Posts Tagged ‘FAQ’

Suboxone FAQ / Subutex FAQ

Monday, December 21st, 2009
DISCLAIMER: The information detailed in this article is not medical advice, nor written by medical professionals. Before making any medical decisions, it is imperative to confer with a licensed medical professional. If you have comments, suggestions, or find an error, please feel free to leave feedback using the comments section at the bottom of this page.


  1. What is Suboxone/Subutex?
  2. How long do I have to wait before taking Suboxone or Subutex?
  3. How is Suboxone taken?
  4. What are some possible side effects of Suboxone and Subutex?
  5. What is precipitated withdrawal?
  6. What are the different stages of Suboxone treatment?
  7. Which is a better treatment for opioid addiction, Suboxone or methadone?
  8. Can a patient on methadone safely switch to Suboxone?
  9. How do I find a doctor that can prescribe Suboxone?
  10. What is the maximum number of patients a doctor may have at any one time?
  11. Is Suboxone addictive?
  12. How long after stopping Suboxone does one have to wait before narcotic painkillers become effective?
  13. Sources

Terms to Know

  • affinity — the strength with which a drug binds to its receptor
  • intrinsic activity — the degree to which a drug activates its receptors
  • rate of dissociation — measure of disengagement or uncoupling of the drug from the receptor

What is Suboxone/Subutex?

Suboxone®, manufactured by Reckitt Benckiser, is the first opioid substitution treatment available without the hassle involved with going to a methadone clinic everyday or even weekly. The two active ingredients in Suboxone® are buprenorphine hydrochloride, and naloxone hydrochloride dihydrate. Subutex® has only buprenorphine as an active ingredient. Suboxone® and Subutex® are available in the following formulations:

2 mg
0.5 mg
Orange / Hexagonal
8 mg
2 mg
Orange / Hexagonal
2 mg
White / Oval
8 mg
White / Oval

In a study involving 220 patients, 16-32 mg of Suboxone proved to be just as effective as high-dose methadone, and more effective than low dose methadone as treatment for opioid dependency. Typical starting dosages range from 8 mg to 32 mg per day; however, some patients believe that it is better to start as low as 2 mg. Buprenorphine is only a partial agonist at the opioid receptors, thereby lowering abuse potential. While a small amount of euphoria may be experienced in some patients, buprenorphine will never provide the same degree of intensity as a full opioid agonist (e.g. heroin, oxycodone, morphine). Because buprenorphine possess the quality of being a partial agonist, it shows a ceiling effect. This means there is a point at which buprenorphine will not increase in effectiveness, despite taking more.

How long do I have to wait before taking Suboxone or Subutex?

If Suboxone is procured legally through a doctor, the prescribing physician will almost always ask that the patient be in mild-to-moderate withdrawal during induction. For short-acting opioids, like heroin and oxycodone, withdrawal takes anywhere from 24-36 hours to kick in. When switching from a longer-acting opioid like methadone, the situation becomes a bit more complicated. The typical scenario goes something like this: (1) taper down to 30 mg methadone per day, (2) wait three days before being inducted. Transferring from methadone to Suboxone is something that has to be discussed with a doctor because it is very easy to precipiate withdrawal if the transfer is not done correctly.

“Why does the patient have to be in withdrawal when he/she comes in?”

If there are high levels of another opioid in the body, Suboxone will, in a sense, compete with the other opioid molecules, and knock them off the receptors. This occurs because buprenorphine has an extremely high binding affinity for the opioid receptors. If this happens, the patient will be thrown into precipitated withdrawal, which is extremely unpleasant, and can last a significant period of time.

“Wait, the opioid molecules that are being replaced are being replaced with another opioid, buprenorphine, so shouldn’t that still quell withdrawal symptoms?”

Buprenorphine is only a partial opioid agonist, therefore, it has less opioid effects than those of a full agonist (e.g. morphine, heroin, oxycodone). If the patient is already in withdrawal when the first dose is taken, he/she will feel better not worse.

How is Suboxone taken?

Sublingual tablets are absorbed through veins under the tongue. Before taking Suboxone, it is a good idea to drink a little water to moisten the mouth, which helps the tablets dissolve easier, and faster. If the doctor prescribes two tablets, put one on the left side under the tongue, and put the other on the right side under the tongue. If more than two are prescribed, Reckitt Benckiser, the makers of Suboxone, recommends waiting until after the first two dissolve to take the rest. It generally takes about 10 minutes for a tablet to dissolve, though it can range anywhere from 5-20 minutes. Some patients have reported holding the “juices” in their mouth for as long as 45 minutes can increase effectiveness. Try not to talk while taking Suboxone, as this can interfere with how well it is absorbed. It is important that Suboxone be taken correctly for it to work, and if a patient does not follow directions he/she may end up feeling sick. The following is a list of ways NOT to take Suboxone:

  • Never swallow the tablet — the reason Suboxone is prescribed as a sublingual tablet is because barely any buprenorphine is absorbed orally. Swallowing the tablet will render Suboxone ineffective.
  • Never suck on the tablet — for the same reason a patient does not swallow the tablet, the patient does not suck on the tablet.
  • Never snort a tablet — although intranasal buprenorphine may work, this method does not work as well as taking the tablet sublingually. Snorting anything is counter-productive to recovery, and only reinforces bad habits. Also, snorting any pill can cause severe damage to the lungs, which most people forget about.
  • Never shoot a tablet — in opioid-dependent individuals, shooting a tablet can cause precipitated withdrawal. Most doctors do not like prescribing Subutex because of the fear that people will try to inject them. The naloxone is present in Suboxone as a deterrent. Shooting any pharmaceutical not specifically prepared for injection can cause serious complications, including death. Don’t do it.

What are some possible side effects of Suboxone and Subutex?

The most common reported side effects of Subutex and Suboxone are:[2]

  • cold or flu-like symptoms
  • headaches
  • sweating
  • sleeping difficulties
  • nausea
  • mood swings

Those side effects do not sound too inviting, do they? I think these are primarily experienced during the induction period, as the body becomes accustomed to buprenorphine, rather than a full agonist. From what I have seen, most people who have become stabilized on Suboxone report very little to no side effects, and those that do report adverse reactions usually only experience trouble sleeping, sweating, and headaches. Other side effects include respiratory depression (as with all opioids), constipation, anxiety, depression, pain, and dizziness. For a full list of side effects, please refer to the prescribing information [PDF] or package insert.

What is precipitated withdrawal?

Precipitated withdrawal can occur when a person who is physically dependent on opioids is administered an opioid antagonist or a partial agonist. In those not physically dependent on opioids, an antagonist typically produces no effects, while a partial agonist would. Depending on the half-life of the antagonist or partial agonist used, the qualitative effects of precipitated withdrawal, when compared with the experience of a typical withdrawal syndrome, are often shorter lived but with a faster onset. It is quite easy to imagine why an antagonist would cause precipitated withdrawal. The antagonist has a very high binding affinity for the opioid receptors, so it displaces any full agonist opioids already present and blocks any molecules from binding for a given period of time (depending on the half-life of the antagonist). Because antagonists block the effects of opioid receptors instead of activating them, there is a drastic reduction in the previous agonist effect, resulting in agonizing withdrawal.

Partial agonists can cause precipitated withdrawal, but the concept is a little more complicated than that of an antagonist causing precipitated withdrawal. If an individual who is physically dependent upon opioids receives a dose of a partial agonist too soon after his or her last dose of a full opioid agonist, precipiated withdrawal occurs. Buprenorphine has a high binding affinity for the mu-opioid receptor, but because of its partial agonist properties, it has low intrinsic activity at that receptor (less opioid-like effects and ceiling effect). If there are full opioid agonist molecules still attached to the opioid receptors at the time of administration, the buprenorphine will displace the full agonist. Though partial agonists do activate opioid receptors, the overall effect is much less than that of a full agonist. This decrease in agonist effect can cause precipitated withdrawal. For this reason, buprenorphine is typically only given when the person physically dependent on opioids is in full-fledged withdrawal.

What are the different stages of Suboxone treatment?

Suboxone treatment should never be used by itself. It is not a cure, but rather a treatment. When used concurrently with some sort of therapy, the success rate is much higher. Suboxone treatment really beings with a phone call called the pretreatment screening; this consists of a brief interview to qualify the person, and a date may be set for intake and induction. Intake is the gathering of medical records to measure suitability for office-based treatment. If the physician feels it is necessary, he or she may perform a physical exam. At this point, the advantages and disadvantages of treatment are discussed, and any questions the patient has are answered. The next step after intake is induction. The goal of induction is to find a dose of Suboxone at which the patient feels comfortable, and withdrawal is suppressed.[3]

Once the patient becomes accustomed to their daily dose of Suboxone, he/she enters the stage of stabilization. At this point, the patient is not feeling any withdrawal symptoms or side effects, has no uncontrollable cravings for opioids, and is not using any additional opioids. During the maintenance phase, which can last anywhere from a few weeks to a few years, the patient is monitored less often, withdrawal symptoms are prevented, cravings are still suppressed, and the need to self-administer opioids is lowered greatly. The next stage is a medically-supervised withdrawal where the patient is slowly tapered off of Suboxone. Only mild withdrawal is felt if the drug is tapered correctly. Either way, the patient should be prepared to have some symptoms of withdrawal, which may include fatigue, reduced appetite, insomnia, and irritability.[3]

Which is a better treatment for opioid addiction, Suboxone or methadone?

Each person differs in what he/she requires as far as treatment in concerned because varying factors such as body chemistry, size of habit, duration of addiction, finances, etc. To help addicts find the right treatment plan, TPC! has put together a side-by-side comparison of Suboxone and methadone. Remember, Suboxone or methadone by themselves should not be considered complete treatment plans, but instead part of a comprehensive plan which leaves no aspect of opioid addiction untended. A link is provided below:

Suboxone vs. Methadone

Can a patient on methadone safely switch to Suboxone?

It is possible for a patient on methadone to switch to Suboxone; however, the difference between the two drugs may cause the former methadone-treated patient to feel unsatisfied, though there have been many successful cases noted. Methadone, being a full-opioid agonist, is more similar to heroin and oxycodone than buprenorphine. Buprenorphine is a partial-opioid agonist, which means it does not provide the same intense release of painkilling chemicals that full agonists provide. As a full agonist, methadone is also more likely to give a patient euphoria.

Because of methadone’s long half-life, it is required that the patient being inducted into Suboxone treatment be at least 72 hours without methadone. If Suboxone is taken prematurely it could cause precipitated withdrawal, a very unpleasant experience. It is important that the patient also be down to 20-30 mg of methadone before making the switch to buprenorphine. A switch should not be attempted with anyone taking over 30 mg of methadone. It is probable that the patient will experience discomfort during the first 3-5 days while his or her body becomes accustomed to buprenorphine, though it is typically fairly mild.

How do I find a doctor that can prescribe Suboxone?

Not all doctors can prescribe Suboxone because it requires special certification. If a doctor wants to be able to prescribe Suboxone, he/she must (1) send a letter of intent to the Substance Abuse and Mental Health Administration, (2) be qualified, and (3) take a special course to learn about Suboxone. Many patients believe their doctors are largely uneducated on the subject. Although every doctor must meet certain criteria, many doctors do not seem to understand addiction or how Suboxone can be used effectively. The qualifications, as taken from SUBOXONE.COM, are listed below:

According to DATA 2000, licensed physicians (MDs or DOs) are considered qualified to prescribe SUBOXONE, if at least 1 of the following criteria has been met:

  • Holds an addiction psychiatry subspecialty board certification from the American Board of Medical Specialties
  • Holds an addiction medicine certification from the American Society of Addiction Medicine (ASAM)
  • Holds an addiction medicine subspecialty board certification from the American Osteopathic Association (AOA)
  • Completion of not less than 8 hours of authorized training on the treatment or management of opioid-dependent patients
  • Organizations currently authorized to provide training: American Academy of Addiction Psychiatry, American Medical Association, AOA (through the American Osteopathic Academy of Addiction Medicine), American Psychiatric Association, and ASAM
  • Participation as an investigator in 1 or more clinical trials leading to the approval of SUBOXONE
  • Training or other such experience as determined by the physician’s state medical licensing board
  • Training or other such experience as determined by the United States Secretary of Health and Human Services

In addition, physicians must satisfy BOTH of the following criteria:

  • Have the capacity to provide or to refer patients for necessary ancillary services, such as psychosocial therapy
  • Agree to treat no more than 30 patients at any one time in an individual or group practice

Finding the right doctor can be a bit hard sometimes. It is very important that the patient be comfortable, and compatible with the doctor. Some of the doctors listed at the site below will not prescribe Suboxone to anyone, or are part of pain management or a clinic, so it may take some looking before the right one is found. The Buprenorphine Physician and Treatment Program Locator is very easy to use, and has an interactive map of the United States to help anyone looking find a doctor. Also, anyone can put their name on a waiting list if a doctor is at full capacity, so that when a spot frees up, he/she gets an e-mail; however, this is largely unnecessary because the patient limit was recently increased from 30 to 100. It should be fairly easy to find a doctor. Below is a link:

The Buprenorphine Physician and Treatment Program Locator

What is the maximum number of patients a doctor may have at any one time?

In December 2006, DATA 2000 was amended, giving Suboxone-certified doctors the ability to treat up to 100 patients; however, for the first year a doctor can only treat 30 patients at any one time. One year after the original letter of intention to treat patients using buprenorphine was submitted, the physician may submit a second notification of the need and intent to treat up to 100 patients.[4]

Is Suboxone addictive?

Yes. The active ingredient in Suboxone that keeps withdrawal at bay is buprenorphine, a partial opioid agonist. Buprenorphine has an extremely high binding affinity to opioid receptors in the brain, but because it is only a partial agonist, full effects, as produced by full agonists (e.g. oxycodone, heroin), are not present. Many people are grossly misinformed about the addictive nature of buprenorphine, and claim that there is no withdrawal syndrome, which is incorrect; however, because of its long half-life and partial agonist properties, the withdrawal is longer, but milder than that of full agonists. Some people have horror stories of their attempts to get off of Suboxone, but most of them come from people who did not taper properly. The bottom line is Suboxone is addictive, and eventually some withdrawal has to be dealt with. Suboxone will soften the fall, and withdrawal from it is certainly not as bad as withdrawal from oxycodone or heroin.

How long after stopping Suboxone does one have to wait before narcotic painkillers become effective?

Suboxone can block opioids for three days, and for individuals on high doses (>16 mg) it may be longer. An individual taking 24 mg for a few days indicated it took 5-6 days before he felt the full effects of the full agonist, oxycodone. It takes 37 hours for half of the buprenorphine in the body to be eliminated. Because of the long half-life of buprenorphine, the drug builds up in the body each day, which is part of the reason it could take a bit more than a day or two for other opioid anagesics to be effective. In summary, the factors that determine the effectiveness of opioids are dosage, frequency of use, length of time using, and individual body chemistry and metabolism.

After doing a bit of research and talking to drug users who have been in this situation, 72 hours seems to be the general consensus. Some people indicated feeling the effects after just 24-36 hours, and others said they felt a fraction of the full effects. Please understand, after taking Suboxone for a given period of time, tolerance may be significantly lower, so do not overdo it. Also, it is important to remember that even though the effects not be felt after 24 hours, it is very possible to overdose. It is impossible to monitor how the body is handling the mixture of buprenorphine and another opioid when it can barely be felt. Always consult a doctor before switching medications.


[1] Johnson, R.E., et al. A comparison of levomethadyl acetate, buprenorphine, and methadone for opioid dependence. New England Journal of Medicine 343(18):1290-1297, 2000. [Abstract]

[2] Subutex and Suboxone: Questions and Answers. FDA/Center for Drug Evaluation and Research. October 8, 2002. [link]

[3] SUBOXONE Treatment Walk-through. Reckitt Benckiser. 2007. Accessed: April 23, 2007 [link]

[4] Buprenorphine-Frequently Asked Questions. Substance Abuse & Mental Health Services Administration. US Dept. of Health and Human Services. 2007. Accessed: April 25, 2007 [link]

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Addiction FAQ

Friday, December 18th, 2009

What is addiction?

Addiction is typically defined as compulsive, and uncontrolled use of a drug even in the face of negative consequences; however, not all healthcare professionals agree with this interpretation. Traditionally, addiction could only occur when a psychoactive substance was involved, but today, some people have expanded the definition to include other behaviors, such as gambling and sex. In addition, addiction usually involves both physical and psychological dependency.

Physical dependency will eventually occur with repeated use of opiates, and is defined as a state where withdrawal symptoms will appear upon abrupt cessation. After a person becomes physically dependent on opiates, discontinuation causes withdrawal symptoms which may include runny nose, gooseflesh, muscle pain, and diarrhea. Some drugs may cause physical dependency, but not addiction. For example, loperamide (an opiate) was originally categorized as a controlled substance because discontinuation of long-term, high doses induced morphine-like withdrawal symptoms; however, the compulsive and uncontrolled behavioral aspects which characterize addiction were not present.

Psychological dependency is noted when upon cessation psychological withdrawal symptoms, such as cravings, irritability, insomnia, depression, and anxiety, appear. “Rewarding” activities such as gambling, sex, and shopping can induce the same sort of psychological withdrawal symptoms as a drug, and are all thought to be due to the effect on the dopamine, a chemical in the brain thought to cause feelings of pleasure. Psychological dependency may also occur when a drug or activity is used to take the place of a typically undesirable activity, making it a habitual behavior. Others consider it to be an emotional, social, or psychological dysfunction, taking the place of “normal” positive stimuli not otherwise present.

How does habitual drug use produce changes in the brain that may lead to drug addiction?

Key Terms

  • dopamine — a neurotransmitter present in brain regions that regulate movement, emotion, motivation, and the feeling of pleasure.
  • locus ceruleus — a region of the brain that receives and processes sensory signals from all areas of the body; involved in arousal and vigilance.
  • noradrenaline — a neurotransmitter produced in the brain and peripheral nervous system; involved in arousal and regulation of blood pressure, sleep, and mood; also called norepinephrine.
  • nucleus accumbens — a structure in the forebrain that plays an important part in dopamine release and stimulant action; one of the brain’s key pleasure centers.
  • ventral tegmental area — the group of dopamine-containing neurons that make up a key part of the brain reward system; key targets of these neurons include the nucleus accumbens and the prefrontal cortex.

The “Changed Set Point” Model

The “changed set point” model of opioid addiction is based on alterations in the neurobiology of dopamine neurons in the ventral tegmental area and of noradrenaline (also called norepinephrine) neurons of the locus ceruleus during early withdrawal and abstinence. The focal point in this model is that drug abuse changes a biological or physiological setting. One variation of this model is based on the idea that neurons of the mesolimbic reward pathways are naturally “set” to release enough dopamine in the nucleus accumbens to produce a normal level of pleasure. When opioids are introduced into this “stable environment” the natural set point is changed; thus, reducing the release of dopamine during typically pleasurable activities (eating, playing, etc.) when opioids are not present. A change also takes place in the locus ceruleus, but in the opposite direction, such that noradrenaline release is increased during withdrawal. This model accounts for the drug liking (increased dopamine levels, decreased noradrenaline levels) and drug withdrawal (decreased dopamine levels, increased noradrenaline levels) aspects of drug addiction.

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Opiate Abuse FAQ for Parents

Friday, December 18th, 2009


  1. How can I tell if my child is using opiates?
  2. What do opiates and opioids look like?
  3. How can I prevent my child from using drugs?

How can I tell if my child is using opiates?

It is extremely difficult to tell with any certainty if a child is using drugs. The effects of opiates can be subtle at lower doses, and completely obvious at others. It is important to be educated on drug abuse, and, worst case scenario, what to do in a situation where an opiate overdose is suspected. Changes in mood or behavior are not necessarily indicative of drug abuse, but may be related to another life issue.

The following symptoms may be indicative of drug abuse in general , but, whether drugs are involved or not, it is important that the following issues be addressed, especially if they are uncharacteristic of your child:

  • mood swings
  • explosive outbursts
  • changes in eating patterns
  • anti-social behavior (family, friends)
  • reduced concentration
  • impaired memory
  • missing money, credit cards, and/or valuables
  • unexplained need for money
  • school/work performance decline
  • abrupt changes in friends
  • finding pawn slips
  • finding small plastic baggies
  • frequent secret phone calls
  • unexplained time away from home

The following symptoms may be indicative of opioid abuse:

  • pinpoint pupils
  • falling asleep at inappropriate times (ex. at the dinner table)
  • vomiting
  • constipation
  • use of laxatives
  • track marks on arms
  • constant itching/scratching
  • finding spoons with burn marks
  • missing spoons
  • aluminum foil or chewing gum wrappers with burn marks
  • bottles of vinegar or bleach (used to clean needles) and cotton balls

What do opiates and opioids look like?

The physical characteristics of opioids depend completely upon where it is they are coming from. There are three possible places opioids can come from.

  • Commercial preparations — Opioids manufactured by pharmaceutical companies come in a few different forms. Most of the time, opioids from a commercial establishment (though they are probably diverted in this case) will be in pill form; however, they are also produced in patches and liquid forms. Some patches, usually containing fentanyl, contain 72 hours worth of medicine, and often people will cut them into smaller pieces or suck the gel out of them to get high, depending on the brand. This is extremely dangerous as there is no guarantee that the medicine will be proportional throughout the patch. Liquid oral doses of opioids are a bit safer to use than the patches, but are by no means safe when used without a doctor’s supervision and prescription. One example of an orally-consumed, opioid-containing, liquid medicine is OxyFast. Codeine is often seen in liquid form as well. Some liquids are marked for injection only, which should be printed somewhere on the label. Fortunately, if you happen to find a commercially-produced opioid in your child’s room or on his/her person, it is fairly easy to find out exactly what it is. Liquid formulations will have a label (unless it is ripped off), and usually the patches have some sort of brand name printed on the back. All pills are required by the FDA to have a unique imprint, shape, and color unique to that one formulation. To identify a pill, feel free to use the search function in our Pill Identification section.
  • The streetsHeroin is typically found as a white to dark brown powder, or a tar-like substance. If you find a bag of white powder, however, it doesn’t necessarily mean that it is heroin. Other drugs, such as cocaine and ketamine, also come in the form of white powder. If you find a needle with the bag of white powder, again, it doesn’t mean that it is heroin because both of these drugs can be injected as well. Opium is another drug found on the streets. Opium is made from the white liquid in the poppy plant, which contains several strong opiates (morphine, codeine, etc.), and is completely natural, though that doesn’t make it any safer. Opium is a black or brown block of a tar-like substance.
  • Nature — This is relatively unheard of, but some people grow their own poppy plants, which is legal only if used for “ornamental purposes.” Poppy plant pods can be used to make a psychoactive tea, which comes equipped with morphine, codeine, among other opiates, and a bitter taste. Believe it or not, pods are fairly easy to order from Internet vendors, though once the pods are made into a tea the person brewing it is in violation of federal law. Opium can also be made by extracting the white juices from the plant.

How can I prevent my child from using drugs?

No parent will successfully control his or her child without creating unnecessary animosity; however, merely talking with a child about drug abuse is a great start. Warning signs will be next to impossible to see if a parent has no communication with his/her child, so be communicative. Prevention involves paying attention to the child, open communication, and early education. Take these measures, and the chances of noticing or preventing a problem are much greater. If a parent suspects a problem, there are a variety of solutions; however, no one solution is perfect for everybody. Somebody who has smoked pot once or twice last year probably doesn’t need to goto rehab for marijuana!

Do not make any decisions without first seeking consultation with some sort of mental health specialist when it comes to substance abuse treatment. Some children may accept the label of “drug addict” which can ultimately make things harder, when it does not necessarily have to be that way. It is also important to be an active part of the young person’s recovery, informed, and supportive. Ridding oneself of opioid addiction may be the single hardest thing a person ever does, and that’s with no exaggeration.

Coming soon: What to do if your child is using drugs…

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Opiate Drug Testing FAQ

Friday, December 18th, 2009


  1. Urine Analysis
    1. Detection Periods in Urine
  2. Hair Testing
  3. Drug Cutoff Concentrations
  4. Substances and conditions which can cause a false positive
  5. Buy Opiate Drug Testing Kit

Urine Analysis

The standard “NIDA 5″ drug test includes testing for cannabinoids, cocaine, amphetamines, phencyclidine (PCP), and opiates. Standard laboratory tests for opiates are performed by immunoassay. Results are confirmed by gas chromatography/mass spectrometry (GC/MS).

The guidelines for positive test results are set by a government organization called the Substance Abuse and Mental Health Services Association (SAMHSA). The target analyte for the standard opiate drug test is morphine, which has a cutoff of 2,000 ng/mL. Additionally, the detection level of the initial screen (immunoassay) for 6-acetylmorphine, a metabolite of heroin, is 10 ng/ml. The GC/MS test, which is required to announce a positive result, also has a cutoff of 10 ng/ml. In other words, the level of opiates in the body must be above this level on both the immunoassay and GC/MS tests to qualify as a positive result.

A standard urine analysis will detect the presence of morphine, codeine, and 6-acetylmorphine. The body breaks down heroin into all three of these substances in the body. The presence of codeine is may indicate heroin, morphine, or codeine use. The ratio of codeine to morphine present in the body can help determine the origin substance, though it is rarely a factor. The test companies do not distinguish between codeine and heroin. Quite simply, a positive result is a positive result. Other opiates not metabolized into the three aforementioned chemicals are not detectable in a standard five-panel drug test.

Typically, low-to-moderate use of oxycodone will not cause a positive result; however, high dose oxycodone use has been reported linked to positive results. Hydrocodone is not converted into morphine or codeine; thus, it is not detectable. However, some testing facilities routinely test for hydrocodone due to its availability and popularity. Although less common, testing facilities have the capability to test for buprenorphine, but it will not cause a positive result in a standard drug screening.

Detection Periods in Urine

3-30 days
3-4 days
3-4 days
1-4 days
3-4 days
3-4 days
4-24 hours
84+ hours
3-4 days
4-5 days

Hair Testing

Hair testing is one of the least invasive methods of testing for drugs. When a drug is ingested, it circulates in a person’s bloodstream, which in turn, nourishes growing hair follicles. As a result, traces of the drug is stored in each piece of hair. The average rate of growth for human hair is about one-half of an inch per month. The typical hair drug test utilizes a 1.5 inch piece of hair, which results in the individual’s drug history for the past 90 days. It takes anywhere from 5-7 days for a drug to be detectable using a hair test.

Substances and Conditions which can cause false positives

  • Diabetes
  • Dextromethorphan (DXM – in most over-the-counter cough medications)
    • Nyquil
    • Vicks Formula 44
  • Kidney disease
  • Kidney infection
  • Liver disease
  • Poppy seeds
  • Prescription painkillers
  • Various quinolones & antibiotics

Drug Cutoff Concentrations

Initial test analyte Initial test cutoff concentration Confirmatory test analyte Confirmatory test cutoff concentration
Source: Analytes and Their Cutoffs (SAMHSA)
Marijuana metabolites 50 ng/mL Delta-9-tetrahydrocannabinol-9-carboxylic acid (THCA) 15 ng/mL
Cocaine metabolites 150 ng/mL Benzoylecgonine 100 ng/mL
Opiate metabolites (codeine/morphine) 2,000 ng/mL Codeine, Morphine 2,000 ng/mL
6-acetylmorphine 10 ng/mL 6-acetylmorphine 10 ng/mL
Phencyclidine 25 ng/mL Phencyclidine 25 ng/mL
Amphetamines (AMP/MAMP) 500 ng/mL Amphetamine, Methamphetamine 250 ng/mL
MDMA 500 ng/mL MDMA, MDA, MDEA 250 ng/mL

Buy Opiate Drug Testing Kit

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OxyContin FAQ

Friday, December 18th, 2009


  1. What is OxyContin?
  2. What strengths does OxyContin come in?
  3. What is the difference between oxycodone and OxyContin?
  4. What is the difference between OxyContin and Percocet?
  5. What does the OXY and CONTIN in OxyContin stand for?

What is OxyContin?

OxyContinOxyContin, manufactured by Purdue Pharma, is a controlled-release formulation of oxycodone effective for 12 hours of pain management. Instant-release formulations, such as Percocet and Tylox, are effective for only 4-6 hours, which results in four to six doses per day. With OxyContin, the medication only needs to be taken twice a day, which simplifies the process for the patient. Though oxycodone has been used since 1917, no time-release formulation was available until December 1995, when OxyContin was introduced as a Schedule II substance in the United States. OxyContin is approved for the treatment of moderate or severe pain, though it is only used in cases of chronic severe pain.

What strengths is OxyContin supplied in?

OxyContin is supplied in seven strengths: 10 mg, 15 mg, 20 mg, 30 mg, 40 mg, 60 mg, and 80 mg. A blue-colored 160 mg formulation was available up until May 2001, when it was discontinued for safety reasons. Each tablet is a different color: (1) 10 mg – white, (2) 15 mg – gray, (3) 20 mg – pink, (4) 30 mg – brown, (5) 40 mg – yellow, (6) 60 mg – red, (7) 80 mg – green. Many of the companies involved in the manufacture of the generic equivalent employ the same color scheme, but not all, so it is always wise to double-check using the Oxycodone Pill Identification Guide.

What is the difference between oxycodone and OxyContin?

OxyContin is merely the brand name under which Purdue Pharma chooses to market its product.  The active opioid ingredient in OxyContin is oxycodone, the same chemical used in Percocet, Tylox, and other popular opioid analgesics.

What is the difference between OxyContin and Percocet?

As stated earlier, OxyContin is a controlled-release formulation containing oxycodone.  It contains doses of oxycodone ranging from 10-80 mg.  Percocet is an instant-release oxycodone formulation, but with doses ranging from 2.5-10 mg.  Compared with OxyContin, Percocet contains a second active ingredient—acetaminophen (Tylenol).  One crushed 10 mg OxyContin tablet is comparable to one 10 mg Percocet tablet.

Some individuals mistakenly believe that abusing Percocet is somehow safer than abusing OxyContin.  In some circles, Percocet may even be socially acceptable, where OxyContin is demonized.  In the end, both formulations contain the same opioid—oxycodone.  Individuals abusing Percocet who also have a high tolerance are forced to take increasingly large doses of acetaminophen, a drug known to cause severe liver damage.  Both Percocet and OxyContin use the same opioid ingredient to achieve analgesia, and both are extremely dangerous when abused.

What does the OXY and CONTIN in OxyContin stand for?

The OXY in OxyContin is a reference to its active opioid ingredient, oxycodone. The word CONTIN, which is also seen in other continuous-release medications such as MS Contin (controlled-release morphine), refers to “continuous.”  CONTIN indicates that the medication is continuously released over the course of a specified period of time, rather than instantaneously like Percocet and Tylox.

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Opiate / Opioid FAQ

Monday, November 23rd, 2009


  1. What is the difference between an opiate and an opioid?
  2. What are the medicinal purposes of opioids?
  3. How are opioids taken?
  4. What are the short-term and long-term effects of opioids?
  5. What parts of the brain and nervous system to opiates affect?
  6. What are opiate receptors and how do they work?
    1. Agonists
    2. Antagonists
    3. Partial Agonists
    4. Mu-opioid receptors
    5. Delta-opioid receptors
    6. Kappa-opioid receptors
    7. Nociceptin-opioid receptors
  7. What drugs and foods should be avoided while on opioids?
  8. How and why are opioids abused?
    1. Heroin
    2. OxyContin
    3. Fentanyl
  9. What is withdrawal and when does it occur?
  10. How does snorting (insufflating) opiates get a person high?
  11. How is an opiate overdose treated?
  12. I have this pill marked xxxxx. What is it?

What is the difference between an opiate and an opioid?

In many cases, the terms opiate and opioid are used interchangeably; however, there are nuances to consider when using either term.  The term opiate refers to the naturally-occurring alkaloids found in the poppy plant (e.g. morphine, thebaine, codeine, and papaverine).  On the other hand, the term opioid refers to any compound resembling opium and its effects (e.g. oxycodone, hydromorphone).  In short, an opiate is naturally occurring, whereas an opioid may be semi-synthetic or synthetic.


Opioids include all semi- and fully synthetic narcotic analgesics (e.g. oxycodone, methadone), as well as the remainder of the opiate class.
— The term opiate describes narcotic analgesics from a natural source (e.g. morphine, codeine).

What are the medicinal purposes of opioids?

Clinical Uses: Analgesic, acute pulmonary edema (slows respiration and calms patient), in preanesthetic medicine for analgesic and sedative effects, anesthetic, antitussive, and antidiarrheal.

Off-Label Uses: Diabetic neuropathy, restless leg syndrome, treatment-resistant depression.

How are opioids administered?

Opioids are administered using a variety of methods from ingestion to injection.  Opioids are generally well-absorbed via intramuscular and subcutaneous routes, as well as at muscosal sites.  Oral consumption is often accompanied by extensive first-pass metabolism rendering it less efficient than the aforementioned methods of delivery.  For opioids like buprenorphine, however, oral administration renders the drug useless; instead, it requires sublingual or intravenous administration to achieve the desired clinical effects.  Because intravenous injection typically provides the highest bioavailability (typically close to 100 percent) and the fastest peak (the “rush”), drug users often prefer this method of administration.

What are the short-term and long-term effects of opioids?


  • POSITIVE — pain relief (analgesia), euphoria, drowsiness, relaxation, cough suppression
  • NEUTRAL — itching, pupillary constriction, stimulation, sweating
  • NEGATIVE — difficulty concentrating, blurred vision, reduced respiratory rate, nausea, vomiting, reduced appetite, anxiety, lethargy, constipation, dysphoria, reduced libido, death, spontaneous abortion


Long-term use of opioids can lead to depression, reduced pain threshold, difficulty concentrating, malnutrition, insomnia, sexual problems, and addiction. As the body becomes accustomed to a specific dosage, the drug will no longer provide the same level of pain relief or euphoria; this is called tolerance. As tolerance builds, the person will find himself requiring increasingly larger doses, sometimes at a higher frequency.  In addition, the body starts producing fewer endorphins and withdrawal becomes more severe.

Injecting opioids carries additional risks, especially when using dirty needles, sharing needles, or injecting incorrectly. The sharing of needles contributes to the spread of diseases such as AIDS/HIV and hepatitis. Intravenous drug use can also lead to collapsed veins, bacterial/viral infections, skin infections, and increased risk of stroke.

What parts of the brain and nervous system do opiates affect?

Picture of brain with limbic system, brainstem, and spinal cord highlighted.AsteriskLimbic system (red) – The limbic system is a part of the brain that controls emotion, motivation, and emotional association with memory. Opiates affect the limbic system leading to feelings of pleasure, relaxation, and contentment.

AsteriskBrainstem (blue) – The brainstem coordinates certain types of movements, as well as automatic functions, such as breathing and coughing. Opiates affect the brainstem causing slowed breathing, and suppression of coughs.

AsteriskSpinal cord (yellow) – The spinal cord is responsible for the communication between the body and brain. One specific function of the spinal cord is the transmission of pain signals from the body. Opiates act on the spinal cord, blocking pain messages, which can sometimes lead to serious injury.

What are opiate receptors and how do they work?

Within the three parts of the brain mentioned above, the limbic system, brainstem, and spinal cord, as well as the large intestines, there are sites on specific nerve cells that recognize opioids. When these sites on the nerve cells are stimulated by an opioid, the brain and body are affected.

There are four major subtypes of opioid receptors: mu, delta, kappa, and recently discovered nociceptin (ORL-1). Each of major receptor subtype is named after a letter of the Greek alphabet. According to Wikipedia, the opiate receptors were named “using the first letter of the first ligand that was found to bind to them.” Each receptor initiates a different response in the body, and there are three different methods of binding to a receptor.

Full Agonists

Opioids that activate opioid receptors in the brain are termed opioid agonists. Opioid agonists bind to opioid receptors and turn them on, or activate them, resulting in some sort of effect in that organism. Full mu-opioid agonists activate the mu-opioid receptors. As the dose of a full agonist is increased, the effects will be increased until a maximum effect is reached or the receptor becomes fully activated. This class of opioids, the opioid agonists, have the highest abuse potential (e.g., heroin, methadone, morphine, oxycodone, hydromorphone).


Antagonists also work by attaching to the opioid receptors, but instead of activating the receptors, they block them. Antagonists also have the property of preventing the receptors from activation from agonists. An antagonist is much like a key that fits in a lock but does not open it and prevents another key from being inserted to open the lock. Examples of opioid antagonists include naloxone and naltrexone.

Partial Agonists

Partial agonists, such as buprenorphine, have qualitative effects similar to both full agonists and antagonists. Like agonists, partial agonists will bind to receptors and activate them, but with lower intrinsic activity. For individuals not opioid-tolerant or dependent upon opioids, full agonists and partial agonists produce indistinguishable effects. Like its counterpart, the agonist, increased doses produce increasing effects; however, at a certain point, the effects of partial agonists reach a maximum and will not increase further, even if the dose is increased. This quality is known as the ceiling effect. At higher doses, partial agonists exert effects much like an antagonist—maintaining binding affinity to the receptor and partial activation (or no activation), while simultaneously displacing or blocking full opioid agonists from the receptors.

Mu-receptors (found in periaqueductal gray region, spinal cord, olfactory bulb, nucleus accumbens) – Activation of the mu-receptor causes analgesia, sedation, reduced blood pressure, itching, nausea, euphoria, decreased respiration, miosis (constricted pupils) and decreased bowel motility. Some of these effects, such as sedation, decreased respiration, and euphoria, tend to disappear as tolerance develops; however, very little tolerance develops to analgesia, miosis, and decreased bowel motility. Tolerance varies from effect-to-effect because of the activation of different mu-receptor subtypes (µ1 and µ2). To be specific, µ1-receptors block pain, while µ1-receptors cause reduced bowel motility and respiratory depression. The mu-receptors possess high affinity for enkephalins and beta-endorphin, and a low affinity for dynorphins.

Delta-receptors Delta-receptor activation produces analgesia, and some research points to the possibility of a lowered seizure threshold. Enkephalins are the endogenous opioids that bind to the delta-receptor. Only recently have scientists been able to study this receptor, and as a result, available information is very limited. On the other hand, there are studies indicating that stimulation of the delta-receptor may result in some sort of cardioprotection, given certain circumstances.

Kappa-receptors (found in periphery by pain neurons, spinal cord, brain) – Like the other opiate receptors, the kappa-receptor also induces analgesia, but also causes nausea and dysphoria. Stimulation of the kappa-receptor is neuroprotective against hypoxia, which may lead to kappa-agonism being used therapeutically in the future. The kappa-receptor has high affinity for dynorphins. Kappa-agonism, whether induced by a full-agonist or partial-agonist, causes psychotomimetic effects, which includes hallucinations, delusions, and other forms of psychotic behavior. Psychotomimetic effects are largely undesirable, which naturally serves to limit abuse potential. Drugs with this sort of effect include buprenorphine (found in Suboxone/Subutex), butorphanol, and nalbuphine. Salvinorin A, the primary active psychotropic chemical in Salvia divinorem, is also a kappa-receptor agonist. Salvia divinorem’s effects are actually sought after, but differ from typical hallucinogens, whose primary method of action is 5-HT2A serotonin receptor agonism.

Nociceptin receptor (also known as ORL-1) – The natural ligands for the ORL-1 receptors are nociceptin, and orphanin FQ.[1] Orphanin FQ was found to inhibit the GABA transporter type I, which indirectly alters dopamine transmission.[2] ORL-1 receptor agonists are currently being researched as possible treatments for heart failure, and migranes. Nociceptin antagonists may be effective for treating depression. Though the implications seem promising, research into the ORL-1 receptors is still in an adolescent stage, so it is hard to tell what the conclusion will be. Buprenorphine, used in the treatment of opioid addiction and also as a painkiller, is a partial agonist at the ORL-1 receptors, while its active metabolite norbuprenorphine is a full agonist at these receptors.[3]

What drugs and foods should be avoided while on opioids?

Combining opiates with any drug that suppresses breathing can be fatal. This includes, but is not limited to:

  • Alcohol
  • EtOH
  • Antihistamines
  • Sedative-hypnotics/benzodiazepines – alprazolam (Xanax), clonazepam (Klonopin), diazepam (Valium), etc.
  • Anesthetics
  • Anti-psychotics

How and why are opioids abused?

Opioids are abused for their euphoric and sedative qualities; however, with repeated dosing tolerance develops. Tolerance develops to many of the effects of opiates, but at different rates for each effect. Tolerance develops very quickly to the ability of opiates to reduce the perception of pain, as well as the suppression of breathing. Two effects that don’t really change as tolerance develops are pinpoint pupils and constipation.

Heroin: Many heroin users begin with insufflation or subcutaneous injection (“skin-popping”) and eventually end up injecting the drug. Smoking heroin, the second fasted method of administration is also popular; however, the fastest way to get heroin to the brain is via intravenous injection.

OxyContin: Abusers generally pulverize the pills and insufflate or “parachute” the resultant fine powder. This is extremely dangerous, especially to opiate-naive individuals, who have little to no tolerance to opioids. An 80 mg OxyContin pill, which is meant to be released over a period of 12 hours, is equivalent to taking sixteen 5 mg Percocets. The instant release of 80 milligrams of oxycodone can be fatal.

Fentanyl: Because fentanyl is very fat-soluble and very fast-acting, it makes it a prime candidate for abuse. One popular form is the transdermal patch, some of which can be worn for three days delivering a steady dose of the drug. Many people cut open the patch and suck the contents out. This is even more dangerous than insufflation of OxyContin; instead of a 12-hour dose, it is a 72-hour dose. It is very hard to determine how much of the drug is actually being taken. Also, by weight, fentanyl is about 80 times stronger than morphine, and is subsequently measured in micrograms. Fentanyl is also frequently found in an injectable preparation.

What is withdrawal and when does it occur?

Withdrawal occurs when an opioid-addicted individual ceases taking opioids. In some cases, withdrawal can begin in as little as a few hours after the last dose, but typically starts within 12-24 hours. For many people, it begins with sweating, yawning, a runny nose and “teary”-eyes. As withdrawal peaks, the individual will be extremely uncomfortable and exhibit symptoms such as diarrhea, shivering, sweating, insomnia, muscle aches, abdominal cramps, restlessness, irritability, loss of appetite, and anxiety. It is often compared to the flu, but for many, the flu is a play day in comparison. Withdrawal generally lasts about a week with the acute symptoms peaking on day three and subsiding by day seven. With long-acting opioids, such as methadone and buprenorphine, the withdrawal can last twice as long.

Recent studies have indicated there is often a “post-acute withdrawal syndrome” which can mean months of muscle aches, insomnia, and depression; however, this doesn’t mean the afflicted individual will be suffering for months on end. PAWS often shows its ugly head in the form of regular “flare-ups.” Sometimes the post-withdrawal feelings may even be the result of a preexisting condition, a condition that the user may or may not have been using drugs to control (self-medicating). This should be discussed with a licensed healthcare professional.

How does snorting (insufflating) opiates get a person high?

In the nose, there is a mucosal lining which can absorb chemicals depending on the fat-solubility of the molecule. The more fat-soluble the opioid, the better it will be absorbed. Perhaps the best example of this is fentanyl, which is the most fat-soluble of the opioid family; not too far behind is its opiate cousin diacetylmorphine, also known as heroin. It is important to remember that insufflation is not without consequence. In general, snorting wears away the tissues in the nose, which can lead to a gaping hole, or unpleasant whistling through the nostril.

How is an opioid overdose treated?

During the movie Pulp Fiction, one of the female characters overdoses on heroin. While trying to save her life, John Travolta is seen screaming at a man to bring over an adrenaline shot. Frantically, the man brought the adrenaline shot, which was subsequently injected directly into her heart, jump-starting her body back to life.  This is not how overdoses are treated in the real world! Adrenaline is not used to reverse an opioid overdose.  To reverse an opioid overdose, an opioid antagonist with a high binding affinity is necessary to strip the opioid from the receptors; thus, eliminating fatal respiratory depression.  In the movie Transpotting, one of the characters is left at the entrance of a hospital emergency room, discovered, and given an opioid antagonist. Within moments the character is seen “jumping out of his skin.” This is a much better representation of the effects of an opioid antagonist.  The drug most frequently used is naloxone, also known as Narcan. Naloxone works in a matter of seconds by stripping any opioids off the opioid receptors. Instant withdrawal, but one life saved.

I found a pill with a particular marking. What is it?

Due to the overwhelming number of requests to identify pills, TPC! has put together an extensive list of pill identification guides for numerous medications with a focus on opioids.

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