Helping a loved one through rehab isn’t easy. Here are some guidelines to follow:
Oxycontin is another type of opiate, says WebMD. Need to assist your loved in looking for an oxycontin rehab treatment in California? Look the right program, doctor and Sacramento detox centers for starters. Then take the time and effort to review the programs. Which one seems a better fit for your loved one? Which one offers a great aftercare program? These choices can help ensure a successful recovery in the future.
Discuss the options
Make them part of the decision-making process if possible. Discuss options. Withdrawal is brutal and can be one of the hardest things your loved one will face. Allowing them to be a part of the decision-making process can help them prepare for what’s coming.
Know what your loved one is going through. If you don’t understand the hold or effects of drugs on the human psyche, behavior and body, there’s no better time to learn than now. The more you know, the better you will understand what your loved one is going through. The more you understand, the easier it will be for you to offer your support and love.
Your support can make a huge difference. Family support has a positive impact on an addict’s recovery and can convince one to finally get help. That’s why you should look for an oxycontin rehab treatment in Florida that allows friends and family to participate in some of the sessions. Being a part of your loved one’s care plan can help not just your loved one but the entire family heal as well. That’s because when drug problems happen, these don’t just involve the individual. It can involve the well-being of the whole family.
It’s easy to pass judgment and believe withdrawal and recovery are easy. But they’re not. Drugs change the way the human brain works. That’s why will power isn’t enough if your loved one wants to recover and live a life free of drugs. It’s best to leave your biases and judgments behind if you want to genuinely connect with and help a friend or family member who’s suffering from opiate abuse.
Relapse and failure can happen. But recovery is always possible. With these tips, you hopefully will know enough to provide your loved one with the help he needs. For assistance and help, call us.
Suboxone, medically known as Buprenorphine, is used to help ease symptoms of opiate addiction. However, by itself, it can be used to provide pain relief for chronic pain. Since it helps patients who suffer from opiate addiction, those who use the drug can inevitably find themselves addicted to the substance. This is where the help and assistance of a suboxone withdrawal facility in Florida will prove helpful.
Factors that affect withdrawal
Once a person has decided to undertake withdrawal and recovery, there are several things that must be considered. If the person is still using suboxone to deal with his opiate addiction, then the withdrawal process will not work, the Mental Health Daily cautions. That’s because the person will still need to be exposed to the drug to counter his opiate addiction, rendering any move toward withdrawal useless. Withdrawal symptoms depend on the length of time the person has been addicted to the drug. Also, before deciding to go through with this process, one must be prepared to go through the withdrawal symptoms.
How long does it last?
The more far along the addiction and drug dependency is, the longer the withdrawal will take. Drugs change the composition of the body. Those who have taken it for months will typically find it easy to come off the addiction, compared to those who have been taking the drug for years. Those who come out of their opiate addiction using the substance also find it difficult to come off Suboxone.
Does physiology matter?
Withdrawal symptoms differ from one person to another. Some might find themselves dealing with slews of painful symptoms while others might only experience mild ones. Your physiology and nervous system will influence the length of the withdrawal process. For instance, someone who’s fit and healthy will have a less difficult time with the withdrawal than someone who’s unhealthy, depressed or stressed.
Can you stop taking it immediately?
It is unsafe for anyone to stop taking the drug without first consulting with their doctors. The wisest course of action is to get in touch with a suboxone withdrawal facility in Florida to help one through the withdrawal process. Medical supervision and monitoring will help alleviate the symptoms and keep the body safe from succumbing to the more severe forms of symptoms that might occur, such as heart attacks or seizures.
By getting professional help, users are well able to get a better chance at recovery and a drug-free life.
Withdrawal is caused by the separation of oneself from something else. In this case; withdrawal refers to the discontinuation using of mind-altering substances such as prescription medications, recreational drugs or alcohol.
Withdrawal symptoms can occur after prolonged usage of a substance suddenly stops. Symptoms of withdrawal vary and depend on the substance used, quantity and length of time used. Typically withdrawals make the person feel worse continuously until they reach a plateau where the symptoms eventually begin to dissipate. In some extreme cases withdrawals can be fatal; for example withdrawals from benzodiazepines or alcohol.
Withdrawal occurs as a result of the building of a tolerance to given substance which in turn builds a physical dependency. Drugs are often abused for the effect they have on the brain. Drugs bind to different parts of the brain and cause different effects on the user. One of the main effects all frequently abused drugs have in common is the effect they have on dopamine. Dopamine is the neurotransmitter responsible for the sensation of pleasure. Drugs will often boost dopamine levels in the brain and so cause pleasure from use. Continuous use of drugs however can lead to withdrawal when the user suddenly stops ingesting the drug.
Dopamine levels will diminish from continuous use of drugs, causing the users ‘level of normality’ being significantly lowered as pleasure cannot be as easily felt; this is one of the factors that cause withdrawal symptoms. When someone stops using drugs or alcohol, the euphoria felt by the drugs, will cause Dysphoria. The main general symptoms of Dysphoria include depression, anxiety and cravings.
An individual withdrawing from a medication for conditions such as epilepsy or heart conditions may endure more severe or life-threatening symptoms. If attempting to quit any medications one should consult their doctor before detoxification. Sometimes substances will mask hunger, sleeplessness, pain or disease. When one goes into withdrawals these will be felt also; this can be dangerous individuals should be aware that some substances can lead to serious malnutrition, worsen illnesses or can cause physical and mental damage.
Withdrawal symptoms very depending on the type of substance the person is withdrawing from. Below is a list of withdrawal symptoms for the most commonly used substances in alphabetical order.
Alcohol Withdrawal Symptoms Include:
- Headache including pulsating sensation in the temple area
- Sweating, especially palms of the hands or the face
- Loss of appetite
- Rapid heart rate
- Enlarged, dilated pupils
- Pale skin
- Abnormal muscle movements or “twitching”
- Involuntary eyelid movements
- Delirium tremens
- Convulsions and seizures
Benzodiazepine Withdrawal Symptoms Include:
- Panic attacks
- Delirium tremens
- Uncontrollable violence and manic episodes
Caffeine Withdrawal Symptoms Include:
- Muscle pain or stiffness
- Loss of concentration
Cocaine/Crack Withdrawals Include:
- Agitation and restless behavior
- Mood Swings
- Variable energy
- Poor concentration
- Low enthusiasm and lethargy
- Vivid and unpleasant dreams
- Increased appetite
- Nausea and vomiting
- Suicidal thoughts
- Strong cravings
Ecstasy or MDMA Withdrawal Symptoms Include:
- Panic attacks
- Loss of reality
- Paranoid delusions
Marijuana Withdrawal Symptoms Include:
- Sleep disruption
- Mood swings
- Appetite changes
- Sex drive fluctuation
- Night sweats
- Weight loss or gain
- Shaking and dizziness
Methamphetamine or Amphetamine Withdrawal Symptoms Include:
- Amphetamine Psychosis
- Increased appetite
- Disruptive sleep patterns
- Panic attacks
Nicotine Withdrawal Symptoms Include:
- Increased appetite
- Intense headaches
- Impaired concentration
- Disturbed sleep or drowsiness
Opiate Symptoms include:
- Aches and pains
- Mood changes (depressed, anxious, irritable)
- Excessive bodily fluids (tears, sweat, runny nose)
- Stomach pain caused by spasms in the digestive system
- Nausea and vomiting
- Sleep problems
- Appetite changes (increased or decreased)
Tranquilizer Withdrawal Symptoms Include:
- Sleeping difficulties
- Impaired memory
- Aches and pains
- Distortions of reality
- Hypersensitivity to light, sound, and touch
Some withdrawal symptoms from drugs will be severe but easily managed without medical care. Others can cause some serious health risks to the user and require medical attention throughout the withdrawal process. Quitting drugs such as nicotine are ones that can be done ‘cold turkey’ without any serious risk to health. Other substances such as benzodiazepines and alcohol can require medical assistance for potentially fatal withdrawals. Severity of withdrawal is normally factored on the drug itself and how dependent the individual has become.
Withdrawals from prescription medications should be closely monitored by the user’s doctor or at least be done under the advice and instruction from a physician. This is not necessarily only due to the withdrawals themselves; medications which are needed for disorders such as schizophrenia and psychosis can be dangerous to withdraw from due to the disorder itself. Always consult the prescribing doctor prior to quitting a prescription medication.
NEW YORK, NY – March 22, 2017 /Press Release/ ––
Heroin use is associated with excessive histone acetylation, an epigenetic process that regulates gene expression, and more years of drug use correlate with higher levels of hyperacetylation, according to research conducted at The Icahn School of Medicine at Mount Sinai and published April 1 in the journal Biological Psychiatry. The study provides the first direct evidence of opiate-related epigenetic alterations in the human brain, indicating that the drug alters accessibility to portions of DNA to be either open or closed, thereby controlling whether genes implicated in addiction are switched on or off.
The Mount Sinai study focuses on epigenetics, the study of changes in the action of human genes caused, not by changes in DNA code we inherit from our parents, but instead by molecules that regulate when, where, and to what degree our genetic material is turned on and off. Histone acetylation of DNA-linked proteins is an essential process for gene regulation by which an acetyl functional group is transferred from one molecule to another, thereby activating gene expression.
To uncover the molecular underpinnings of heroin addiction, the Mount Sinai study team focused on the striatum, a brain region implicated in drug addiction because of its central role in habit formation and goal-directed behavior. Studying postmortem human tissue from 48 heroin users and 37 controls, they found acetylation changes at genes that regulate the function of glutamate, a neurotransmitter that regulates the drug reward system and controls drug-seeking behavior. Specifically, changes were identified at the glutamate receptor gene GRIA1, which has previously been implicated in drug use.
“We hypothesized that the epigenetic impairments uncovered in our study reflect changes that would increase accessibility to DNA that is required to enhance gene transcription that subsequently plays an important role in addiction behavior,” says Yasmin Hurd, PhD, Professor of Psychiatry and Neuroscience at the Icahn School of Medicine at Mount Sinai and Director of The Center for Addictive Disorders at the Mount Sinai Behavioral Health System, who led the study. “Because epigenetic impairments are physical alterations to the DNA that do not change the sequence of a gene, they have the potential to be reversed, so our next step was to address this possibility.”
Using a rat model of heroin addiction, researchers allowed rats to self-administer heroin and observed the same hyperacetylation alterations that were found in the postmortem human brains. The study team then treated the heroin-addicted rats with JQ1, a compound originally developed against cancer pathology, which inhibits the readout of acetylated epigenetic proteins thereby reducing accessibility to the DNA that was previously induced by heroin. The drug reduced heroin self-administration among study rats. Importantly, JQ1 also reduced drug-seeking behavior after abstinence from heroin, suggesting it might be beneficial for long-term heroin users.
“Our findings suggest that JQ1 and similar compounds might be promising therapeutic tools for heroin use disorder,” says Dr. Hurd. “Furthermore, the animal model we created that displayed analogous epigenetic impairments related to heroin use will be useful for future studies looking to identify addiction-related changes that translate to the human brain.”
Researchers from Semmelweis University in Budapest, Hungary, contributed to this study.
About the Mount Sinai Health System
The Mount Sinai Health System is an integrated health system committed to providing distinguished care, conducting transformative research, and advancing biomedical education. Structured around seven hospital campuses and a single medical school, the Health System has an extensive ambulatory network and a range of inpatient and outpatient services—from community-based facilities to tertiary and quaternary care.
The System includes approximately 7,100 primary and specialty care physicians; 12 joint-venture ambulatory surgery centers; more than 140 ambulatory practices throughout the five boroughs of New York City, Westchester, Long Island, and Florida; and 31 affiliated community health centers. Physicians are affiliated with the renowned Icahn School of Medicine at Mount Sinai, which is ranked among the highest in the nation in National Institutes of Health funding per investigator. The Mount Sinai Hospital is in the “Honor Roll” of best hospitals in America, ranked No. 15 nationally in the 2016-2017 “Best Hospitals” issue of U.S. News & World Report. The Mount Sinai Hospital is also ranked as one of the nation’s top 20 hospitals in Geriatrics, Gastroenterology/GI Surgery, Cardiology/Heart Surgery, Diabetes/Endocrinology, Nephrology, Neurology/Neurosurgery, and Ear, Nose & Throat, and is in the top 50 in four other specialties. New York Eye and Ear Infirmary of Mount Sinai is ranked No. 10 nationally for Ophthalmology, while Mount Sinai Beth Israel, Mount Sinai St. Luke’s, and Mount Sinai West are ranked regionally. Mount Sinai’s Kravis Children’s Hospital is ranked in seven out of ten pediatric specialties by U.S. News & World Report in “Best Children’s Hospitals.”
For more information, visit http://www.mountsinai.org or find Mount Sinai on Facebook, Twitter and YouTube.
Source: The Mount Sinai Hospital
In a randomized controlled trial conducted by researchers at the New York State Psychiatric Institute and Columbia University College of Physicians and Surgeons, an 8-day detoxification process using low-dose oral naltrexone showed superior efficacy to the standard 15-day approach that uses an agonist taper leading to induction with extended-release naltrexone (XR-naltrexone).1
Results from a 2014 survey found that the monthly prevalence of nonmedical prescription opioid and heroin use in the United States was 4.3 million and 435,000, respectively.2 Such estimates, along with the rising rates of opioid overdose and related deaths, highlight the urgent need for effective approaches to detoxification and help for chronic relapse prevention. There are Medicare addiction treatment programs out there for people who need the help. Although the US Food and Drug Administration (FDA) has approved XR-naltrexone in injectable form for this purpose, its success is limited by the 7- to 10-day waiting period during which individuals must abstain from opioids prior to receiving the medication.
“An 8-day detoxification process using low-dose oral naltrexone showed superior efficacy to the standard 15-day approach.“
“This waiting period, combined with conventional methods of opioid detoxification employing agonist tapers over several days, represents a delay of 2 weeks or more before XR-naltrexone can be administered,” wrote the investigators in the present study, which was supported by grants from the National Institute on Drug Abuse (NIDA). Such a long delay is unrealistic in outpatient settings, however, in which greater numbers of patients are seeking treatment as inpatient detoxification beds become increasingly scarce, and the tapered approach has been linked with high relapse and attrition rates.3
While earlier findings suggest that accelerated detoxification methods using buprenorphine and low doses of naltrexone to transition to XR-naltrexone may be effective in outpatient settings, no previous trials have compared such methods with the traditional approach.4 To that end, the current researchers compared 2 treatment methods in 150 individuals seeking outpatient treatment for prescription opioid or heroin dependence.
The rapid treatment included a single day of buprenorphine followed by low doses of naltrexone and adjuvant medications such as clonidine on days 2 to 7, and the standard treatment consisted of a 7-day buprenorphine taper followed by a 7-day waiting period. On day 8 in the first group and day 15 in the second group, patients were administered the initial dose of XR-naltrexone, and all participants who remained in treatment at week 5 received a second dose.
The results demonstrated that rates of XR-naltrexone induction were 56.1% in the rapid naltrexone-assisted group, compared with 32.7% in the buprenorphine-assisted group. In addition, the naltrexone-assisted group was more likely to receive the second dose vs the buprenorphine-assisted group (50% vs 26.9%). Although withdrawal severity and dropout rates were similar between the 2 groups during the first 7 days of treatment, 29% of patients in the standard treatment group relapsed during the 7-day waiting period and thus did not receive XR-naltrexone.
These findings “support the feasibility of ascending low doses of oral naltrexone, in combination with an initial dose of buprenorphine and standing non-opioid ancillary medications, as an outpatient regimen for opioid,” the researchers concluded. “By circumventing the need for a protracted period of abstinence and mitigating the severity of withdrawal symptoms experienced during detoxiﬁcation, this strategy has the potential to considerably increase patient acceptability of, and access to, antagonist therapy.”
Source: Psychiatry Advisor
- Sullivan M, Bisaga A, Pavlicova M, et al. Long-acting injectable naltrexone induction: a randomized trial of outpatient opioid detoxification with naltrexone versus buprenorphine [published online January 10, 2017]. Am J Psychiatry. appiajp201616050548. doi: 10.1176/appi.ajp.2016
- Center for Behavioral Health Statistics and Quality. Behavioral health trends in the United States: results from the 2014 National Survey on Drug Use and Health. https://www.samhsa.gov/data/sites/default/files/NSDUH-DetTabs2014/NSDUH-DetTabs2014.htm. Accessed February 1, 2017.
- Day E, Ison J, Strang J. Inpatient versus other settings for detoxification for opioid dependence. Cochrane Database Syst Rev. 2005;(2):CD004580.
- Mannelli P, Wu LT, Peindl KS, Swartz MS, Woody GE. Extended release naltrexone injection is performed in the majority of opioid dependent patients receiving outpatient induction: a very low dose naltrexone and buprenorphine open label trial. Drug Alcohol Depend. 2014; 138:83-88. doi: 10.1016/j.drugalcdep.2014.02.002
END ARTICLE CONTENT
Rajendra D. Badgaiyan1,2*, Sampada Sinha1 and Kenneth Blum3
1Laboratory of Molecular and Functional Imaging, Department of Psychiatry, University of Minnesota, Minneapolis MN 55414, USA
2Laboratory of Advanced Radiochemistry, University of Minnesota, Minneapolis MN 55414, USA
3Department of Psychiatry, McKnight Brain Institute, University of Florida Gainesville, FL, USA
It is unclear whether pharmacotherapy for opioid use disorder (OUD) should be continued for short or long-term. Before introduction of buprenorphine, methadone was the primary pharmacotherapy for OUD in the United States. Because of its specific pharmacokinetic properties methadone was recommended for long-term use with some justification. Introduction of buprenorphine however has altered the treatment protocol because of milder adverse effects and withdrawal symptoms. The adverse effects of buprenorphine are milder but not negligible. Therefore, indefinite prescription is justified only if there is a significant benefit. Studies that have compared short and long-term treatment of buprenorphine protocols do not show a significant benefit of long-term treatment over relatively short-term (few months) treatment protocols. Obviously, the ultra short-term treatment lasting a few days has very little or no benefit on long-term treatment of buprenorphine protocols that use buprenorphine for 3 to 9 months is comparable to that of the long-term (years to lifetime) treatment without financial and medical consequences of the long-term treatment.
Pharmacotherapy, Opioid Use Disorder (OUD), Buprenorphine/naloxone, Mood changes
After introduction of buprenorphine and buprenorphine/naloxone combination (BUP) in the US in 2002, pharmacological treatment of opioid use disorder (OUD) has become more popular and easily accessible because it can be dispensed/prescribed in the office and individuals have to visit the clinic only once in several weeks. This is a departure from methadone treatment protocol, which requires patients to report to the clinic on a daily basis. Relatively low incidence of adverse effects and ease of prescription has made a significant difference in the way OUD is treated pharmacologically.
This change has prompted debate on appropriate treatment protocol. Because of limited data and clinical experience, determination of the dose and length of treatment with BUP remains unclear. Gustin et al.  recommend indefinite continuation of treatment. They argue that the chronic disease model of addiction proposed by American Society of Addiction Medicine  suggests that the addiction treatment should be continued for the rest of life, as is the case with the most chronic diseases like diabetes mellitus and hypertension. This is in contrast to the suggestions made by other investigators who favor short-term treatment to avoid adverse consequences associated with long-term BUP use . We favor this approach and discuss some of its advantages over the long-term protocols and why we think it is not appropriate to continue pharmacological treatment for OUD indefinitely.
Methadone was introduced in the US for OUD treatment in 1947. Because of long exposure and experience, there are a number of well-designed studies that have established dosing and duration of treatment with methadone. The data on BUP is not that extensive and because it can be prescribed by only a small number of physicians (8777 in the United States as of 2008), there is limited experience. Because of this limitation most prescribers use their own experience to guide treatment protocol and duration. This has led to controversy concerning the length of treatment. Initial thought was to follow the methadone model, which requires continuation of treatment for several years. The United States Federal Guidelines for Opioid Treatment compiled by the Substance Abuse and Mental Health Services Administration recommends lifelong treatment with methadone .
Long-term treatment with methadone is justified on several counts: being an agonist of μ receptor it activates these receptors to full extent depending on the dose and develops tolerance and physical dependence. As a result, its withdrawal or dose reduction result in serious withdrawal symptoms and craving leading to relapse. It also has relatively short half-life of 14.3 hrs . Since substances with shorter half-life have greater addictive potential , methadone works as a kind of substituted drug of addiction. Moreover, most methadone programs do not require patients to go for psychotherapy/counseling. It makes the treatment a substitution therapy that needs to be continued for several years if not lifelong.
Treatment of opioid addiction with BUP however is a different story. Since it is a partial agonist of μ receptors. It does not fully activate these receptors and therefore has milder withdrawal symptoms  but still very significant. It is significantly milder and sets in slower than that of the methadone partly due to slow dissociation from receptor sites [8, 9]. Because of the slow dissociation it has longer halflife of 27.72 hrs as compared to methadone . Because of these differences treatment strategies that are effective for methadone cannot be applied to BUP.
Most independent clinics prefer the methadone model and prescribe BUP for several years without a break. The expert consensus panel convened by the US Department of Health and Human Services however recommended BUP treatment for one week, followed by a taper for two weeks . It recommended long-term treatment for patients who are unable to maintain to stay clean. Since publication of this clinical guideline, several trials were conducted to examine relapse rates after a short or long term treatment. In a large study 990 patients were randomly assigned a protocol in which they received BUP either for 7 or 28 days . Three months after termination of the treatment, there was no significant difference in the rate of relapse in the group that received BUP for 7 or 28 days. The two groups had similar levels of withdrawal symptoms and craving. The relapse rate however was high in both groups. Only 12.16% of the 7-day group and 13.41% of the 28-day group were opioid free three months after the treatment. While the result is disappointing, the authors concluded that the duration of treatment does not significantly affect the outcome and treatment success does not depend on the duration of treatment.
When we examine the results of this study with the other similar studies, we did find that relatively longer duration allows more patients to stay opioid-free after cessation of treatment [11–13]. For example, if patients receive BUP for 12 weeks instead of 4 weeks more than 60% patients remain drug-free after a year of treatment termination . This is encouraging data because no intervention, even BUP maintenance for life achieve 100% opioid-free outcome. Even patients on longterm treatment and on BUP maintenance treatment achieve mean abstinence of only 5.2 weeks as compared to 2.7 weeks achieved by graduates of a short-term program.
Thus no protocol at this time can make all patients opioidfree but most of them are able to stay that way following a 12- week BUP treatment . A certain number of patients will not stop abusing opioid no matter what treatment strategy is employed. Therefore, we have to accept a certain degree of treatment failure. The correct approach therefore is to strike a balance between treatment outcome and adverse effect of long-term BUP use.
A reasonable approach to strike this balance is to increase the duration of treatment to include even more patients. So, if after 7 days’ treatment 12.16% patients stay drug free and the number increases to 13.41 after 28-day and 60% after 12 weeks’ treatment, the duration can be increased to a few more weeks to include 90% of patients. In our clinic when we tapered BUP over 6-9 months period, over 90% of patients were opioid-free after a year of treatment termination (manuscript in preparation). Achieving over 90% success following 6-9 months’ treatment is the best outcome we should hope for. However, we have not accessed the possibility of transfer addiction.
These studies make it clear that there are individual differences in the ability of individuals to respond to pharmacotherapy. A number of variables are known to affect the recovery and ultimately treatment success . In this context we agree with Gustin et al.  that the treatment protocol should be individualized but the variables that affect the outcome are difficult to quantify. It is difficult to precisely predict the length of treatment a particular individual would need. It is therefore best to use a treatment protocol that would make a vast majority of patients opioid-free (for example 90% patients in 6-9 month treatment protocol). For the patients that do not respond to this protocol, the treatment can be continue for another few months. Of course there will be few patients that will never respond. Because a few patients will not respond to any length of treatment does not justify recommending long-term (lifelong) treatment protocol for all patients as suggested by Gustin et al. .
Thus, a regimented relatively short-term treatment protocol not only will treat a vast majority of patients at a relatively lower cost but will also avoid long-term consequences of BUP use. In the short term BUP has relatively low adverse effects, consequences of its long-term use are still largely unknown because of a short clinical history. But there is very high probability of it making long-term alterations in the receptor activity. In laboratory animals BUP is known to down regulate or upregulate a variety of receptors . It downregulates μ receptors in several brain areas (frontal cortex, parietal cortex, thalamus, hippocampus, striatum, brain stem) and upregulate κ1 receptors in the striatum and in the frontal, parietal, and occipital cortex. It is not yet known whether long-term use of BUP will have the same adverse effects that are associated with long-term use of opioids. Since it is a partial opioid agonist it is likely to have at least some of those adverse effects. These effects include lower immunity, hyperalgesia, prolonged QTc interval, respiratory depression and reduced levels of a number of hormones . There are a number of reports of serious withdrawal symptoms in individuals using BUP [18, 19]. Additionally, long-term users of BUP (average 1.6 years) have difficulty experiencing pleasure and other emotions . They discount happiness and tend to be unaware of the feeling of sadness and anxiety. Long term use therefore takes away normal pleasures of life and leads to reward deficiency syndrome . Additionally since BUP inhibits the CYP2D6 and CYP3A4 enzyme systems , it interacts significantly with a number of medications. This is a potential problem for an individual who is on a lifelong BUP treatment. The most important problem is the possible anti dopaminergic effect of chronic administration leading to increased relapse potential . Long-term treatment could therefore be counterproductive.
Thus, does it make sense to expose all OUD individuals to significant medical and financial stress of lifelong treatment because a small number of individuals would not respond to short-term therapy? We think that the stress of long term therapy should be restricted only to a small subset of individuals who are resistant to short-term treatment. For some of these individuals pharmacotherapy or other forms of dopamine agonistic therapy [23, 24] may be effective for some but not all, while others may benefit from psychological and social interventions, which should be used to maximize benefits of the short-term treatment. We can achieve better outcome with this approach without adverse consequences of long-term use.
The authors thank the expert editorial assistance of Margaret A Madigan.
This work was supported by the National Institutes of Health grants 1R01NS073884 and 1R21MH073624, and the VA Merit Review Awards CX000479 and CX000780 awarded to RDB.
Conflict of Interest
Dr. Blum is a member of the scientific advisory board of Dominion Diagnostics, LLC and a member of the Board of Directors of RDSolutions Inc. He also serves as Chief Scientific Advisor to Dominion Diagnostics, LLC and is currently the Chief Scientific Officer of RDSolutions, Inc. and Victory Nutrition International, LLC. There are no other conflicts of interest to report.
All the authors contributed equally.
1. Gustin R, Nichols J, Martin PR. 2015. Individualizing opiate use disorder (OUD) Treatment: Time to fully embrace a chronic disease model. J Reward Defic Syndr 1(1): 10-15.
2. American Society of Addiciotn medicine. 2011. Definition of Addiction.
3. Ling W, Hillhouse M, Domier C, Doraimani G, Hunter J, et al. 2009. Buprenorphine tapering schedule and illicit opioid use. Addiction 104(2): 256-265. doi: 10.1111/j.1360-0443.2008.02455.x
4. Substance Abuse and Mental Health Services Administration. 2013. Federal Guidelines for Opioid Treatment 2013.
5. Verebely K, Volavka J, Mule S, Resnick R.1975. Methadone in man: pharmacokinetic and excretion studies in acute and chronic treatment. Clin Pharmacol Ther 18(2): 180-190.
6. Volkow ND, Swanson JM. 2003. Variables that affect the clinical use and abuse of methylphenidate in the treatment of ADHD. Am J Psychiatry 160(11): 1909-1918. doi: 10.1176/appi.ajp.160.11.1909
7. Eissenberg T, Greenwald MK, Johnson RE, Liebson IA, Bigelow GE, et al. 1996. Buprenorphine’s physical dependence potential: antagonist precipitated withdrawal in humans. J Pharmacol Exp Ther 276(2): 449-459.
8. Eissenberg T, Johnson RE, Bigelow GE, Walsh SL, Liebson IA, et al. 1997. Controlled opioid withdrawal evaluation during 72 h dose omission in buprenorphine-maintained patients. 45(1-2): 81-91. doi: 10.1016/S0376-8716(97)01347-1
9. Mello NK, Bree MP, Mendelson JH. 1982. Comparison of the effects of buprenorphine and methadone on opiate self-administration in primates. NIDA Res Monogr 41: 67-73.
10. Kuhlman JJ Jr, Lalani S, Magluilo J Jr, Levine B, Darwin WD. 1996. Human pharmacokinetics of intravenous, sublingual, and buccal buprenorphine. J Anal Toxicol 20(6): 369-378.
11. Amass L, Bickel WK, Higgins ST, Hughes JR. 1994. A preliminary investigation of outcome following gradual or rapid buprenorphine detoxification. J Addict Dis 13(3): 33-45. doi: 10.1300/J069v13n03_04
12. Galanter M, Dermatis H, Resnick R, Maslansky R, Neumann E. 2003. Short-term buprenorphine maintenance: treatment outcome. J Addict Dis 22(3): 39-49. doi: 10.1300/J069v22n03_04
13. Katz EC, Schwartz RP, King S, Highfield DA, O’Grady KE, et al. 2009. Brief vs. extended buprenorphine detoxification in a community treatment program: engagement and short-term outcomes. Am J Drug Alcohol Abuse 35(2): 63-67. doi: 10.1080/00952990802585380
14. Woody GE, Poole SA, Subramaniam G, Dugosh K, Bogenschutz M, et al. 2008. Extended vs short-term buprenorphine-naloxone for treatment of opioid-addicted youth: a randomized trial. JAMA 300(17): 2003-2011. doi: 10.1001/jama.2008.574
15. Mintzer IL, Eisenberg M, Terra M, MacVane C, Himmelstein DU, et al. 2007. Treating opioid addiction with buprenorphine-naloxone in community-based primary care settings. Ann Fam Med 5(2): 146-150. doi: 10.1370/afm.665
16. Belcheva MM, Ho MT, Ignatova EG, Jefcoat LB, Barg J, et al. 1996. Buprenorphine differentially alters opioid receptor adaptation in rat brain regions. J Pharmacol Exp Ther 277(3): 1322-1327.
17. Benyamin R, Trescot AM, Datta S, Buenaventura R, Adlaka R, et al. 2008. Opioid complications and side effects. Pain Physician 11: S105-120.
18. Blum K, Oscar-Berman M, Femino J, Waite RL, Benya L, et al. 2013. Withdrawal from Buprenorphine/Naloxone and Maintenance with a Natural Dopaminergic Agonist: A Cautionary Note. J Addict Res Ther 4(2). doi: 10.4172/2155-6105.1000146
19. Makhinson M, Gomez-Makhinson J. 2014. A successful treatment of buprenorphine withdrawal with the dopamine receptor agonist pramipexole. Am J Addict 23(5): 475-477. doi: 10.1111/j.1521-0391.2014.12133.x
20. Hill E, Han D, Dumouchel P, Dehak N, Quatieri T, et al. 2013. Long term Suboxone emotional reactivity as measured by automatic detection in speech. PLoS One 8(7): e69043. doi: 10.1371/journal.pone.0069043
21. Blum K, Oscar-Burman M, Jacobs W, McLaughlin T, Gold M. 2014. Buprenorphine Response as a Function of Neurogenetic Polymorphic Antecedents: Can Dopamine Genes Affect Clinical Outcomes in Reward Deficiency Syndrome (RDS)? J Addict Res Ther 5(3): 1000185. doi: 10.4172/2155-6105.1000185
22. Umehara K, Shimokawa Y, Miyamoto G. 2002. Inhibition of human drug metabolizing cytochrome P450 by buprenorphine. Biol Pharm Bull 25(5): 682-685. doi: 10.1248/bpb.25.682
23. Blum K, Chen TJ, Bailey J, Bowirrat A, Femino J, et al. 2011. Can the chronic administration of the combination of buprenorphine and naloxone block dopaminergic activity causing anti-reward and relapse potential? Mol Neurobiol 44(3): 250-268. doi: 10.1007/s12035-011-8206-0
24. Blum K, Liu Y, Wang W, Wang Y, Zhang Y, et al. 2015. rsfMRI effects of KB220Z™ on neural pathways in reward circuitry of abstinent genotyped heroin addicts. Postgrad Med 127(2): 232-241.