Europe for anesthesia, but never used in the US before. It has three to four times the affinity for the NMDA receptor as ketamine and fewer intolerable side effects (such as hallucinations, dissociation, and dangerous fluctuations of vital signs). A phase two study of esketamine was published in April 2018, a randomized controlled trial of suicidal depressed patients. They agreed to be monitored on an inpatient unit for five days after the first administration of the medicine, followed by twice-a-week administration for four weeks in addition to standard antidepressant treatment. To empathize how ill the population in this study was, three (placebo) patients out of 68 made suicide attempts during the follow up period, and half needed additional suicide precautions during their inpatient stay (usually decreased time between nursing checks which is, at the low end, every 15 minutes on a standard inpatient unit). Esketamine results separated from those of placebo treatment by four hours and at 24 hours, with rapid relief from suicidal thoughts and depressive symptoms, but there seemed to be no difference with esketamine and placebo at 25 days.

This study seems to support the old case study observations, that ketamine can be amazingly helpful short term, but is not really a long-term intervention. But it’s hard to tell, and we need more data. No one really knows why there’s such a rapid ketamine poop-out, but from a clinical perspective, who cares? A fast intervention that decreases suicidal ideation could save lives while our other, proof-tested, slower interventions take their time to work. This could also shorten inpatient hospital stays for depression, freeing up precious resources and getting people back to their families, work, and communities. While the use in observed settings such as inpatient units and emergency rooms is likely to accelerate, we need way more-real world data before we start prescribing nasal spray in outpatient treatment, especially for dangerously suicidal patients.

Ketamine studies have also opened the doors for other NMDA receptor antagonist interventions. Some drugs in development include new formulations of dextromethorphan and rapastinel. Given that psychiatric drugs have been endless renditions of the same tricyclic antidepressants,  SSRIs, dopamine blockers, and dopamine partial agonists for decades, we could use a new approach.

And remember, there are plenty of ways to unstick that gas pedal early in the game, with proper self care and healthy living. Modern life, in America at least, doesn’t much incentivize vacation or sleep, both of which help that recovery and repair cycle. As a psychiatrist I’ll use whatever evidence-based intervention I can at any stage to treat the patient where he or she is to make them start getting better in the moment. As a health writer I can suggest eating a (mostly) home-cooked whole foods diet, avoiding a lot of alcohol and smoking, and getting enough physical movement, rest, and recharging time. In the brain, it’s all about reducing that excitotoxicity. In life, it’s all about a clear head, good energy, and serenity.

*Magnesium is also felt to work, in some respects, by antagonizing NMDA receptors “

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Ketamine offers a rapid solution for many when their other treatments for depression have failed. Most patients studied for Ketamine treatment have failed standard therapies. Sanjay Gupta discusses this below in the link:

 

KETAMINE as a rapid antidepressant – CNN article Sanjay Gupta

Suicide in the United States

 

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A lot of depression is out there. There are a lot of hopeful measures to take in resolving it. The link below is to several documentaries regarding depression:

7 Documentaries About Depression To Check Out

Hope to Cope

I added another interesting feature below as well – addiction to aggression:

Addiction to aggression – NIDA

The NIDA Blog Team

Aggressive behavior can be physical (shoving or hitting somebody) or verbal (yelling at someone or saying something mean to them). What does a person who exhibits behavior like that have in common with someone who has a substance use disorder?

Your first guess may be, “Nothing!” They seem like completely separate problems. However, research is finding that’s not totally true.

What’s the link?

Scientists who study the brain and behavior have discovered that those who tend to be aggressive and hostile and those with substance use disorders are alike in two ways:

  1. Both groups are likely to engage in behaviors that could hurt others or themselves—even when they knowthe result could be harmful.
  2. If they stop doing those harmful behaviors, both groups can relapse (engage in the behaviors again), even if they haven’t done them for a long time.

What’s going on here? Scientists think that some people are more likely than others to develop “compulsive” (uncontrollable) aggression—and that this involves some of the same brain activity that gets disrupted with a substance use disorder. Further research into the brain could reveal why some people are more inclined than others to use drugs or to act aggressively.

Observers have noted parallels between aggression and addiction. People with either problem pursue a harmful behavior, even despite negative consequences. A new study by scientists at the National Institute on Drug Abuse’s (NIDA) Intramural Research Program (IRP) showed that when mice are exposed to experimental protocols adapted from those that are used to model human addictive behaviors, some animals develop an addiction-like propensity to aggression.

Scrabble tiles showing Aggression and Addiction intertwined
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NIDA IRP researchers observed that about 70 percent of the male mice pressed a lever in their cages for the opportunity to show aggression toward a mouse of a smaller, subordinate strain. About 19 percent were “compulsive aggression-seeking” animals who worked harder (lever pressed more times) for a chance to aggress, and were more likely to continue lever pressing even when doing so meant forgoing food.

The researchers conclude that under certain conditions, a portion of the mouse population is susceptible to developing compulsive aggression. They hypothesize that this susceptibility is a product of evolution, that it involves some of the same motivational circuits in the brain that are disrupted in addiction—and that it may also occur in people. Their findings also indicate that the same animal models researchers have developed to investigate addiction can also be used to study compulsive aggression.

Here are some articles related to the biology and meaning of aggression:

Adversity-driven changes in hypothalamic-pituitary-adrenal axis functioning during adolescence

How Does Adversity Get Under the Ski to Lead to the Development of Antisocial Behavior

Scanning for Justice With Functional Magnetic Resonance Imaging

Exogenous Testosterone Rapidly Increases Aggressive Behavior in Dominant and Impulsive Men

Testosterone and Aggression More Than Just biology

COmpulsive addiction like aggressive behavior in mice

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More from NIDA Blog posted below regarding stimulants:

https://teens.drugabuse.gov/blog/post/your-brain-stimulants-part-1-how-stimulants-work

The NIDA Blog Team

Stimulants are drugs that increase alertness, attention, and energy by raising the levels of key chemicals in the brain and other parts of the body. This may be helpful for people with certain health conditions, such as attention-deficit hyperactivity disorder (ADHD).

It’s estimated that more than 10 percent of teens have been diagnosed with ADHD.  For them, ADHD can make it difficult to complete schoolwork or other tasks.

If someone with ADHD has difficulty paying attention, how can something called a stimulant help? The reason is that stimulants increase the amount of a chemical needed to help a person stay focused.

Research by NIDA’s Dr. Nora Volkow found that the symptoms of ADHD are associated with having lower levels of dopamine in the brain. Prescription stimulants slowly increase the level of dopamine, similar to the way it’s naturally produced in the brain. A doctor will usually prescribe a low dose (amount) of a stimulant and increase it gradually if necessary.

Prescription stimulants can also have some unpleasant side effects: fatigue, anxiety, depression, and raising a person’s blood pressure, rate of breathing, and heart rate. Misusing prescription stimulants can also lead to stimulant use disorders—but people with ADHD who use them as prescribed are not at the same risk.

In our previous post, we described how prescription stimulants can reduce symptoms of ADHD. Treating ADHD with stimulants (sometimes combined with counseling) can help improve ADHD symptoms, as well as a person’s self-esteem and their interactions with friends and family.

However, other, non-prescribed stimulants don’t help with ADHD, and each one has its own side effects and risks:

  • Caffeine is found in coffee, many kinds of soda and energy drinks, and chocolate. It also comes in pills and tablets that are advertised as helping you stay awake. Caffeine produces a small rise in dopamine. Consuming too much of it can be harmful, but scientifically speaking, it isn’t addictive—although you can feel withdrawal symptoms if you stop consuming it all of a sudden.
  • Nicotine is found in cigarettes and chewing tobacco. Nicotine stimulates both dopamine and the body’s adrenal glands to release epinephrine (also called adrenaline). Nicotine is extremely addictive.
  • Illegal stimulants include cocainemethamphetamine or meth, and MDMA (Ecstasy or Molly). These drugs produce a large surge of dopamine that unbalances the reward system in the brain and produces the “high.” This surge also increases the risk for addiction.
  • The NIDA Blog Team

    Read part 1 of this series here; part 2 is here.

     What does it mean to misuse prescription stimulants?

    • Taking more of a stimulant than the doctor prescribed;
    • Taking it more frequently than prescribed;
    • Taking a stimulant that was prescribed for someone else, like a friend; or
    • Taking it if you don’t have ADHD.

    Sometimes, people misuse prescription stimulants just to get high, or because they think the stimulants will help them lose weight, or boost their study performance. While prescription stimulants do promote wakefulness, studies have found they don’t enhance learning or thinking ability when taken by people who don’t have ADHD.

    However, misusing prescription stimulants can lead to:

    • Sleep problems, depression, and paranoia;
    • Serious heart complications, including stroke (at high doses); and
    • Abnormally high levels of dopamine in the body. This produces the “high,” which increases the risk for misusing the drug again and, in some cases, becoming addicted.

    The good news is that teens’ misuse of the stimulants Adderall and Ritalin has been decreasing in recent years. For example, about 6 percent of teens reported misusing Adderall last year, a slight decrease from 2015, and only about 1 percent report misusing Ritalin, down from a peak level of 5 percent in 2004.

    You can keep this positive trend going. Avoid using prescription stimulants unless they’re prescribed for you, and spread the word about the risks in misusing them.

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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

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Traditional antidepressants may take weeks to work on individuals. There have been associations with increased suicidality in some studies. The need for a more rapidly acting antidepressant is important. The study below investigated the antidepressant effect of Ketamine by looking through an FDA database and observing associations of pain and depression reduction with the use of Ketamine. They were clearly present. Of note, minocycline and Diclofenac also seemed to be associated with improved depression parameters.

Ketamine provides both pain relief and anti-depression effects in refractory patients, who by definition, have failed multiple therapies.   ::

 

______________________________________________________________________________

Ketamine for Pain Management, Treatment of Depression << Article Link

Article below:

Ketamine may alleviate depression, pain, and adverse effects associated with opioid treatment, and may thus represent an attractive adjunct therapy for pain management, according to a novel population analysis recently published in Scientific Reports.1

Nearly half of all patients with depression taking conventional antidepressants discontinue their treatment prematurely.2 Researchers have sought alternatives to standard antidepressants, for which therapeutic effects are delayed by 2 to 10 weeks.3

Ketamine, an N-methyl-D-aspartate antagonist, was shown to provide acute benefits for treatment-resistant depression, bipolar depression, and major depressive disorder with suicidal ideation, when administered intravenously, however, those studies were conducted on limited samples (20 to 57 participants).4-7

The history of ketamine as an illicit drug favored for its hallucinogenic effects presents ethical obstacles to its use in large clinical trials. Researchers from the University of California San Diego in La Jolla, therefore employed an Inverse-Frequency Analysis approach to investigate whether ketamine, when administered in addition to other therapeutics, has antidepressant properties.

The team applied the inverse frequency analysis method, which looks for negative statistical patterns in the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) post-marketing database of more than 8 million patient records. They observed reductions in depression and pain in patients receiving ketamine, as indicated by negative log odds ratio (logOR) values (logOR, -0.67 ± 0.034 and logOR, -0.41 ± 0.019, respectively). “The data we analyzed are indirect and skewed by cases of bad or lethal adverse effects. Nevertheless the statistics were sufficient to notice the trends,” explained study co-author, Ruben Abagyan, PhD, in an interview with Clinical Pain Advisor.

According to Dr Abagyan, a study recently published by a British team indicates that ketamine might be effective in nearly 40% of patients with severe, treatment-resistant depression, results that are concordant with those from the current study.8

The IFA method was also used to evaluate ketamine efficacy and associated side effects reported in the FAERS database. The investigators found significant reductions in a number of side effects associated with opioid therapies, including constipation (LogOR −0.17 ± 0.023), vomiting (LogOR −0.16 ± 0.025), and nausea (LogOR −0.45 ± 0.034) compared with other drug combinations used for pain management.

The authors concluded that their findings are in line with those from smaller studies, indicating beneficial effects for ketamine as a monotherapy or adjunctive therapy for depression, particularly treatment-resistant depression, with particular indication for patients with suicide ideation, because of its rapid onset of action. “The results should serve as a motivation to conduct a proper clinical trial for the rapid onset treatment of severe depression,” Dr Abagyan noted.

The novel analysis employed in this study may help investigate off-label indications for other drugs. “Ideally the method we proposed should be applied to the actual clinical data rather than the somewhat biased set of un-normalized FAERS reports,” Dr Abagyan added. “The method [can be used] to observe unexpected effects of a treatment by looking at the reduction of the baseline of this effect upon treatment. It can be applied to any effect that is being recorded including cancer, viral diseases mortality, longevity.” he concluded.

 

References

  1. Cohen IV, Makunts T, Atayee R, Abagyan R. Population scale data reveals the antidepressant effects of ketamine and other therapeutics approved for non-psychiatric indicationsSci Rep 2017;7:1450.
  2. Sansone RA, Sansone LA. Antidepressant adherence: are patients taking their medications?. Innov Clin Neurosci. 2012;9(5-6):41-46.
  3. Frazer A, Benmansour S. Mol Psychiatry. Delayed pharmacological effects of antidepressantsMol Psychiatry 2002;7:S23-8.
  4. Price RB, Iosifescu DV, Murrough JW,  et al. Effects of ketamine on explicit and implicit suicidal cognition: a randomized controlled trial in treatment-resistant depressionDepress Anxiety 2014;31:335-343.
  5. DiazGranados N, Ibrahim LA, Brutsche NE, et al. Rapid resolution of suicidal ideation after a single infusion of an N-methyl-D-aspartate antagonist in patients with treatment-resistant major depressive disorderJ Clin Psychiatry 2010;71:1605-1611.
  6. Alberich S, Martínez-Cengotitabengoa M, López P,et al. Efficacy and safety of ketamine in bipolar depression: A systematic reviewRev Psiquiatr Salud Ment 2017;10:104-112.
  7. Larkin, G. L. & Beautrais, A. L. A preliminary naturalistic study of low-dose ketamine for depression and suicide ideation in the emergency departmentInt J Neuropsychopharmacol 2011;8:1127-31.
  8. Singh I, Morgan C, Curran V, et al. Ketamine treatment for depression: opportunities for clinical innovation and ethical foresightLancet Psychiatry 2017;4:419-42

 

Population scale data reveals the antidepressant effects of Ketamine  ::  << Article below

Population scale data reveals the
antidepressant effects of ketamine
and other therapeutics approved
for non-psychiatric indications

Isaac V. Cohen, Tigran Makunts, Rabia Atayee & Ruben Abagyan

Current therapeutic approaches to depression fail for millions of patients due to lag in clinical response
and non-adherence. Here we provide new support for the antidepressant efect of an anesthetic
drug, ketamine, by Inverse-Frequency Analysis of eight million reports from the FDA Adverse Efect
Reporting System. The results of the examination of population scale data revealed that patients who
received ketamine had signifcantly lower frequency of reports of depression than patients who took
any other combination of drugs for pain. The analysis also revealed that patients who took ketamine
had signifcantly lower frequency of reports of pain and opioid induced side efects, implying ketamine’s
potential to act as a benefcial adjunct agent in pain management pharmacotherapy. Further, the
Inverse-Frequency Analysis methodology provides robust statistical support for the antidepressant
action of other currently approved therapeutics including diclofenac and minocycline.

We found that patients listed in the FAERS database who received ketamine in addition to other therapeutics
had signifcantly lower frequency of reports of depression than patients who took any other combination of drugs
for pain (LogOR−0.67±0.034)

Te analysis of the whole FAERS database revealed several other unintentional depression reducing drugs
among antibiotics, cosmeceuticals and NSAIDS.Our data supported previous studies that observed the
psychiatric polypharmacology of minocycline, a tetracycline antibiotic.The NSAID, diclofenac, was also
observed to have some antidepressant properties.It is theorized that both of these drugs may accomplish
antidepressant effects through an anti-inflammatory mechanism.Because of the antidepressant activity of several
NSAIDs, we further separated the non-ketamine pain cohort. Ketamine patients were then compared to
patients who received any other combination of drugs for pain excluding NSAIDs. It was observed that depression
event rates remained low (LogOR−0.56±0.035).As an important side note, we also evaluated efcacy and side efects with the use of ketamine for pain management.
We found that patients who were on ketamine had reduced opioid induced side effects including constipation, vomiting, and nausea. Our data supports ketamine’s
opioid-sparing properties and alludes to the fact that patients may receive benefts of improved pain, reduced
requirement of opioids, and ultimately less opioid reduced side effects.

References
1. Murray, C. J. & Lopez, A. D. Evidence-based health policy–lessons from the Global Burden of Disease Study. Science 274, 740–743,
doi:10.1126/science.274.5288.740 (1996).
2. Kessler, R. C. et al. Te epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication
(NCS-R). JAMA 289, 3095–3105, doi:10.1001/jama.289.23.3095 (2003).
3. Bromet, E. et al. Cross-national epidemiology of DSM-IV major depressive episode. BMC Med 9, 90, doi:10.1186/1741-7015-9-90
(2011).
4. Andrade, L. et al. The epidemiology of major depressive episodes: results from the International Consortium of Psychiatric
Epidemiology (ICPE) Surveys. Int J Methods Psychiatr Res 12, 3–21, doi:10.1002/(ISSN)1557-0657 (2003).
5. Sansone, R. A. & Sansone, L. A. Antidepressant adherence: are patients taking their medications? Innov Clin Neurosci 9, 41–46
(2012).
6. Frazer, A. & Benmansour, S. Delayed pharmacological effects of antidepressants. Mol Psychiatry 7, S23–28, doi:10.1038/
sj.mp.4001015 (2002). Suppl 1.
7. Braun, C., Bschor, T., Franklin, J. & Baethge, C. Suicides and Suicide Attempts during Long-Term Treatment with Antidepressants:
A Meta-Analysis of 29 Placebo-Controlled Studies Including 6,934 Patients with Major Depressive Disorder. Psychother Psychosom
85, 171–179, doi:10.1159/000442293 (2016).
8. Seemüller, F. et al. Te controversial link between antidepressants and suicidality risks in adults: data from a naturalistic study on a
large sample of in-patients with a major depressive episode. Int J Neuropsychopharmacol 12, 181–189, doi:10.1017/
S1461145708009139 (2009).
9. Rush, A. J. et al. Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D
report. Am J Psychiatry 163, 1905–1917, doi:10.1176/ajp.2006.163.11.1905 (2006).
10. Price, R. B. et al. Efects of ketamine on explicit and implicit suicidal cognition: a randomized controlled trial in treatment-resistant
depression. Depress Anxiety 31, 335–343, doi:10.1002/da.22253 (2014).

11. DiazGranados, N. et al. Rapid resolution of suicidal ideation afer a single infusion of an N-methyl-D-aspartate antagonist in
patients with treatment-resistant major depressive disorder. J Clin Psychiatry 71, 1605–1611, doi:10.4088/JCP.09m05327blu (2010).
12. Alberich, S. et al. Efcacy and safety of ketamine in bipolar depression: A systematic review. Rev Psiquiatr Salud Ment (2016).
13. Larkin, G. L. & Beautrais, A. L. A preliminary naturalistic study of low-dose ketamine for depression and suicide ideation in the
emergency department. Int J Neuropsychopharmacol 14, 1127–1131, doi:10.1017/S1461145711000629 (2011).
14. Miyaoka, T. et al. Minocycline as adjunctive therapy for patients with unipolar psychotic depression: an open-label study. Prog
Neuropsychopharmacol Biol Psychiatry 37, 222–226, doi:10.1016/j.pnpbp.2012.02.002 (2012).
15. Rosenblat, J. D. et al. Anti-infammatory agents in the treatment of bipolar depression: a systematic review and meta-analysis.
Bipolar Disord 18, 89–101, doi:10.1111/bdi.2016.18.issue-2 (2016).
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