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Coron, Palawan Philippine Islands

Getting Away With Murder: The Philippines’ Brutal Drug War

Coron, Palawan Philippine Islands

A quick search on the internet regarding the state of the Philippine drug war reveals a shocking reality. Bystanders describe the bloodied bodies of victims lying callously in the street after encounters with police force; families recall husbands and fathers being taken from their homes by masked vigilantes. If the tales of the widows and children left behind aren’t enough to paint a horrifying picture, the devastating photos that emerge certainly do.

In a country currently experiencing our own struggles with drug use and trafficking, such a reality can be hard to process, to say the least. It’s difficult to imagine how a federal operation intended to protect the public has strayed so far as to leave 7 of every 10 Filipinos fearing they will become victims at the hands of their own government. To understand how the Philippines got here, it’s helpful to examine the history of President Rodrigo Duterte’s anti-drug initiative.

A Violent Past

In the mid-to-late 90’s, while drug hysteria seemed to be reaching a global peak, Rodrigo Duterte was in the middle of serving 22 years as Mayor of Davao City in the Philippines. He was notorious, but praised by citizens no less, for his zero-tolerance attitude toward drugs and criminal activity, earning him popular sensationalist nicknames like “The Punisher.”

After local media sources connected over 60 unexplained deaths throughout Davao City with a vigilante group of killers known as the Davao Death Squad (DDS), human rights activists began to suspect Duterte of assembling the force. Though he denied involvement in the group’s creation, he had no problem publicly encouraging and approving of their actions.

In these early days, the DDS was believed to be comprised of only ten members, a number that quickly grew alongside death tolls. Throughout the entirety of Duterte’s time as Mayor, both hitmen and human rights groups have estimated at least 1,000 casualties as the result of Duterte’s orders.

The Present President

President Rodrigo Roa Duterte
President Rodrigo Roa Duterte

Unfortunately, as the death count rose, it appeared Duterte’s approval ratings did as well. In June of 2016, running on a hostile platform that candidly threatened to kill drug users and traffickers, Duterte won the presidential election, promising to rid the Philippines of their drug problem within six months. The Philippine National Police force (PNP) were immediately pressured and given all-encompassing immunity to kill anyone suspected of using or selling drugs. Just two months into Duterte’s presidency, the official death count had already climbed to over 2,000.

It wasn’t until January of 2017, when a South Korean businessman was kidnapped and murdered at the hands of two PNP officers, that Duterte first began to question the integrity of the police force. Official anti-drug operations were temporarily suspended until late February, and on March 6th the PNP launched a new plan to redirect focus on “big fishes” instead of low-level users. But in practice, neither the suspension nor the new plan (dubbed “Oplan Double Barrel Reloaded”) changed much of anything on the ground, and Duterte’s approval ratings still soared, so the killings relentlessly continued. It would take a tragedy to wake the nation up.

During August 2017, in a one-week crackdown in Caloocan City, the PNP killed 17-year-old Kian Delos Santos, reporting that he was armed and killed after fighting back when officers tried to arrest him. This report is identical to countless others, but surveillance footage of officers dragging Kian outside, giving him a gun, and shooting him as he tried to run finally confirmed the corruption among the PNP that citizens have long feared. It was finally enough for the Senate to open an investigation, and for Duterte’s satisfaction ratings to take a massive hit.

Hope for the Future?

With Duterte’s violent methods rapidly drawing criticisms from the public eye, as of October 12 he has once again detached the PNP from the anti-drug campaign, pulling Oplan Double Barrel and ordering all drug-related operations to be left to the Philippine Drug Enforcement Agency (PDEA). The PNP is now limited only to intelligence gathering, and the officers responsible for Kian’s murder has been detained despite Duterte’s past promises to protect the police. Whether or not these actions will have a tangible effect remains yet to be seen, but in the meantime, there exists a lesson for the rest of the world.

Though Duterte’s approach is no doubt extremist, it demonstrates the devastating consequences of criminalizing addicts instead of treating their disease. Waging war against drug users is a hostile tactic that destroys countless lives. Fostering a culture of prevention and rehabilitation is far more effective, and could have saved actual thousands in the case of the Philippines: While the police force currently claims a death count of 3,451 people, human rights groups factoring in victims of vigilante killings estimate numbers upwards of 12,000. Meanwhile, PNP reports state that 2,465 kilograms of methamphetamine have been seized since the start of Duterte’s drug war.

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Understanding Addiction


Addiction is a life-shattering illness. It rips families apart and destroys lives. It is historically defined as a physical and/or psychological dependency on a mood-altering chemical (e.g. alcohol, heroin, prescription drugs, etc.) or behavior (sex addiction, gambling addiction, internet addiction), although it can also be viewed as a continued involvement with a substance or activity despite the negative consequences associated with it. It often starts with experimentation and social use coupled with the thought that one can quit whenever he/she wants. It has many end results: living on the streets, alienating one’s family and friends, and in some cases death. For most addicts, addiction is a lifelong illness, with relapses occurring even after long periods of abstinence or sobriety. Addiction is rarely arrested without the help of an addiction treatment center.

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Alcohol Abstinence May Resolve Neurocongnitive Defects

Long-term abstinence may resolve many of the neurocognitive deficits associated with alcoholism

Alcoholism can cause neuropsychological deficits.


  • A new study looks at alcoholics who have been sober for six months to 13 years.
  • Results indicate that long-term abstinent alcoholics can recover many of their neurocognitive deficits, except for spatial-processing abilities.

Alcoholism can cause neuropsychological deficits, that much is clear. There is much less clarity, however, concerning to what degree recovery may occur with abstinence from alcohol. New findings indicate that long-term abstinence from alcohol can resolve many – but not all – neurocognitive deficits.

Results are published in the September issue of Alcoholism: Clinical & Experimental Research.

“Previous research has shown some but not total recovery with abstinence from alcohol,”

said George Fein, president of and senior scientist at Neurobehavioral Research, as well as the corresponding author for the study.

“The continuing presence of deficits is not a trivial issue as it may interfere with day-to-day functioning.”

“The nature of alcoholism as a dynamic condition is largely underappreciated by most people, including clinicians,”

added Edith Sullivan, a professor in the department of psychiatry and behavioral sciences at Stanford University School of Medicine. “Alcoholics may have periods of abstinence, during which time they give their nervous system time for repair. Thus, longitudinal studies of alcoholics are critical for identifying functional areas that are targeted by alcoholism, those that are relatively spared, and those that can recover with sobriety.”

Longitudinal studies in alcoholism, however, are very difficult to conduct, Sullivan added. “Tracking active alcoholics is challenging, finding alcoholics in recovery is also difficult – there is still a stigma associated with the condition. Furthermore, those who are in denial of their condition, by definition, will not avail themselves for study.”

In this case, researchers performed a number of neuropsychological assessments on 96 participants, divided into two groups: 48 (25 males, 23 females) long-term abstinent alcoholics, and 48 (25 males, 23 females) age-matched “controls” who either drank lightly or not at all. The alcoholics were abstinent from six months to 13 years, for an average of 6.7 years. Performance was measured in nine domains: abstraction/cognitive flexibility, attention, auditory working memory, immediate memory, delayed memory, psychomotor function, reaction time, spatial processing, and verbal skills. Fein said that the only domain they did not examine was gait and balance, regarding it as separate.

“We found that the cognitive and mental abilities of middle-aged alcoholics who had been abstinent for six months to 13 years are indistinguishable from those of age and gender comparable non-alcoholics,” said Fein, “with the possible exception of spatial processing abilities. Recovered functions would include short- and long-term memory, planning, learning, comprehension, etc. In other words, they would be able to support a normal home, work and social life; these people should be able to function cognitively normally.”

“These findings further indicate the selectivity of alcoholism’s untoward effect on visuospatial processes,” added Sullivan, “which are important for many daily activities, including driving. We might also predict that these recovering alcoholics would have difficulties in reading a map, assembling things, and performing tasks that require spatial orientation.”

Both Fein and Sullivan noted that these findings provide hope for recovering alcoholics, and can be used to encourage abstinence from alcohol.

However, cautioned Sullivan, “it is important to conduct careful investigation of cognitive and motor functions because they are multifaceted and complex, and component processes and functions can be impaired or recover piece by piece,” she said. “It may be that only when enough of the pieces recover to at least some minimum level that we can then observe improved function.”

In addition, said Fein, “we cannot definitively say that these individuals had deficits when they stopped drinking. We don’t have data on this. Furthermore, these people were middle-aged. We’re not saying that you will have full recovery if you stop drinking in your 50s or 60s; we are saying that these people stopped drinking earlier, and they appear to have close-to-full recovery function.”

Researchers believe that the older brain may be more vulnerable than the younger and middle-aged brain to the damaging effects of alcohol. Fein and his colleagues are now examining recovery of cognitive functioning among abstinent alcoholics 65 to 85 years of age who stopped drinking before the age of 50, between 50 and 60, and after 60 years of age. This data, said Fein, will address the degree to which alcohol abuse is more damaging to the older brain, as well as the extent of recovery of function with long-term abstinence among older alcoholics.

“Whatever their nature,” said Sullivan, “follow-up and/or longitudinal studies are of the utmost importance because of the vast number of factors that can contribute to cognitive and motor abilities, such as pre-existing family history and genetic factors, education, gender differences, age at onset of drinking, drinking pattern, age of drinking, nutrition, non-alcohol substance abuse comorbidity, and psychiatric comorbidity, such as anxiety or depressive disorders.”

Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, “Cognitive Performance in Long-Term Abstinent Alcoholics,” were: Jennifer Torres and Victoria Di Sclafani of Neurobehavioral Research, Inc.; and Leonard J. Price of the Alta Bates Medical Center at Herrick Campus, Berkeley. The study was funded by the National Institute on Alcohol Abuse and Alcoholism.

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Gene-on-gene Interactions May Influence Risk for Developing Alcoholism

Gene-on-gene interactions may influence risk for developing alcoholism

One variant of the alcohol dehydrogenase gene can influence alcohol response among some Caucasians

Not only do both genes and environment have an impact on the development of alcohol-use disorders, but now researchers have found that certain genes may influence scientists’ ability to interpret other genes’ effects. One variant of the alcohol dehydrogenase (ADH) gene – the ADH1B genotype – appears to be able to influence level of response (LR) to alcohol among non-Asians.

Results are published in the September issue of Alcoholism: Clinical & Experimental Research.

There are at least two known groups of gene mutations that can effect how individuals metabolize alcohol, explained Marc A. Schuckit, director of the Alcohol Research Center, Veterans Affairs San Diego Healthcare System, professor of psychiatry at the University of California, San Diego, and co- author of the study. One group of mutations is in an enzyme called aldehyde dehydrogenase (ALDH) and the other group is in the ADH enzyme. These mutations – predominantly observed among Asians – tend to impart protection from alcohol-use disorders because they cause a larger, more intense LR to alcohol, including facial flushing.

“The question was raised,” continued Schuckit, “do the ADH mutations affect LR to alcohol in Caucasians? There are some fairly consistent reports in the literature that some Caucasians do have a bit of facial flushing with alcohol similar to what you see in Asians. Accordingly, if you can find this same increased response to alcohol in the roughly 10 percent of the Caucasian population that carries these ADH gene mutations, the next question is: ‘how does that effect our ability to study people’s LR to alcohol as it might be influenced by another gene?'”

For this study, participants numbered 117 (81 females, 36 males), ranging in age from 18 to 29 years of age, were primarily Caucasian (70.1%) and Black (26.5%), and recruited from San Diego, California. Researchers used various tools to assess demographic, substance use, psychiatric history, and first-degree family history of alcohol dependence. In addition, all participants provided a blood sample for genotyping, and were given an alcohol challenge in order to examine their LR to alcohol during a 210-minute session.

Results showed that participants with the ADH1B*1/*2 genotype had a higher LR to alcohol early in the alcohol challenge (that is, 30, 60 and 90 minutes after drinking), as measured by subjective feelings of intoxication and body sway.

“These findings suggest that there indeed might be a genetically influenced factor of a possible mildly increased LR to alcohol associated with the two genes that we studied,” said Schuckit, “and that may decrease some people’s risk for alcoholism slightly.”

Schuckit said that these findings will likely change how he approaches his own research in the future. “In the kind of work that I’m doing, I had better evaluate people with those two gene forms of ADH separately, because I think they may wash out the effects of some of the other genes that I’m trying to look for. For the field in general, it’s important for researchers to know that there are milder effects of alcohol-metabolizing enzymes similar to what’s seen in Asians that might have an effect of slightly decreasing the risk for alcoholism.”

He added that the implications of these findings go beyond significance for just researchers. “This is the sort of finding that reinforces the fact that genes impact on your response to alcohol, and impact on your risk for alcoholism,” he said. “There are some people who think it’s hard to see behavioral problems like alcoholism being impacted by genes, but of course it is, because genes affect what you were like before you took the alcohol, and also genes absolutely impact on how the alcohol will affect you. The clearest example we have of this are the alcohol-metabolizing genes.”

Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, “Associations of Variations in Alcohol Dehydrogenase Genes with the Level of Response to Alcohol in Non-Asians,” were: Nicole C. E. Duranceaux, Mimy Y. Eng, Shannon K. Robinson, and Tamara L. Wall of the Department of Psychiatry at the University of California, San Diego; and Lucinda G. Carr of the Departments of Medicine and Pharmacology at Indiana University. The study was funded by the Veterans Affairs Research Service, the State of California, and the National Institute on Alcohol Abuse and Alcoholism.

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Alcoholism Treatment Medication Acamprosate May Help Abstinent Alcoholics Sleep Better

Alcoholism treatment medication Acamprosate may help abstinent alcoholics sleep better

New findings suggest that Acamprosate shows promise as a treatment method for alleviating sleep disturbances experienced by alcoholics during abstinence

Alcoholics generally don’t sleep well. Nor does abstinence improve the situation much. In fact, sleep difficulties during alcohol abstinence may be responsible for a relapse to alcoholism as individuals attempt to self medicate their sleeping problems. New findings show that an alcoholism – treatment drug called acamprosate, widely used in Europe, can alleviate post-withdrawal sleep disturbances by influencing glutamatergic transmission.

Results are published in the September issue of Alcoholism: Clinical & Experimental Research.

“During chronic and excessive use of alcohol, short periods of deep sleep become interrupted by brief periods of restlessness,” said Luc Staner, director of the Sleep Laboratory of the Centre Hospitalier de Rouffach. “This may also be accompanied by sleep terrors, sleepwalking and exacerbation of loud snoring or sleep apnea. During the day, alcohol intake can exacerbate sleepiness, which disrupts performance and contributes to accidents even when an individual is not significantly intoxicated.” Staner is also a researcher at FORENAP, an organization that specializes in early drug development and research in neuroscience, located in Rouffach, France.

Sleep dysfunction does not necessarily improve with abstinence from alcohol, added Staner, who is also the corresponding author for the study. “Sleep is initially characterized by occasional nights of very little sleep and nightmares, followed by either progressive improvement or, very often, long-lasting sleep difficulties,” he said. “If the latter, consequences may include decreased attention, vigilance, energy and concentration; increase in fatigue and malaise, irritability, etc. These often protracted symptoms lead some patients to resume drinking in an attempt to self-medicate their sleep problems. Probably for this reason, persistent post-withdrawal sleep complaints have been shown to predict relapse to alcoholism.”

“These sleep problems among abstinent alcoholics construe a critical issue, as they can remain for up to three years,” added Timothy A. Roehrs, director of research at the Sleep Disorders and Research Center at Henry Ford Hospital, as well as professor of psychiatry and neurobehavioral sciences at Wayne State University School of Medicine in Detroit. “This would be the first study of its kind to show positive effects of acamprosate on sleep disorders.”

The seemingly greater popularity of acamprosate in Europe, noted Staner, is probably due to the fact that the drug was approved by many European countries in the early 1990s, long before naltrexone (another alcoholism-treatment medication). “The drug is very safe to use and there is no cross-tolerance with alcohol,” he said.

Study participants (n=24 males) were recruited through physician referral or a local hospital outpatient department; all were confirmed as alcohol dependent according to the Diagnostic and Statistical Manual of Mental Disorders – Fourth Edition. Beginning eight days before alcohol withdrawal, in order to reach steady levels in patient plasma, and continuing for 15 days following withdrawal, researchers administered either acamprosate (two tablets of 333 mg) or a placebo. Polysomnographic assessments were recorded during acute withdrawal (the first two nights following withdrawal), as well as during post-withdrawal abstinence (the last two nights of the study period).

“Compared to the placebo,” said Staner, “results indicate that acamprosate objectively improves sleep disturbances of alcohol-dependent patients who are trying to stop alcohol intake. This effect was observed during the first withdrawal night and was maintained after two weeks of treatment. On a more mechanistic level, these results appear to implicate glutamate in both sleep disturbances and withdrawal symptoms, and acamprosate appears to be able to decrease the physiological effects of glutamate in the brain.”

Given that this was a very short-term study, Roehrs said he is hopeful that future research will address what the long-term impact of acamprosate may be. He would also like to learn more about helping those individuals for whom acamprosate does not alleviate sleep problems.

Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, “The Effects of Acamprosate on Sleep During Alcohol Withdrawal: A Double-Blind Placebo Controlled Polysomnographic Study in Alcohol-Dependent Subjects,” were: Peter Boeijinga, IsabelleGendre, Muriel Muzet and Rémy Luthringer of FORENAP at Centre Hospitalier de Rouffach, France; Thierry Danel of the Unité de psychopathologie et alcoologie clinique de l’anxiété of Lille, France; and Frédéric Landron of MERCK Santé of Lyon, France. The study was funded by Merck Santé.

Anesthesia Drug Rapidly LIfts Depression, Researchers Say

Anesthesia Drug Rapidly Lifts Depression, Researchers Say

MONDAY, Aug. 7 (HealthDay News) — A single dose of an anesthesia drug produced relief from depression in as little as two hours in a small group of patients for whom several other treatments had failed, U.S. government researchers report.
The researchers said, however, that the drug, ketamine, is unlikely to be used in the treatment of depression because of possible side effects, including psychosis. But the new finding does signal an important direction for future research.
Currently available antidepressants can take weeks to work. “That was similar to the sound barrier. We felt we couldn’t pass it,” said Dr. Carlos A. Zarate Jr., lead author of the study and chief of the mood disorders research unit at the National Institute of Mental Health.

He added, “Now the sound barrier is broken. That doesn’t mean you can get on the plane and take off right away, but it means it’s possible that we can come up with a treatment that works very rapidly. That’s down the road.”
Ketamine is novel not only for the speed of its effect, but also because it targets a new system in the brain.

“It’s novel because all antidepressants that are currently available work on neurotransmitters that are monoamines like dopamine and serotonin. That’s the focus of the current antidepressant armamentarium,” explained Dr. Richard A. Friedman, director of the psychopharmacology clinic at Cornell University’s Medical Center in New York City. “Ketamine involves a particular system of the brain called glutamate. It’s the main excitory neurotransmitter in the brain,” he said.

Depression is a chronic, disabling condition affecting almost 15 million Americans — almost 7 percent of the adult U.S. population — in any given year. Some 4 percent of people with depression will end their own lives, resulting in 30,000 suicides each year.
Unfortunately, about half of people with depression don’t receive treatment and, of those who do get treatment, only about 40 percent get the best, “evidence-based” treatment. Some people still don’t get better even with this type of treatment, however.
This is one of the first studies in humans to look at the effect of ketamine on depression, although previous animal studies had shown promising results.
For the study, which is published in the August issue of the Archives of General Psychiatry, 18 treatment-resistant patients with depression were randomly assigned to receive either one intravenous dose of ketamine or a placebo. Participants had tried an average of six antidepressant medications without success in the past.
Depression improved within one day in 71 percent of participants who received ketamine; 29 percent of those became nearly symptom-free within one day. Thirty-five percent of those receiving ketamine still showed benefits after several weeks. Those in the placebo group showed no improvement.

One week later, participants were given the opposite treatment, unless they were still showing a benefit from the ketamine.
“People had tried six to seven antidepressants on average and had been ill for 30 years. The current episode was three years in duration,” Zarate said. “All people who went through this reported a tremendous relief of suffering.”
Short-term side effects, including perception disturbances, went away usually before the antidepressant effect kicked in. Participants were given a relatively low dose, so they did not experience the more severe side effects.
Ketamine works by blocking the N-methyl-D-aspartic acid (NMDA) receptor, which receives signals for glutamate. Using ketamine to block glutamate’s action on the NMDA receptor also seemed to have a secondary effect on another brain receptor, the AMPA receptor.
Zarate and his team are now looking at several ways to use this information for depressed patients. “We’re looking to see if we can refine ketamine for clinical use by taking care of side effects,” he said. “We’re also looking at other drugs.”

More information

For more on depression, head to the National Institute of Mental Health –

Heroin Addicts Clamor for Scarce Medicine

Heroin Addicts Clamor for Scarce Medicine

The Associated Press
Source: Washington Post
Date: 28 April 2005

WILKES-BARRE, Pa. — Krystal began using heroin when she was 14, and soon hit bottom. But at 18, she says she is drug-free, holds down a job, attends beauty school and cares for her toddler son. She credits a relatively new medication called buprenorphine with freeing her from heroin’s grip.

“Amazing,” “incredible” and “lifesaving” are a few of the words addicts use to describe buprenorphine, a pill that blocks heroin cravings.

The problem, some say, is that Congress has made it hard to get the drug, and health professionals are pressuring the government to expand access.

Available in this country since 2002, buprenorphine is an alternative to methadone, which has been used to treat heroin addiction since the 1960s. Buprenorphine is also used to treat addictions to prescription painkillers like OxyContin, Percocet and Vicodin.

“It has been extraordinarily effective in the patients we have given it to,” said psychiatrist Dr. Herbert Kleber of Columbia University.

Doctors say buprenorphine is longer-acting than methadone, more difficult to overdose on and easier to withdraw from. Addicts say “bupe” gives them a feeling of clearheadedness they do not get with methadone. Also, they can be treated in the privacy of a doctor’s office; methadone, under federal law, is available only at public clinics.

But federal law says individual doctors and medical practices can prescribe buprenorphine to no more than 30 patients at a time _ a provision aimed at preventing “prescription mills,” where drugs are doled out indiscriminately by doctors trying to make a fast buck.

Krystal’s doctor, J. Charles Lentini, said he has a waiting list of 185 addicts _ many of whom are continuing to abuse drugs while they wait.

Even more problematic is the restriction on large medical practices. For example, Kaiser Permanente, the nation’s largest not-for-profit health maintenance organization with 8.2 million members, operates eight medical groups around the country, meaning it can treat only 240 patients at any one time nationwide.

Bills pending in Congress would eliminate the 30-patient restriction for group medical practices while retaining it for individual doctors. The Senate passed similar legislation last year, but it died in the House.

“It clearly was not our intention” that addicts have less access to buprenorphine because they go to a group practice, said Sen. Carl Levin, D-Mich., co-author of the 2000 law that paved the way for doctors to prescribe buprenorphine but also established the 30-patient limit. Levin introduced the bill now pending.

Meanwhile, the U.S. Substance Abuse and Mental Health Services Administration is working on a regulatory fix to expand access to buprenorphine. “The group practice issue we see very much as a critical barrier,” said Robert Lubran, the agency’s director of pharmacologic therapies.

Krystal said she spent eight agonizing months on Lentini’s waiting list before finally getting her buprenorphine prescription last month. She entered detox two or three times while she waited, and returned to heroin each time she was discharged.

“It was torture,” she said. “I just wanted to feel normal again.”

Another of Lentini’s patients, David, used heroin for six years and has been on buprenorphine for 13 months. The 43-year-old day trader, who spent time in prison for accidentally killing a woman with his car while high, said he thanks God that he got the drug when he did.

“If there was a waiting list, I’d be in jail now, because my urine would be hot,” he said.

Both Krystal and David spoke on condition that their last names not be used.

The Office of National Drug Control Policy estimates there are 800,000 heroin addicts in the United States, and about 20 percent of them receive methadone.

The 30-patient limit on buprenorphine is not the only barrier. Fewer than 1 percent of the nation’s doctors _ 4,850 out of 600,000 _ have received Drug Enforcement Administration certification to prescribe buprenorphine, which is manufactured by Reckitt Benckiser and sold under the brand names Suboxone and Subutex.

Kleber said the manufacturer told him last year that only 1,500 doctors had written a buprenorphine prescription. Reckitt Benckiser officials did not return a call.

Many doctors shy away from treating heroin addicts because they believe those patients will be disruptive, Kleber and others said. Also, buprenorphine is expensive, at around $300 to $350 a month, and is not always covered by insurance.

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Moss Rehab Again Named Among “America’s Best Hospitals”

Moss Rehab Again Named Among “America’s Best Hospitals”

Elkins Park, PA, July 7, 2006 – Once again, MossRehab, a member of the Albert Einstein Healthcare Network, has been recognized as one of the nation’s leading rehabilitation facilities in the annual US News & World Report survey of “America’s Best Hospitals.”

“We are honored that MossRehab is consistently recognized as one of the leading rehabilitation facilities in the country,” said Ruth Lefton, Chief Operating Officer, MossRehab. “This recognition clearly reflects the ongoing commitment of our entire staff to providing the highest level of quality patient care and services.”

MossRehab offers a wide range of specialized services, including comprehensive programs for brain and spinal cord injury, stroke, amputation and orthopaedic conditions. In addition, MossRehab is one of only a few rehabilitation hospitals in the nation to be designated by the National Institute on Disability and Rehabilitation Research as a Model System of Care for traumatic brain injury.

Rehabilitation medicine was one of five out of the 16 medical specialties ranked whose outcome was based solely on reputation. The survey, conducted over a three-year period by RTI International in Triangle Park, N.C., involved a sampling of board-certified physicians randomly selected from the American Medical Association’s database. The physicians were asked to list up to five hospitals they believe to be top in this specialty, without considering cost or location. The reputational score, which corresponds to the hospital’s overall USNews ranking, represents the percentages of responding doctors who named that hospital.

Complete survey information will be published in the July 17, 2006 edition of US News & World Report, which hits newsstands on July 10, or visit

MossRehab has two main facilities – MossRehab at Elkins Park at 60 East Township Line Road in Elkins Park, PA, and MossRehab at 1200 West Tabor Road in Philadelphia. It also operates inpatient units, outpatient sites and various community programs in Pennsylvania, New Jersey and Delaware. For more information about MossRehab’s programs and services, call 1-800-CALL MOSS or visit

Heroin Gene Identified and Blocked

Heroin addiction gene identified and blocked

* 15:00 31 May 2005
* news service
* Jennifer Viegas

Scientists have not only identified a critical gene involved in heroin addiction relapse, but they have also successfully blocked it, eliminating cravings for the drug.

The study was conducted on heroin-addicted rats. But the researchers now think that, within a few years, better treatments will become available to human heroin users who cannot quit due to insidious cycles of relapse.

“Many people try to stop taking heroin, but in a few months almost all of them go back to using the drug,” said Ivan Diamond, at the Ernest Gallo Clinic and Research Center in California, US, and one of the research team.

David Shurtleff, director of the Division of Basic Neuroscience and Behavioral Research at the National Institute on Drug Abuse in Maryland, US, is encouraged by the research. “It will take creativity and additional research to translate this into usable therapies, but it does provide hope that we will be able to prevent compulsive drug seeking behaviour,” he told New Scientist.

Reward circuitry

Previous research has indicated that a section of the midbrain called the nucleus accumbens plays a central role in the “mental reward circuitry” of animals, such as rats and humans. This circuitry generates feelings of pleasure in response to drugs, as well as in response to other things, including food, sex and, in humans, work accomplishments.

Drugs like heroin, however, seem to over-stimulate the normal reward process to the point where users value their next fix more highly than food, water and other essentials. In 2004, a study revealed that cocaine causes a gene in the nucleus accumbens, called AGS3, to rapidly encode masses of proteins that are involved in the cravings and pleasure associated with the drug.

Diamond and his team isolated AGS3 genes and proteins in nucleus accumbens cells taken from newborn baby rats. After cloning and studying the cells in the lab, the researchers determined that AGS3’s drug-related functions are most active in the inner nucleus accumbens core as opposed to its outer shell region.

An AGS3 blocker was then created from a herpes virus. This temporarily binds to proteins within the reward circuit and blocks the cravings-pleasure cycle until the virus “washes out” of the body a few weeks later.

Eliminated desires

Heroin-addicted rats that were trained to give themselves the drug using a lever were injected with the AGS3 blocker into their nucleus accumbens after they had gone through a short period of withdrawal. A small dose of heroin then was administered to each rat.

Normally even such a tiny “taste” of the drug leads to cravings for more, but the blocker prevented the addiction relapse by eliminating these desires. The treatment produced no other observed behavioural side effects.

Diamond told New Scientist that a related treatment could become available to humans within the next couple of years. His colleague Krista McFarland, at the Medical University of South Carolina, added that one of the challenges will be to find a safe method of administering the blocker to people.

Journal reference: Proceedings of the National Academy of Sciences (DOI: 10.1073/pnas.0503419102)

Useful New Addiction Treatment News

Useful New Addiction Treatment News

All major classes of drugs of abuse in our society, including opioids (fentanyl, hydrocodone, and Oxycontin) and cocaine, exert their addictive properties through the mesolimbic dopamine system in the brain where the receptors for these chemicals reside.  It has been assumed that pharmacologic treatments for cocaine or heroin abuse would have to be somehow different.  Despite acting on the same area of the brain, different drugs bond to different receptors within this system, even though the concurrent abuse of both drugs is common.

A new synthetic opioid medication originally developed as a pain reliever has shown great promise for the treatment of “polydrug” abuse involving both cocaine and opioids. This drug, called buprenorphine, is unusual in that it both activates opiate receptors in the brain and then blocks them from further binding with other opiates. Thus, like most opioids, it effectively relieves pain but the risk for overdose is minimal.

Clinical studies found buprenorphine to be effective as a treatment for heroin addiction and to have some advantages over methadone in terms of safety. However, researchers were surprised to discover that buprenorphine was also found to reduce cocaine abuse in individuals who are dependent on both heroin and cocaine. Finding these dual effects by buprenorphine provides new insights into the mechanisms of cocaine and heroin dependence and suggests that these mechanisms may be more closely related than was previously thought.

The Harvard Mahoney Neuroscience Institute Letter “On The Brain” Snapshot

More info on buprenorphine (Subutex, suboxone tablets)