Suboxone FAQ

Q: Is buprenorphine treatment just trading one addiction for another?

No- with successful buprenorphine treatment, the compulsive behavior, the loss of control of drug use, the constant cravings, and all of the other hallmarks of addiction vanish. When all signs and symptoms of the disease of addiction vanish, we call that remission, not switching addictions.

The key to understanding this is knowing the difference between physical dependence and addiction.

Buprenorphine will maintain some of the preexisting physical dependence, but that is easily managed medically and eventually resolved with a slow taper off of the buprenorphine when the patient is ready. Physical dependence, unlike addiction, is not a dangerous medical condition that requires treatment. Addiction is damaging and life-threatening, while physical dependence is an inconvenience, and is normal physiology for anyone taking large doses of opioids for an extended period of time.

It is essential to understand the definition of addiction and know how it differs from physical dependence or tolerance.

The American Academy of Pain Medicine (AAPM), American Pain Society (APS), American Society of Addiction Medicine (ASAM), and (NAABT) National Alliance of Advocates of Buprenorphine Treatment, have recognizes these definitions below.


Addiction is a primary, chronic, neurobiologic disease, with genetic, psychosocial, and environmental factors influencing its development and manifestations. It is characterized by behaviors that include one or more of the following: impaired control over drug use, compulsive use, continued use despite harm, and craving.

Physical Dependence: Physical dependence is a state of adaptation that is manifested by a drug class specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist.

Tolerance: Tolerance is a state of adaptation in which exposure to a drug induces changes that result in a diminution of one or more of the drug's effects over time.

Physical dependence and tolerance are normal physiology. Addiction is a disorder that is damaging and requires treatment.

When a patient switches from an addictive opioid to successful buprenorphine treatment, the addictive behavior often stops. In part due to buprenorphine's long duration of action, patients do not have physical cravings prior to taking their daily dose. The drug seeking behavior ends. Patients; regain control over drug use, compulsive use ends, they are no longer using despite harm, and many patients report no cravings. Thus all of the hallmarks of addiction disappear with successful buprenorphine treatment.

Therefore, one is not trading one addiction for another addiction. They have traded a life threatening situation (addiction) for a daily inconvenience of needing to take a medication (physical dependence), as some would a vitamin. Yes the physical dependence to opioids still remains, but that is vast improvement over addiction, is not life threatening, and it can easily be managed medically. It's also important to note that the physical depndence pre-existed the buprenorphine treatment and was not caused by it.

Addiction is a brain disease that affects behavior. This addictive behavior can be devastating to the patient and their loved ones. It's not the need to take a medication that is the problem, many people need to take a medication, but rather it is the compulsive addictive behavior to keep taking it despite doing harm to one's self or loved ones that needs to stop. Whether or not the person takes a medication to help achieve this shouldn't matter to anyone. If a medication helps stop the damaging addictive behavior, then that is successful treatment and not switching one addiction for another.

Q: What exactly is Buprenorphine?

Buprenorphine (BYOO-pre-NOR-feen) ('b?-pre-'nôr-f?n) is an opioid medication used to treat opioid addiction in the privacy of an AHC facility. Buprenorphine can be dispensed for take home use, by prescription. This in addition to buprenorphine’s pharmacological and safety profile makes it an attractive treatment for patients addicted to opioids.

Buprenorphine is different from other opioids in that it is a partial opioid agonist3. This property of buprenorphine may allow for;

less euphoria and physical dependence
lower potential for misuse
a ceiling on opioid effects
relatively mild withdrawal profile
At the appropriate dose buprenorphine treatment may:

Suppress symptoms of opioid withdrawal
Decrease cravings for opioids
Reduce illicit opioid use
Block the effects of other opioids
Help patients stay in treatment
* When compared with full opioid agonists (such as oxycodone and heroin)

Buprenorphine ('b?-pre-'nôr-f?n) (C29H41NO4) is a semi-synthetic opioid derived from thebaine, an alkaloid of the poppy Papaver somniferum. Buprenorphine is an opioid partial agonist. This means that, although Buprenorphine is an opioid, and thus can produce typical opioid effects and side effects such as euphoria and respiratory depression, its maximal effects are less than those of full agonists like heroin and methadone. At low doses Buprenorphine produces sufficient agonist effect to enable opioid-addicted individuals to discontinue the misuse of opioids without experiencing withdrawal symptoms. The agonist effects of Buprenorphine increase linearly with increasing doses of the drug until it reaches a plateau and no longer continues to increase with further increases in dosage. This is called the "ceiling effect." Thus, Buprenorphine carries a lower risk of abuse, addiction, and side effects compared to full opioid agonists. In fact, Buprenorphine can actually block the effects of full opioid agonists and can precipitate withdrawal symptoms if administered to an opioid-addicted individual while a full agonist is in the bloodstream. This is the result of the high affinity Buprenorphine has to the opioid receptors. The affinity refers to the strength of attraction and likelihood of a substance to bind with the opioid receptors. Buprenorphine has a higher affinity than other opioids and as such will compete for the receptor and win. It will "knock off" other opioids and occupy that receptor blocking other opioids from attaching to it. If there is enough Buprenorphine to knock the opioids off the receptors but not enough to occupy and satisfy the receptors, withdrawal symptoms can occur; in which case the treatment is more Buprenorphine until withdrawal symptoms disappear.

Suboxone, contains both buprenorphine and the opiate antagonist naloxone. Naloxone has been added to Suboxone to guard against intravenous abuse of buprenorphine by individuals physically dependent on other opiates. If misused by injection, the naloxone (along with the buprenorphine itself) will help cause immediate withdrawal in opioid dependent people, however when taken sublingually, as indicated, the naloxone is clinically insignificant.

Q: What are common Buprenorphine side effects?

Headache is one of the most commonly reported buprenorphine side effects. A common remedy for headaches is aspirin or other OTC (over the counter) pain remedies with a glass of water; but water alone may be all that's needed. Medications, including laxatives and all opioids, can contribute to dehydration; and one of the first symptoms of dehydration is a headache. Just by staying hydrated throughout the day may be enough to solve the headache side effect, and reduce some of the other side effects as well.

Be mindful there are other things that can cause headaches such as caffeine and nicotine withdrawals. Drinking plenty of water is the easiest first step in trying to figure out the cause of headaches. But if the headaches persist, consult with a medical professional to be on the safe side.

Many medications can cause constipation, including opioids, and especially long-acting opioids. Fast-acting, short-duration opioids, such as heroin and hydrocodone, cycle through periods of great effect to periods of lesser effect. It is during those periods of lesser effect that the body is able to produce bowel movements. However, long-acting opioids, such as buprenorphine, methadone and time-released oxycodone, have a continuous influence on the body without the period of lesser effect that would allow for bowel movements. This can lead to chronic constipation if preventative strategies aren't employed.

Constipation can become serious, and, in extreme cases, require surgery, but for most, it's an unnecessary inconvenience and discomfort. Fortunately, it is usually avoidable with OTC remedies, exercise, good diet and good hydration.

If drinking more water along with a high fiber diet and increased exercise isn't enough, stool softeners such as docusate sodium (brand name Colace®) which comes in soft gel tablets are an option. This product softens stools and has a lubricating effect, but is not a laxative. Polyethylene glycol 3350 (brand name Miralax®) is a powder that dissolves into drinks and both softens stools and increases the frequency of bowel movements. It works by drawing water into the colon, and for that reason drink plenty of water to avoid dehydration - a contributor to constipation. According to an informal survey conducted online, either one or a combination of both has been effective at relieving most buprenorphine-induced constipation. Avoid harsh laxatives if possible; and, of course, consult your doctor before using any of the remedies mentioned here.

Too late for prevention, I have severe constipation now, what can I do?

Dry mouth (xerostomia): This may seem like an innocuous symptom and is not often cited as a buprenorphine side effect, but it can be very serious and very costly.

Saliva is the mouth’s primary defense against tooth decay, gun disease, and maintains the health of the soft and hard tissues in the mouth. Saliva washes away food and other debris, neutralizes acids produced by bacteria in the mouth and provides disease-fighting substances throughout the mouth.

With dry mouth (which is a side effect from all opioids) these benefits are diminished which allows bacteria to multiply and often leads to gingivitis which can lead to periodontitis disease, and eventually bone and tooth loss

Gingivitis: This is the earliest stage of gum disease, some bleeding with brushing and inflammation of your gums caused by plaque buildup at the gumline. At this early stage in gum disease, damage can be reversed, since the bone and connective tissue that hold the teeth in place are not yet affected.

Periodontitis: At this stage, the supporting bone and fibers that hold your teeth in place are irreversibly damaged. Your gums may begin to form a pocket below the gumline, which traps food and plaque. Proper dental treatment and improved home care can usually help prevent further damage.

Advanced Periodontitis: In this final stage of gum disease, the fibers and bone supporting your teeth are destroyed, which can cause your teeth to shift or loosen. This can affect your bite and, teeth may need to be removed.

Bacteria in plaque are the main cause of gingivitis and periodontitis. Plaque is a sticky film of microorganisms (biofilm) that continuously forms on the teeth and under the gumline. These bacteria may release toxins, especially below the gumline, that irritate the gum tissue and cause inflammation. Toxins or poisons -- produced by the bacteria in plaque as well as the body's "good" enzymes involved in fighting infections -- start to break down the bone and connective tissue that hold teeth in place. The gums may eventually break down and separate from the teeth causing a deep space called periodontal pockets. These pockets are very difficult to clean, allowing the bacteria to grow and multiply. As the disease progresses, the pockets deepen and more gum tissue and bone are destroyed. When this happens, teeth are no longer anchored in place, they become loose, and tooth loss occurs. Gum disease is the leading cause of tooth loss in adults, not tooth decay.

Other contributors to the risk and severity of periodontal gum disease and oral health problems are smoking and diabetes.

According to the CDC, researchers have uncovered potential links between gum disease and other serious health conditions. In people with healthy immune systems, the bacteria in the mouth that makes its way into the bloodstream is usually harmless. But under certain circumstances, these microorganisms are associated with health problems such as stroke and heart disease.

Avoid the pain and cost from the consequences of opioid-induced dry mouth by keeping well hydrated, use OTC treatment for dry-mouth such as Biotene®, and pay especially close attention to good oral hygiene with routine dentist visits. Water flossers may be even more effective than floss at reducing plaque buildup. Preventative oral care might be the single best way to save money associated with your addiction treatment. Do not overlook the importance of it.

Above buprenorphine side effects can occur when dosed correctly. When doses incorrectly however, other symptoms have been reported. Here are some of them.

Too high of a dose: lethargy, a medicated feeling ( described as “ cloudy” “foggy” or “ slow”), tiredness, nausea, constricted pupils in low light, a general unmotivated feeling, unjustified feeling of contentment, dehydration (indicated by dark urine)

Too low of a dose: sweating, chills, goose bumps, dilated pupils in normal light, diarrhea, cramps, insomnia, nausea, anxiety, depression, dehydration, cravings

The optimal dose of buprenorphine, when prescribed for addiction, is the lowest dose that suppresses cravings and withdrawal symptoms. Dose requirements may change as treatment progresses.

Q: What drugs are opioids?

Examples of opioids are: Painkillers such as; morphine, methadone, Buprenorphine, hydrocodone, and oxycodone. Heroin is also an opioid and is illegal.

Opioid drugs sold under brand names include: OxyContin®, Percocet®, Palladone®(taken off the market 7/2005), Vicodin®, Percodan®, Tylox® and Demerol® among others.

Drugs that are not opioids are; Cocaine, methamphetamines, ecstasy, LSD, GHB, Ketamine, other club drugs, or steroids.

Q: What’s this agonist / antagonist stuff?

This is an important concept, it is why Buprenorphine is so unique as a treatment medication. An agonist is a drug that activates certain receptors in the brain. Full agonist opioids activate the opioid receptors in the brain fully resulting in the full opioid effect. Examples of full agonists are heroin, oxycodone, methadone, hydrocodone, morphine, opium and others. An antagonist is a drug that blocks opioids by attaching to the opioid receptors without activating them. Antagonists cause no opioid effect and block full agonist opioids. Examples are naltrexone and naloxone. Naloxone is sometimes used to reverse a heroin overdose. Buprenorphine is a partial agonist meaning, it activates the opioid receptors in the brain, but to a much lesser degree then a full agonist.

Buprenorphine also acts as an antagonist, meaning it blocks other opioids, while allowing for some opioid effect of its own to suppress withdrawal symptoms and cravings.

This is why it would be misleading to classify buprenorphine as a replacement therapy. It would be equally misleading to classify it solely as an opioid blocker. Buprenorphine is in a category of its own and therefore should not be seen as “replacement” or "substitution" for anything else.

Q: How do opioids work in the brain??

Opioids attach to receptors in the brain. Normally these opioids are the endogenous variety that are created naturally in the body. Once attached, they send signals to the brain of the "opioid effect" which blocks pain, slows breathing, and has a general calming and anti-depressing effect. The body cannot produce enough natural opioids to stop severe or chronic pain nor can it produce enough to cause an overdose.

opioids can activate receptors because their chemical structure mimics that of a natural neurotransmitter. This similarity in structure "fools" receptors and allows the drugs to lock onto and activate the nerve cells. Although these drugs mimic brain chemicals, they don't activate nerve cells in the same way as a natural neurotransmitter, and they lead to abnormal messages being transmitted through the network.

Opioids target the brain's reward system by flooding the circuit with dopamine. Dopamine is a neurotransmitter present in regions of the brain that regulate movement, emotion, cognition, motivation, and feelings of pleasure. The overstimulation of this system, which rewards our natural behaviors, produces the euphoric effects sought by people who misuse drugs and teaches them to repeat the behavior.

Our brains are wired to ensure that we will repeat life-sustaining activities by associating those activities with pleasure or reward. Whenever this reward circuit is activated, the brain notes that something important is happening that needs to be remembered, and teaches us to do it again and again, without thinking about it. Because drugs of abuse stimulate the same circuit, we learn to abuse drugs in the same way.

Q: How does Buprenorphine work in the brain?

Opioids attach to receptors in the brain, with three main effects; reduced respiration, euphoria, decreased pain. The more opioids ingested the more of an effect. The process of opioids binding to the opioid receptors can be thought of as a mechanical union, the better the fit the more the opioid effect. Buprenorphine is different. It too binds to the receptors, however, without a perfect fit. As a result the Buprenorphine tends to occupy the receptors without all of the opioid effects. The receptor is tricked into thinking it has been satisfied with opioids without producing strong feelings of euphoria, and without causing significant respiratory depression. This, in turn, prevents that receptor from joining with full opioids; therefore if the patient uses heroin or painkillers, they are unlikely to experience additional effect. Buprenorphine tends to stay with the receptors, blocking them, much longer then opioids do. This stickiness, is what makes Buprenorphine last so long, up to 3 days.

Q: What exactly are opioid receptors?

These are protein molecules that exist on the surface of some nerve cell membranes. They provide a way for the body to experience the effects of opioids.

Q: What is addiction?

To understand fully you must be aware of the difference between tolerance, physical dependence, and addiction:

As a person takes opioids for an extended period of time, they become less sensitive to it and require more to achieve the same effect. Receptors in the brain become less sensitive. This means they need more and more opioid to achieve the same effect. This is called tolerance. When the body can no longer make enough natural opioids to satisfy the less sensitive receptors, the body becomes dependent on the external source. This is physical dependence.

"Physical Dependence" is a physiological state of adaptation to a substance, the absence of which produces symptoms and signs of withdrawal. It is possible to be physically dependent on a drug without being addicted to it. Physical dependence is the result of physical changes in the brain. It is not a matter of willpower rather it is actual physiology.

Addiction is defined as a behavioral syndrome characterized by the repeated, compulsive seeking (psychological dependence) or use of a substance despite adverse social, psychological, and/or physical consequences, along with the physical need for an increased amount of a substance as time goes on to achieve the same desired effect. Addiction is often (but not always, as with an addiction to gambling) accompanied by tolerance, physical dependence, and withdrawal syndrome.

People are dependent on water and food but are not addicted to them. If a cancer patient is taking large doses of painkillers, he/she will become tolerant and physically dependent on them (meaning they will experience withdrawal symptoms if the drug is abruptly removed) but they are not necessarily addicted to it (meaning they will not seek out the drug despite adverse consequences once the drug is no longer needed for pain).

Addiction is a disorder that requires treatment while physical dependence is not. This is important to understand in order to be able to discern between switching one addiction for another and treatment.

The American Academy of Pain Medicine, American Pain Society, and American Society of Addiction Medicine, recognizes these definitions below as the current accepted definitions.

I. Addiction: Addiction is a primary, chronic, neurobiologic disease, with genetic, psychosocial, and environmental factors influencing its development and manifestations. It is characterized by behaviors that include one or more of the following: impaired control over drug use, compulsive use, continued use despite harm, and craving.

II. Physical Dependence: Physical dependence is a state of adaptation that is manifested by a drug class specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist.

III. Tolerance: Tolerance is a state of adaptation in which exposure to a drug induces changes that result in a diminution of one or more of the drug’s effects over time.

Summary: Addiction is uncontrollable compulsive behavior caused by alterations of parts of the brain from repeated exposure to high euphoric responses.

Q: What is withdrawal?

Withdrawal syndrome consists of a predictable group of signs and symptoms resulting from abrupt removal of, or a rapid decrease in the regular dosage of, a psychoactive substance. The syndrome is often characterized by over activity of the physiological functions that were suppressed by the drug and/or depression of the functions that were stimulated by the drug. In other words, opposite of what the drug did. If the drug suppressed depression then the person would be depressed while in withdrawal. If the substance suppressed pain then the person will experience pain while in withdrawal.

Withdrawal from opioids can be severe and excruciating. Withdrawal generally begins between 4 to 72 hours after the last opioid use (depending on dose and opioid), The symptoms are both physical and emotional and include: dilated pupils, goose bumps, watery eyes, runny nose, yawning, loss of appetite, tremors, panic, chills, nausea, vomiting, muscle cramps, insomnia, stomach cramps, diarrhea, shaking, chills or profuse sweating, depression, irritability, jitters, and increased sensitivity to pain.

Withdrawal is a symptom of brain adaptations caused by some substances. As someone takes more and more of an opioid they increase their tolerance and require more and more to achieve the same effect. The level of tolerance where the body can no longer naturally compensate for the absence of the substance is called physical dependence. Withdrawal is a symptom of physical dependence. If you are not physically dependent on a substance you will not experience withdrawal from it. To achieve a comfortable transition off a medication you have become physically dependent on requires matching your taper off of the drug with your brain's ability to adapt to each decrease. Too fast will cause discomfort.

Q: Is continued addictive behavior a voluntary behavior?

The initial decision to take drugs is mostly voluntary. However, when drug misuse takes over, a person's ability to exert self control can become seriously impaired. Brain imaging studies from drug-addicted individuals show physical changes in areas of the brain that are critical to judgment, decision making, learning and memory, and behavior control. Scientists believe that these changes alter the way the brain works, and may help explain the compulsive and destructive behaviors of addiction.(1) The patient's struggle for recovery is in great part a struggle to overcome the effects of these brain adaptations.(3)

Behavior modification can help recondition the brain and reverse some of the brain changes, medication can sometimes help too, but often it is a combination of both. Not all of the brain adaptations resulting from addiction can be reversed, so patients need to develop strategies to compensate. Cognitive tools may be enough for some patients while others will require a combination of cognitive tools and medication to keep the addictive behavior in remission.(4)

Q: Why is counseling an important tool in the treatment process?

Physical connections create pathways in the brain that can be altered when we learn something new. These changes to the brain can be seen with medical imagery. With long term difficult things like learning to play a musical instrument, these changes can be permanent. Addiction is a learned behavior that changes the brain as well. The brain becomes conditioned to want the substance. Through counseling and other behavioral modification we can actually, in some cases, change the brain physically. By changing our environment, starting a new job, new hobbies and friends, all will alter our brain in some way. It is possible to undo some of the changes that occurred while addicted. Therapy will recondition the brain closer to pre-addiction status. This will better prepare the patient for a time when they may no longer require medication.

Medication alone can reduce cravings and withdrawal, but recovering from an addictive disorder requires a rewiring of the brain and medication alone is not enough. Attention to eliminating things in life that cause stress or depression will help minimize the chance of relapse. Disassociating with friends who are in active addiction can be difficult but very necessary. An experienced counselor/therapist will be able to teach other techniques that will further help undo some of the brain changes and conditioned learning that occurred while becoming and once addicted.

Q: Can someone switch from methadone to buprenorphine?

YES, it is best to SLOWLY reduce your therapeutic dose of Methadone to 30 mg a day or less for at least a week, before discontinuing it completely for at least 36 hours before starting Buprenorphine. You MUST be in mild to moderate withdrawal before you take your first dose of Buprenorphine. If you are doing well in Methadone treatment it may not be advisable to change treatments at all unless you and your doctor determine it is in your best interest.

It is VERY important to follow these guidelines and prevent precipitated withdrawal.

Q: What if I miss a dose?

If you miss a dose and remember it hours later, take it upon remembering. If you forget until it is close to the time of the next day's dose, do not take a double dose. Not because you will take too much but rather you will just be wasting it, due to the ceiling effect. After being on treatment for a relatively short period of time you will feel so normal it may be difficult to remember unless you tie taking your medication to an activity you do every day at the same time. For example, after you have coffee or orange juice in the morning, or while reading the newspaper.

Q: What if I need pain medication for surgery, or acute pain?

You will still be able to be treated for pain with elective dental or surgical procedures. Our medical director should coordinate with your treating physician. They will likely stop your Buprenorphine medication, at least 36 hours before the procedure, and then when you are ready to go back on Buprenorphine you will need to be re-induced, which means stopping your pain medicine, experiencing mild withdrawal (for a very short time) and restarting your Buprenorphine.

Q: How soon can a work schedule be resumed?

It is recommended to take the first day of treatment off. Some are able to work even on Day One. Certainly after Day One, you should be able to work with greater attentiveness and clarity than before starting treatment. The transition from addictive substance to Buprenorphine is usually painless and most patients experience no adverse physical effects. In fact most say that they feel normal again, like they were never on drugs at all.

Q: What is Precipitated withdrawal?

Precipitated withdrawal can occur when an antagonist (or partial antagonist, such as buprenorphine) is administered to a patient dependent on full agonist opioids. Due to Buprenorphine’s high affinity but low intrinsic activity at the mu receptor, the partial antagonist displaces agonist opioids from the mu receptors, without activating the receptor to an equivalent degree, resulting in a net decrease in agonist effect, thus precipitating a withdrawal syndrome.

It is a common misconception that the Naloxone in Suboxone initiates precipitated withdrawal. This is false. The Naloxone can only initiate precipitated withdrawal if injected into a person tolerant to opioids. Taken sublingually the Naloxone has virtually no effect.

How to avoid precipitated withdrawal: The best way to avoid this condition is through patient education. The patient should be informed, prior to the induction appointment, of what precipitated withdrawal is and how they can avoid it. The patient who understands that under reporting last use puts him/her at high risk for rapid and intense onset of withdrawal syndrome, is more likely to accurately report last use. Ask the patient what their first few symptoms and signs of withdrawal have been in the past. Look for these S/S before administering the first dose at induction.

Precipitated withdrawal puts the patient at risk for concluding that Buprenorphine is ineffective, or the doctor may not know how to help, or both. Either situation leaves the patient in a precarious state physically and emotionally.

Begin the induction by assessing last use of all Opioids, short and long acting, objective and subjective symptoms and calculate a COWS score. If not in sufficient withdrawal explain that it is in the patient’s best interest to wait.

Short-acting Opioids: (Heroin, Crushed OxyContin®, Percocet®, Vicodin®, Oxycodone®) Short- acting Opioids have a half life of approximately 8 hours or less. Prior to induction, patients must abstain from all short-acting Opioids for 12 to 24 hours and/or have objective withdrawal symptoms sufficient to produce a score of 5 to 6 on the COWS (Clinical Opiate Withdrawal Scale) such as dilated pupils.

Methadone; Patients transitioning from methadone to Buprenorphine require a slow taper to 30mg./day of methadone, for at least one week. Last dose must be no less than 36 hours prior to induction. A minimal score of at least 5 to 6 on COWS is recommended.

OxyContin® (taken orally) Discontinue use for at least 24 hours prior to induction, with a COWS score of at least 5 to 6.

How to Treat Precipitated Withdrawal If the patient experiences precipitated withdrawal, administer additional 2mg. to 4 mg. doses of Buprenorphine hourly, until symptoms dissipate.