NOVA Heath Recovery Ketamine Treatment Center | Call 703–844-0184 for a Ketamine Treatment | Alexandria, Va 22306 | 7 days a week and evening appointments as well! We also evaluate depression, ADHD, PTSD. Intranasal Ketamine available. The email is EMAIL@novahealthrecovery.com
Learn How Ketamine Can Treat Post Traumatic Stress Disorder
For decades, ketamine has been used as a medicinal intervention for treating depression, anxiety, mood disorders, and post-traumatic stress disorder (PTSD). While most ketamine advocates recognize its therapeutic potential for treating depression, the many benefits available to those suffering from PTSD are less understood.
Do you or a loved one suffer from post-traumatic stress disorder? If so, ketamine infusion therapy may be able to help alleviate your symptoms and provide the relief you need. However, public knowledge about medicinal ketamine is lacking. In this article, we go over everything there is to know about ketamine for treating PTSD.
PTSD 101: What You Need to Know
Post-traumatic stress disorder has a medical diagnostic code of ICD-10, which is the code used for reimbursing treatment through your insurance provider. PTSD, unlike other mental illnesses, is characterized by its triggering from a single or series of traumatic events. This explains why PTSD is common among military veterans and first responders.
According to a summary article from Mayo Clinic, PTSD is a mental health condition triggered by a terrifying experience. The sufferer subsequently experiences flashbacks, night terrors, and anxiety attacks that they cannot control as a result of the event. It takes a significant amount of time, therapy, and self-care to overcome the trauma of PTSD.
There is no known cure for PTSD. However, many experimental medicinal interventions are breaking ground when it comes to finding a cure. For example, the psychoactive drugs MDMA and ketamine have both been studied for their potential to alleviate the negative effects of PTSD.
Ketamine Infusion Therapy
Since the early 2000s, ketamine has gained popularity among medical providers for its application in infusion therapies. In recent years, clinics all around the world have embraced the healing power of ketamine by offering ketamine infusion therapy. This unique therapy involves one or more intravenous injections of ketamine under the supervision of an anesthesiologist.
What Is Ketamine?
Although ketamine has garnered a reputation as a party drug, its primary value is in its ability to provide fast-acting and potent relief for those with chronic pain issues. Ketamine was first synthesized in the 1960s and was later adopted as an anesthetic in veterinary medicine by the end of the decade. However, use in humans was initially sparse.
Ketamine is both an analgesic and anesthetic drug, which means its primary quality is to reduce or prevent pain. This makes ketamine highly effective for treating major depressive disorder, chronic back pain, and PTSD.
Ketamine and PTSD
Ketamine infusion clinics across the United States are now offering specialty treatments for those suffering from PTSD. For example, the renowned Ketamine Clinics of Los Angeles has treated hundreds of PTSD patients over the years. Led by Dr. Steven Mandel, M.D., the team at Ketamine Clinics of LA has a proven track record of helping relieve the pain of PTSD.
An increasing amount of scientific research has proven that ketamine is effective in treating PTSD. Most notably, a breakthrough 2014 study in JAMA Psychiatry discovered that a single intravenous subanesthetic dose of ketamine resulted in “significant and rapid reduction in PTSD symptom severity.”
Over the past few years, many articles and news reports have heralded ketamine as a potential wonder drug for treating PTSD. A recent article published by Medscape discussed how a team of researchers at the Icahn School of Medicine at Mount Sinai in New York City used ketamine to fight depressive symptoms in patients with PTSD and severe depression.
Is Ketamine Safe for PTSD?
There is no doubt that ketamine is a novel treatment for many PTSD sufferers. Since it is a relatively new medicinal intervention, there is some skepticism within the medical community regarding whether it is safe for human use. However, many of these doubts have been quelled over the years thanks to numerous studies and experiences that have proven its safety.
The most compelling evidence suggesting that ketamine infusion is safe in humans comes from a 2014 clinical study. This study managed to safely administer low doses of ketamine to treat neuropathic pain states in adults. Over the two-week monitoring period, the patients exhibited numerous benefits while experiencing only marginal or negligible side effects.
It should be noted that ketamine is not safe if taken recreationally. Since its inception, ketamine has gained a reputation as a party drug for its ability to induce dissociative states and euphoria. However, ketamine is not safe to use unless administered by a licensed physician. It is possible to overdose on ketamine, and the side effects of using high doses of ketamine can be fatal.
Ketamine: A PTSD Prevention Tool?
Interestingly, ketamine has found success as a tool for preventing the onset of PTSD. In one case, a research team gave a family of mice a low dose of ketamine before exposing them to electric shocks. Usually, mice exhibit symptoms of PTSD after being exposed to such a severe stressor. However, the mice that were given ketamine did not exhibit these symptoms at all.
Typically, traumatized mice freeze up when they are placed back in the cage in which they were shocked. In this case, the mice who were sedated with ketamine did not freeze when placed in the cage or froze for a significantly reduced duration. This led the research team to believe that ketamine may have value in both preventing and treating PTSD in humans.
Is Ketamine Right for You?
Ketamine may be an appropriate treatment option for you if you have treatment-resistant PTSD. In other words, you must first be diagnosed with PTSD and have sought the traditional frontline treatments for the condition before considering ketamine infusion therapy. We recommend speaking with your doctor about your PTSD symptoms and the appropriate therapies available to you. Usually, SSRIs or benzodiazepine pharmaceutical drugs, in conjunction with cognitive behavioral therapy (CBT) is the first method of treatment. However, if you do not respond well to this treatment option you should consider seeking ketamine therapy.
Cocaine use disorder has been difficult to treat.Certainly motivational enhancement therapy works to a degree, but few pharmcotherapies have been productive. An article in the American Journal of Addiction in December 2017 demonstrated the use of Sertraline to help in cocaine use disorder. The net effect of the study showed that 200 mg a day given to patients with some depressive symptoms and two weeks of abstinence had a decreased relapse rate of almost TWISE.
Bashiri M et al. Moderators of response to sertraline versus placebo among recently abstinent, cocaine dependent patients: A retrospective analysis of two clinical trials. Am J Addict 2017 Dec; 26:807. (http://dx.doi.org/10.1111/ajad.12635)
Those most likely to benefit are OLDER people and alcoholics.
Higher risk of relapse with cocaine used disorder: Current alcoholics, older age, male, lower depressive ratings.
Whether the selective serotonin re-uptake inhibitor sertraline at 200 mg/day delays relapse in recently abstinent cocaine-dependent individuals.
The study involved a 12-week, double-blind, placebo-controlled clinical trial with 2-week residential stay followed by 10-week out-patient participation.
Veterans Affairs residential unit and out-patient treatment research program.
Cocaine-dependent volunteers (n = 86) with depressive symptoms (Hamilton score > 15), but otherwise no major psychiatric or medical disorder or contraindication to sertraline.
Participants were housed on a drug-free residential unit (weeks 1-2) and randomized to receive sertraline or placebo. Participants then participated on an out-patient basis during weeks 3-12 while continuing to receive study medication. Patients participated in a day substance abuse/day treatment program during weeks 1-3 and underwent weekly cognitive behavioral therapy during weeks 4-12. The primary outcome measure was thrice-weekly urine results and the secondary measure was Hamilton Depression scores.
Pre-hoc analyses were performed on those who participated beyond week 2. Generally, no group differences in retention or baseline characteristics occurred. Sertraline patients showed a trend towards longer time before their first cocaine-positive urine (‘lapse’, χ(2) = 3.67, P = 0.056), went significantly longer before having two consecutive urine samples positive for cocaine (‘relapse’, χ(2) = 4.03, P = 0.04) and showed significantly more days to lapse (26.1 ± 16.7 versus 13.2 ± 10.5; Z = 2.89, P = 0.004) and relapse (21.3 ± 10.8 versus 32.3 ± 14.9; Z = 2.25, P = 0.02). Depression scores decreased over time (F = 43.43, P < 0.0001), but did not differ between groups (F = 0.09, P = 0.77).
Sertraline delays time to relapse relative to placebo in cocaine-dependent patients who initially achieve at least 2 weeks of abstinence.
No consistently effective pharmacotherapy exists for preventing relapse in cocaine use disorder. However, sertraline has shown promise in abstinent individuals with some depression symptoms. The current researchers pooled data from two similarly designed, 12-week, double-blind studies in Connecticut and Arkansas (N=126; median age, 39).
All participants were cocaine dependent, were randomized as inpatients to sertraline at 200 mg/day or placebo, and completed 2 weeks of residential treatment. Rates of current major depression were 74% in the Connecticut study and 50% in the Arkansas study. In both treatment groups, current alcohol dependence diagnosis, older age, male sex, lower depression ratings, and a negative urine screen at baseline predicted a higher risk for relapse. Overall, sertraline was associated with relapse prevention (relapse was defined as two sequential positive or missing urine cocaine results). The abstinence rate with sertraline was nearly double that of placebo (34% and 18%). Older age and current alcohol dependence predicted a stronger response to sertraline than placebo.
Studies of sertraline at lower doses and in outpatients and of other selective serotonin reuptake inhibitors have yielded disappointing results. Here, however, sertraline, dosed at 200 mg and given to participants with some depression symptoms and at least 2 weeks of abstinence, prevented relapse. Sertraline might work best to sustain rather than to initiate abstinence. This fairly low-risk intervention should be considered even if individuals don’t currently have major depression, similar to a significant portion of this sample. Older people and those with current alcohol dependence may be especially likely to benefit from sertraline, although these findings need replication.
In the seminal trial, cocaine-dependent subjects were randomly assigned to
receive D-amphetamine (15 or 30 mg/day; n = 26 and
28, respectively) or placebo (n = 40) for 25 weeks
(Grabowski et al., 2001). During the fifth week, the
D-amphetamine dose was doubled. Subjects maintained
on the higher D-amphetamine dosing regimen
(30/60 mg/day) used significantly less cocaine during
the trial than subjects maintained on either the lower
dosing regimen (15/30 mg/day) or placebo as determined
by benzoylecgonine-free urines. In the next study, dependent
cocaine injectors were assigned to placebo (n =
14) or 60 mg/day D-amphetamine (n = 16) for 14 weeks
(Shearer et al., 2003). In the D-amphetamine maintenance
group, the percent of cocaine-positive urines
decreased from 94% at baseline to 56% by the end of the
trial. In contrast, the percent of cocaine-positive urines
in the placebo maintenance group remained stable at
approximately 79% from the beginning to the end.
In the more recent trial, 48 subjects were
randomly assigned to placebo or methylphenidate over
14 weeks (Levin et al., 2007). The methylphenidate dose
was titrated upward to a target dose of 60 mg/day.
Methylphenidate-treated individuals demonstrated a
significant decrease in the probability of providing a
cocaine-positive urine sample during the trial.
Two studies meeting inclusion criteria for this review
evaluated desipramine for managing cocaine use disorder
(Gawin et al., 1989; Campbell et al., 2003). In the
first study, which lasted 6 weeks, cocaine-dependent
subjects were assigned to receive placebo (n = 24) or
2.5 mg/kg desipramine daily (Gawin et al., 1989).
Subjects who received desipramine were more likely
to achieve abstinence for longer periods, as verified by a
combined use indicator of a cocaine-negative urine
sample and self-report of no cocaine use, than subjects
assigned to receive placebo. In the more recent study,
cocaine-dependent subjects were maintained on placebo
(n = 50) or desipramine (n = 49) in an 8-week trial
(Campbell et al., 2003). The desipramine dose started at
50 mg/day and was titrated up to 200 mg/day. Groups
did not differ in their ability to sustain cocaine abstinence
or in proportion of cocaine-positive urine samples. < Ambivalent
Three prospective trials have tested the efficacy of
amantadine for treating patients with cocaine use
disorder (Kampman et al., 1996, 2006; Shoptaw et al.,
2002). Three prospective trials have tested the efficacy of
amantadine for treating patients with cocaine use
disorder (Kampman et al., 1996, 2006; Shoptaw et al.,
2002). In the earliest study, cocaine-dependent subjects
were assigned to placebo (n = 30) or 300 mg/day
amantadine (n = 31) for 4 weeks (Kampman et al., 1996).
The proportion of urine samples indicating cocaine use
was not significantly different across groups, with 57.5%
of samples being positive in the placebo group and 49.6%
of samples being positive in the amantadine group when
counting missing samples as positive. In the next study,
cocaine-dependent subjects were assigned to receive
placebo (n = 35) or 200 mg/day amantadine (n = 34) for
18 weeks (Shoptaw et al., 2002). Amantadine maintenance
increased the probability that subjects would
provide a cocaine-negative urine sample, with statistically
significant differences observed at a priori comparison
time points (i.e., weeks 8 and 16). In the most recent
study, 199 cocaine-dependent subjects with severe
withdrawal symptoms were assigned to receive placebo,
300 mg/day amantadine, 100 mg/day propranolol
or combined amantadine and propranol for 10 weeks
(Kampman et al., 2006). There was no difference between
the amantadine-treated and the placebo-treated groups
on cocaine use outcomes. Taken together, the results are
equivocal. Differences in the subjects’ severity of cocaine
use may have played a role in the discrepancy.
The only human
laboratory study of D-amphetamine reported results
similar to those of rodent and nonhuman primate laboratory
studies and several clinical trials that all support the
effectiveness of chronic D-amphetamine to decrease cocaine
use. Although three animal studies did not show
that reductions in self-administration were selective for
cocaine (versus food) self-administration, all three of
those studies examined acute D-amphetamine treatment,
whereas all studies that showed positive results
involved chronic D-amphetamine administration. Thus
it is clear that the predictive validity of these animal
models, at least with respect to D-amphetamine, is
critically dependent on chronic treatment with the
Data with methylphenidate that may appear equivocal
at first glance are reconciled when the ADHD
status of subjects is considered. Results were negative
in rats (Hiranita et al., 2009), rhesus monkeys (Czotyet al., 2013), and a clinical trial in subjects without
comorbid ADHD (Grabowski et al., 1997). When tested
in an ADHD population, however, more encouraging
results were found in the only human laboratory study
(Collins et al., 2006) and one of two clinical trials (Levin
et al., 2007). The effects of modafinil were positive in the
one preclinical study in monkeys and one study in
humans. Four of the six reviewed clinical trials reported
negative results, although in some cases positive results
were found in subsets of the subjects based on sex or
history of alcohol dependence. Likewise, negative results
were found with the norepinephrine uptake
blocker desipramine in laboratory studies in nonhuman
primates and humans and in one of two clinical trials
(Campbell et al., 2003). However, positive results were
seen with lower doses of desipramine in the other
clinical trial (Gawin et al., 1989). Finally, negative
results with amantadine were reported in monkey and
human laboratory studies as well as two of three clinical
Taken together, results with D-amphetamine (when
administered chronically) and amantadine are clearly
consistent across settings; negative results with
desipramine have been found in all but one study and
apparent discrepancies with methylphenidate can
largely be explained when ADHD status is taken into
consideration. Only modafinil resulted in clearly discordant
conclusions across settings. However, as noted
above, recent data suggest that the effectiveness in
clinical trials may require the absence of lifetime
alcohol dependence: if true, this would bring clinical
trial results more in line with the only nonhuman
primate study conducted to date (Newman et al.,
2010). Moreover, investigators have enumerated other
reasons for the discordance across clinical trials that
may affect translation.
Conclusions regarding the promise of
baclofen as a putative pharmacotherapy for treating
cocaine use disorder are similar across animal, human
laboratory, and clinical studies in that all three settings
have produced mixed results. Acute baclofen treatment
in rodents produced positive results (i.e., a selective
decrease in cocaine versus food self-administration)
only in the laboratory that used food pellets as a
reinforcer but not in two others where liquid food
was used. Baclofen did not selectively decrease cocaine self-administration in monkeys. Thus we concluded
mixed findings as 5 of 8 studies showed that baclofen
reduced cocaine self-administration (Table 2) similar to
studies in the other two settings. The two human
laboratory studies produced opposite results and the
results of clinical trials were also mixed, perhaps based
on the extent of cocaine use of the subjects. In addition,
because of the relatively short duration of action of
baclofen and documented side effects (e.g., Brebner
et al., 2002; Bowery, 2006), it is tempting to speculate
that experimental parameters, such as dose, duration of
treatment, and drug pretreatment times (in acute
experiments), may contribute to the discordant results
obtained with baclofen. The tiagabine results are more
clearly concordant, showing no differential effects on
cocaine taking observed as a function of tiagabine
treatment across nonhuman primate and human laboratory
and clinical trial research (Lile et al., 2004b;
Weerts et al., 2005; Winhusen et al., 2005, 2007).
Two clinical trials evaluated the efficacy of buspirone
for treating cocaine use disorder (Moeller et al., 2001;
Winhusen et al., 2014). In the earlier study, cocainedependent
subjects were randomized to receive placebo
(n = 18) or 45 mg/day buspirone (n = 17) for 12 weeks
(Moeller et al., 2001). The two groups did not differ in
percent of cocaine negative urines nor did they differ in
semiquantitative levels of cocaine metabolites in urine
samples. In the second study, which lasted 16 weeks
and was designed to evaluate the ability of buspirone to
prevent cocaine relapse, subjects were first admitted to
an inpatient treatment unit to achieve cocaine abstinence.
While on the unit, subjects were randomized to
receive placebo (n = 27) or 60 mg/day buspirone (n = 35;
Winhusen et al., 2014). There were no differences
between the groups assigned to receive placebo or
buspirone in their ability to maintain cocaine abstinence
after discharge from the inpatient unit or in the
number days using cocaine after discharge from the
In the first study, 30 cocaine- and opioid-dependent
subjects received ascending daily doses of buprenorphine
(2, 4, 8, 12, and 16 mg, doses varied across
individual subjects) for 21 days at each dose (Schottenfeld
et al., 1993). The buprenorphine dose was then tapered.
During the taper, the proportion of cocaine-positive
urines was lower than during the dose escalation period,
with similar effects across doses. In the next study,
116 opioid-dependent cocaine abusers were randomly
assigned to receive 4 or 12 mg/day buprenorphine or 20
or 65 mg/day methadone for 24 weeks (Schottenfeld
et al., 1997). None of the treatment groups differed in
rates of cocaine use. The third study evaluated 2, 8, or
16 mg/day buprenorphine or 16 mg buprenorphine
every other day in 200 cocaine and opioid-dependent
subjects (Montoya et al., 2004). Urine toxicology
testing revealed significantly reduced benzoylecgonine
concentrations in the subjects randomized to 8 or 16 mg
buprenorphine daily. The 16 mg/day buprenorphine
group also displayed significant reductions in the
number of cocaine-positive urines during withdrawal
from opioid maintenance. The most recent trial
compared maintenance on 12–16 mg buprenorphine
to maintenance on 65–85 mg methadone in 162
individuals assigned to contingency management or
performance feedback using a 2 2 factorial design
over 24 weeks (Schottenfeld et al., 2005). Subjects
assigned to methadone, regardless of behavioral
therapy platform, were significantly more likely to
provide cocaine-negative urines and achieved longer
consecutive periods of abstinence from cocaine than
their buprenorphine-treated counterparts.
Sleep is so important to re-structuring your brain for success, yet it is so difficult to get good quality sleep. Our circadian rhythms and general health are tied to our sleep-wake schedules and this impacts our longevity and healthspan. It is known that addiction is a lot harder to treat when you don’t get good quality sleep. The information below is a copy of an article that discussed the circadian rhythm and health and how there is genetic basis to sleep-wakefulness.
What’s your chronotype? Are you a morning lark or a night owl? The manner in which your brain processes light, an activity known as phototransduction, is responsible for whether you find yourself nodding off in the chair every evening about 8:30, or whether you regularly stay up until the wee hours and sleep as late as you can. If you are such an owl that you have trouble getting to work or school on time and feel groggy most of the day, you might have delayed sleep phase disorder (DSPD). Too early, and it’s advanced sleep phase disorder (ASPD), which is less common. Circadian misalignment of this kind can affect everything from your risk of clinical depression to your chances of cardiovascular disease. It can alter your BMI and play a role in whether or not you smoke cigarettes.
A 2012 study in Annals of Neurology found that variations in the PER1 and PER2 genes, members of a gene group responsible for circadian rhythms, were strongly involved in determining who rises early and who rises late. Genome-wide association studies undertaken using data from the UK Biobank and from the genetics company 23andMe also support the conclusion of a genetic origin for delayed and advanced sleep phase disorders.
Our intrinsic 24-hour clock mechanism resides in the brain’s suprachiasmatic nucleus (SCN), a set of neuron clusters in the hypothalamus that receive input from the retina via the optic nerve. Via phototransduction, the amount of light captured by the brain is translated into electrical signals. This system evolved to allow early life forms to accurately peg light and dark cycles caused by the rising and setting of the sun. The SCN also controls the synthesis of melatonin in the pineal gland, a crucial component of wake/sleep cycles. Both larks and owls inherit variations of these genetically determined behaviors that produce something very much like jet lag without the plane ride. Clock-dependent alertness pathways in the brain stay activated later at night in the owls, and give out earlier in the larks. Peak performance times, body temperature cycles, and hormonal rhythms are all canted away from the norm in people with sleep phase disorders.
In a commentary for Proceedings of the National Academy of Sciences (PNAS), Joseph Bass of Northwestern University’s department of medicine wrote that “alignment between behavioral cycles and the light-dark cycle may also provide health benefits to humans, since at clinical and epidemiological levels, a strong correlation has emerged between chronic sleep and circadian disruption and metabolic disease.” (This correlation is especially noticeable among shift workers, who forcefully alter their circadian rhythms to fit the needs of the workplace).
The body clock also helps establish our eating cycles, body weight, and glucose levels. Circadian misalignment results in “a decrease in leptin, increase in glucose and insulin, increase in mean arterial blood pressure, and reduced sleep efficiency” according to Frank Scheer and coworkers who authored the PNAS study. Scheer adds that people with disordered body clocks also show mild hypertension, “indicating that over the long term, cumulative cardiovascular risk may increase as a result of circadian misalignment.”
It should be noted that most people with sleep phase disorders are able to sleep just fine when they are allowed to choose the hours. And while they share certain metabolic risks, morning people and night people have different profiles and problems. In a study of people with DSPD in San Diego, published in the Journal of Circadian Rhythms, night owls reported bedtimes of 2 am on average, compared with 10:45 pm in a control group. As children, more than 80 percent of late-nighters said they had gone to bed later than their contemporaries, and about 30 percent were able to identify at least one grandparent who stayed up late. They were also six times more likely than controls to have consulted a doctor about sleep problems, and most strikingly, almost half of delayed sleep phase subjects reported seeing a counselor for emotional problems, primarily depression.
Thus it is not surprising that scientists have raised the possibility that DPSD and depression share common genetic underpinnings. In 2014, a survey in BMC Psychiatry suggested that delayed sleep phase disturbances were twice as common among depressed young people in Australia compared with the population at large. Higher levels of tobacco use were also associated with this group (38 percent compared with the national smoking rate of roughly 17 percent). The researchers called smoking “the only independent predictor of delayed sleep onset.” They also suggest that the onset of DSPD may represent a marker signifying “a circadian pathophysiological profile of depression that may have a different prognosis and response to treatment.”
Indeed, there is additional evidence of a link between delayed sleep phase disorder and seasonal affective disorder (SAD). Night owls are more than three times as likely to report seasonal affective disorder during winter months than normal sleepers, Heon-Jeong Lee and colleagues report in theJournal of Affective Disorders: “DSPD might share similar pathophysiological mechanisms” with seasonal affective disorder (SAD), “since both manifest problems of delayed circadian rhythm phase and both are treated by morning light therapy and melatonin before bedtime.”
This treatment protocol, used for both delayed and advanced sleep disorders as well as for SAD, is a form of chronotherapy, or the deliberate shifting of sleep-wake cycles. Full-spectrum light therapy for two hours in the morning and melatonin treatment in the early evening help advance the body clock in night owls. Similarly, with early risers, bright light in the evening and melatonin supplements in the morning serve to delay the circadian cycle to align it with normal day-night cycles.
As for morning people, the overall profile is less worrisome, though those with ASPD often have an impaired social life because evening activities conflict with their desire to sleep. In addition, according to work published in Nature Communications, genetic correlations suggest that a morning chronotype may share underlying biology with a slightly higher BMI.
Nonetheless, it seems that morning larks present a healthier profile than the owls.
“There is little if any evidence that early morning risers have more depression than the average person,” says Daniel F. Kripke, a sleep researcher and emeritus professor of psychiatry at the University of California, San Diego. “At our sleep clinic, we probably see ten cases of delayed sleep phase for every case with advanced sleep phase.” Sleep patterns of morning people, Kripke notes, resemble those of “an agricultural society without electric light.”
In sum, says Kripke, “people in the ‘morningness’ half of the population do not complain of it much except in unusual or extreme cases.
Norway’s parliament has voted to decriminalize drug use this week, moving instead to focus on treatment for addicted drug users in place of punitive measures.
The vote, with the majority of parliament voting to decriminalize, asks the government to prepare for reform. Parliament wants to stop punishment drug users who struggle to provide assistance and professional treatment. Those found with small amounts of drugs from heroin to marijuana but won’t be arrested and instead offered treatment.
Members of parliament have said the effort will focus on treatment and follow-up programs. They also emphasized that they do not want to legalize drugs, only decriminalize drug use.
The process of changing the policies will take time, but the vote is a symbolic change for the new direction and vision. Currently, those who are struggling with substance abuse are treated as criminals with sanctions like fines and imprisonment, but the Norwegian parliament believes that they should be treated as ill.
Some members of parliament are calling the vote a “historic transformation of Norwegian drug policy.” The process aims to bequeath the responsibility from the justice system to health agencies.
Norway has considered decriminalizing drug use for several years, even starting a test program in Olso and Bergen that would sentence drug users to treatment rather than jail in 2006. In 2016, the courts were allowed to use this option on a national level.
Recently the Norwegian Minister of Health, Bent Høie, changed his position on the issue, saying he believed in treatment in place of punishment. The shift, however, is not a unanimous one. Some members of parliament believe decriminalization sends a signal to drug users that the offense is not serious, but that has never stopped addicted users from getting and taking drugs.
Portugal similarly decriminalized all drug use in 2001 after harsh punishments did not improve the opioid crisis, and it set the precedent for that approach at the national level. Over 15 years, the country has seen a decline in drug use, and drug-related deaths.
Can energy drinks lead to future drug and alcohol addiction?
Objectives: This longitudinal study examined the prevalence and correlates of energy drink use among college students, and investigated its possible prospective associations with subsequent drug use, including nonmedical prescription drug use.
Methods: Participants were 1060 undergraduates from a large, public university who completed 3 annual interviews, beginning in their first year of college. Use of energy drinks, other caffeinated products, tobacco, alcohol, and other illicit and prescription drugs were assessed, as well as demographic and personality characteristics.
Results: Annual weighted prevalence of energy drink use was 22.6%wt and 36.5%wt in the second and third year of college, respectively. Compared with energy drink nonusers, energy drink users had heavier alcohol consumption patterns, and were more likely to have used other drugs, both concurrently and in the preceding assessment. Regression analyses revealed that Year 2 energy drink use was significantly associated with Year 3 nonmedical use of prescription stimulants and prescription analgesics, but not with other Year 3 drug use, holding constant demographics, prior drug use, and other factors.
Conclusions: A substantial and rapidly growing proportion of college students use energy drinks. Energy drink users tend to have greater involvement in alcohol and other drug use and higher levels of sensation seeking, relative to nonusers of energy drinks. Prospectively, energy drink use has a unique relationship with nonmedical use of prescription stimulants and analgesics. More research is needed regarding the health risks associated with energy drink use in young adults, including their possible role in the development of substance use problems.
College students who often consume energy drinks are more at risk of forming an alcohol addiction, using cocaine, or misusing prescription stimulants by the age of 25, according to a new study.
The paper — funded by the National Institute on Drug Abuse and conducted by researchers from the University of Maryland’s School of Public Health — asked over 1,000 college students about their habits concerning the past-year consumption of highly caffeinated energy drinks.
In a three-year span, the participants were interviewed annually. Researchers observed whether their energy drink consumption decreased, increased or remained steady, and at the five-year mark, the subjects were evaluated again for drug use in the past year.
The researchers discovered an increased likelihood of alcohol addiction, prescription drug misuse, and cocaine use in groups that revealed increasing or consistent probabilities of energy drink use over the time period.
These groups were previously categorized based on their energy-drinking habits. “Intermediate” and “persistent” groups who drank energy drinks consistently were the most at-risk. The groups were not gathered based on the level of consumption, but rather on their consistency of consumption.Although the data is in line with similar animal-based studies that suggest caffeine can influence future drug use, this research does not confirm energy drinks as a direct cause.
The results remained accurate regardless of how often — frequently, occasionally or infrequently — students drank these beverages.
In a direct response to the study, the American Beverage Association released a statementthat emphasized the safety of energy drinks and mentioned the extensive government studies that affirm their safety.
“Nothing in this study counters this well-established fact,” the association added.
Long-term effects aren’t the only concerns — beverages with excessive amounts of caffeine also have short-term effects. For example, drinking more than four cups of brewed coffee a day can result in muscle spasms, irritability, speeding heart-rate, severe headaches, upset stomach, and restlessness at night.
The Mayo Clinic says the daily consumption of up to 400 milligrams of caffeine “appears” to be safe. This amount is found in about
10 cans of soda, two energy shot drinks, or four cups of coffee. The caffeine amounts in these comparisons can vary drastically, especially with energy drinks, the clinic clarified.
They also emphasized the dangers of caffeine use in children and urged adolescents to minimize their intake; alcohol and other substances should not be mixed with caffeine either.
The Mayo Clinic encourages pregnant women or those trying to become pregnant to seek professional guidance about limiting their use of caffeine.
The benefit of Sublocade is it forces one to be compliant with treatment – no more stopping the films so you can have a relapse. Also it doesn’t require you to detox to go on Vivitrol. Obviously those who detox have a higher rate and risk of overdosing if they relapse.
You need a license to cut-and-paste this copyrighted news content. Use this link to purchase your paid subscription ($200/year for individuals and $1,000/year for companies of every size): https://endpts.com/subscribe Already a paid subscriber? Sign in to Endpoints News to remove this message.
The FDA has given Indivior the OK to sell its monthly injectable version of Suboxone, shoring up the company’s tenuous hold on the opioid addiction market as competition looms near.
The drug, to be marketed as Sublocade (RBP-6000), is a monthly injection of buprenorphine, which contains a mild opioid to help stymie withdrawal for addicts quitting opioid use. The medicine is meant to be used as part of a treatment plan that includes counseling and psychosocial support.
The news doesn’t come as a surprise. Considering the growing addiction to opioid-based painkillers and heroin in the US, the FDA’s advisory committee made a strong recommendation to approve the drug earlier this month. And rivals will be well received at the FDA.
“Everyone who seeks treatment for opioid use disorder deserves the opportunity to be offered the treatment best suited to the needs of each individual patient, in combination with counseling and psychosocial support, as part of a comprehensive recovery plan,” said FDA Commissioner Scott Gottlieb. “As part of our ongoing work in supporting the treatment of those suffering from addiction to opioids, the FDA plans to issue guidance to expedite the development of new addiction treatment options. We’ll continue to pursue efforts to promote more widespread use of existing, safe and effective FDA-approved therapies to treat addiction.”
Max Herrmann, Stifel
Indivior’s film version of this drug, which is dissolved under the tongue or inside the cheek, has been the market leader in this field for the past two decades. But the company’s grip on the market was compromised when generics and other competitors began to creep onto the scene. In September the company warned investors that a US court ruling that cleared the way for a generic rival had “significantly increased” the risk of new competitors. In a press release back in September, Indivior said it could lose up to 80% of its market share “within a matter of months” thanks to the new competition.
And then there’s Suboxone’s branded rival Vivitrol (made by Alkermes), which recently made its case for equal efficacy to Indivor’s drug. This monthly injection works differently than Suboxone, blocking the effect of opioids. Alkermes’ central branding message is that Vivitrol is cleaner, containing no opioids. But the drug also requires patients to be detoxed entirely from opioids, which can prove problematic for addicted patients.
Although not great news for competitors, this new approval for Indivior could mean significant revenue for the company. Max Herrmann, an analyst at Stifel, expects the drug could capture 30% of the broader buprenorphine market. He expects annual sales of about $700 million by 2021, while Jefferies analysts expect peak sales of $1.3 billion by 2025.
There is a new treatment for Opioid dependence, Sublocade, which is a monthly depot injection of buprenorphine in a slow release formulation. I can see the benefits in people who seem to relapse on Suboxone as it will enforce compliance as they work on the cues and triggers that drive them to use. The links are below for articles related to this new product sold through Avella pharmacies : https://www.avella.com/ Avella Pharmacies
In a press release issued November 30, 2017, the US Food and Drug Administration (FDA) announced it has approved Sublocade, a once-monthly buprenorphine injection for moderate to severe opioid use disorder (OUD).1
Current buprenorphine-based treatments for OUD employ an oral mode of administration (in the form of a dissolvable film or tablets) and require daily intake, thus posing the issue of medication adherence. These treatments are also available in the form of an implant (Probuphine), which provides stable delivery of low-dose buprenorphine over a 6-month period.2 The agency’s commissioner, Scott Gottlieb, MD, noted in the press release the importance of providing an array of treatment options for OUD. “Everyone who seeks treatment for opioid use disorder deserves the opportunity to be offered the treatment best suited to the needs of each individual patient, in combination with counseling and psychosocial support, as part of a comprehensive recovery plan,” he said.1
Also in the press release, the FDA emphasizes that providing “the full range of medication-assisted treatments” is one of its focuses, and is in line with the US Department of Health and Human Services’ first point in their “Five-Point Strategy to Combat the Opioid Crisis.”3
Sublocade (RBP-6000) allows the sustained delivery of buprenorphine over a 1-month period, thanks to the Atrigel Delivery System, which, on subcutaneous injection, forms a solid deposit, subsequently broken down to steadily release the drug. The treatment is meant to be delivered in the form of a prefilled syringe by a clinician, and should be included in a comprehensive biopsychosocial treatment program.
In a study investigating the efficacy of RBP-6000 in subjects with moderate to severe OUD, initiated on a buprenorphine/naloxone sublingual treatment before receiving 2 RBP-6000 injections on days 1 and 29, the treatment was found to reduce “drug-liking” and reinforcing behaviors on challenges with the μ-opioid agonist hydromorphone (administered before and after RBP-6000 injections on 3 consecutive days of each week of the study period at 6 and 18 mg, and compared with placebo).4The clinical development of RBP-6000 included a phase 1 study (ClinicalTrials.gov identifier: NCT03002961), evaluating a single-ascending dose of the drug, and a phase 2 multiple dose study (ClinicalTrials.gov identifier: NCT01738503), which demonstrated the safety and tolerability of the treatment for patients ages 17 to 65 years. A population/pharmacodynamic model indicated that “200 mg RBP-6000 dose should achieve 2–3 ng/mL buprenorphine average concentrations and desired efficacy.”5 Clinical studies showed that patients treated with Sublocade had fewer weeks with positive urine tests and self-reported opioid use vs patients receiving placebo.
Treatment side effects include constipation, vomiting, nausea, and drowsiness. Postmarketing studies will assess the necessity of the pretreatment stabilization regimen with sublingual buprenorphine, the benefits of higher doses of Sublocade in patient subpopulations, and the efficacy of longer interdose intervals.
“We’ll continue to pursue efforts to promote more widespread use of existing, safe and effective FDA-approved therapies to treat addiction,” concluded Dr Gottlieb in the press release.
The article below is from the Fairfax county Police site regarding overdoses: Treatment is available for all these people, so they are all preventable deaths. Unfortunately, seeking treatment is a choice that the disease of addiction just doesn’t always allow:
In just the past week, our detectives have investigated six deaths as overdoses, five of which are believed to be caused by opioids. The first overdose death occurred Friday, December 1 in Alexandria. The second death happened on Sunday in Fairfax Station. The third and fourth deaths were on Wednesday in McLean and Clifton. The fifth death occurred yesterday in Fairfax. The victims were between the ages of 22 and 34.
Our detectives believe there are batches of heroin currently on our streets which could be laced with fentanyl and carfentanil,synthetic opioids which can be lethal even in the smallest doses. Until lab results are received, we cannot confirm the five overdose victims died due to a result of these new batches appearing in the county.
“In my 20 years in Narcotics, I have never seen anything like this. Before this week, the highest number of opioid overdoses we had in a weekend was five, and fortunately, everyone lived,” said Second Lt. James Cox of the Organized Crime and Narcotics Division. “We don’t want to see anyone else die. Please have a plan in place. You may remain anonymous. Help is also available through the Community Services Board for anyone, including families suffering from addiction. Narcan is available and the Chris Atwood Foundation will give it out this evening between 6 and 8 p.m. at 11890 Sunrise Valley Drive in Reston.”
Since the start of 2017, there have been 102 fatal overdoses in Fairfax County.
Of those 102 overdose fatalities, about 70% have been confirmed to be opioid related.
Our detectives are still awaiting lab results for overdose cases reported within the last 90 days, but they expect the majority of them to also be opioid related.
Cases have involved people of varying ages, from their early 20s to mid-60s, with higher numbers seen between the ages of 25 and 35.
Since the rise of opioid use in late 2014, we have partnered with a number of local offices and organizations to educate members of our community on the dangers of opioid use and the resources available within our community to combat this growing concern. The outreach includes students, nurses, Parent Teacher Associations, Rotary Clubs, Citizen Advisory Committees and more.
In addition to general outreach and education on opioid use, some groups also offer free Narcan training. Narcan is a medicine that can reverse an overdose when used quickly and correctly. It is available without a prescription at local pharmacy stores in Virginia. Free training on how to use Narcan is available through the Fairfax-Falls Church Community Services Board (CSB). Please visit https://www.fairfaxcounty.gov/csb/revive/ for upcoming training dates and information. This training is open to everyone.
If you feel you may have overdosed or are concerned someone around you has, please call 9-1-1 immediately. Fairfax County Fire and Rescue personnel also carry Narcan and are trained in its use.
Symptoms of opioid overdose include some of the following:
Loss of consciousness
Snore-like gurgling sounds
Breathing is low, shallow or erratic
Bluish purple, or ashen skin color
Nausea or vomiting
Fingernails turn blue or close to black
Our officers and detectives are working diligently and around the clock to reduce the number of deaths caused by opioids. Please call 9-1-1 if you suspect an overdose. Help is available 24 hours a day. If you or someone you know needs help to overcome drug dependence, please call the Community Services Board at Merrifield Center at 703-573-5679 to help find appropriate treatment and recovery services. Walk-ins are also welcome Monday through Friday from 9 a.m. to 5 p.m.