Home Study

• Stop Obsessing!
  Chapter 1. Do You Have Obsessions or Compulsions?
• Chapter 2. The Lives of Obsessive-Compulsives
• The Stop Obsessing! Audio-Tapes
  Tape 1-1: Common Features & The Four Challenges

Obsessions are repetitive, unproductive thoughts that almost all of us have experienced from time to time. We can be driving down the road, ten minutes from home, heading for a week's vacation. Suddenly the thought enters our mind, "Did I unplug the iron after I finished with that shirt?" Then we think, "I must have . . . but I don't know, I was rushing around so at the last minute. Did I reach down and pull the cord out of the socket? I can't remember. Was the iron light still on as I walked out the door? No, it was off. Was it? I can't leave it on all week; the house will burn down. This is ridiculous!" Eventually we either turn around and head home to check as the only way to feel relieved, or we convince ourselves that we did indeed take care of the task.

This is an example of what can take place inside the mind of any of us when worrying about a particular problem. Obsessive-compulsive disorder, however, is much more serious. In the mind of the person with obsessive-compulsive disorder, this pattern of thought is exaggerated, highly distressing and persistent.

The second form of the problem is : compulsions: repetitive, unproductive behaviors that people engage in ritualistically. As with obsessive thoughts, there are a few compulsive behaviors in which the average person might engage. As children, we played with superstitions, such as never stepping on a sidewalk crack or turning away when a black cat crossed our path. Some of these persist as we become adults: many of us still never walk under a ladder.

Intense anxiety and even panic can come whenever the person attempts to stop the ritual. The tension and anxiety build to such an intense degree that he surrenders once again to the thoughts or behaviors. Unlike an alcoholic, who feels compelled to drink but also enjoys the drinking experience, the obsessive-compulsive person achieves relief through the ritual, but no pleasure.

We have written a self-help book specifically for anyone suffering from OCD, titled Stop Obsessing! How to Overcome Obsessions and Compulsions, by Dr. Edna Foa and Dr. Reid Wilson (Bantam Books).

Common Features of Obsessions and Compulsions

There are seven common features of obsessions and compulsions. The first three are related to obsessions and worrying in general; the last four are for people who experience both obsessions and compulsions. Find out which ones fit you.

1. Your obsessions involve a concern with disastrous consequences. You are usually afraid that some harm will come to you or others. For instance, you'll forget to lock the doors of your house, and someone will break in and harm your family. Or you'll neglect to thoroughly wash your hands, and you'll develop some dreaded disease. Some people have compulsions, and they don't have that sense of obsession. They don't really know what they're worried about. But usually you will get a sense of dread, like something terrible is going to happen.
2. There are times when you know your obsessions are irrational. Some people believe their worries are accurate reflections of reality, and it's hard for them to get a perspective. But for most people there are times when you know that your worries are senseless. During good times, when you're not under stress, and you're not involved in your ritual or really worried, you can say, "This is crazy. This doesn't make any sense." You know that you're not really going get sick if you fail to wash your hands five times. You don't really believe that your boss will humiliate you if you make one typing error. Nonetheless, when you start to worry, you believe those fearful thoughts.
3. You try to resist your obsessions, but that only makes them worse. You want to get rid of these worries because they cause so much fear. But when you fight these thoughts it often makes them more intense. This gives us a clue to one of the ways we can start to change this negative pattern. If resisting the thoughts makes them worse, what might help lessen them? ...Believe it or not, accepting your fearful thoughts will help lessen them! We'll talk more about acceptance in a few minutes.
4. Compulsive rituals provide you temporary relief. Some people just worry, and they don't have compulsive rituals, so this one wouldn't fit them. But when people do use compulsions, they provide relief and restore a sense of relative safety, even if just for a little while.
5. Your rituals usually involve specific sequences. This means that you often have a set pattern for how you wash, or check or count or think in order to be released from your distressing worries.
6. You try to resist your compulsions too. If your compulsions are brief, and don't interfere with your daily living, then you can probably tolerate them. But if the rituals are inconvenient and take a while to perform, then you probably try to avoid the rituals or to complete them as soon as possible.
7. You seek out others to help with your rituals. Compulsions can be so distressing that you enlist the help of those close to you. You may ask family members to help count for you, or friends to check behind you, or your boss to please read over a letter before you seal it up.

These seven features should give you a better sense of your symptoms.

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Causes

Until recently OCD was regarded as a rare condition, but studies now indicate that up to 3% of the population, or nearly 6 million Americans, will experience an obsessive-compulsive disorder at some point in their life. Symptoms tend to begin in the teen years, or in early adulthood. About one third of people with OCD showed the first signs of a problem in childhood.

Men and women are equally likely to suffer from OCD, although men tend to show symptoms at an earlier age. Cleaning compulsions are more common in women, while men are more likely to be checkers.

No one can say for certain what causes obsessive-compulsive disorder. At one time researchers speculated that OCD resulted from family attitudes or childhood experiences, including harsh discipline by demanding parents. Recent evidence suggest that biological factors may contribute to the development of OCD. Some recent tests have found high rates of OCD in people with Tourette's Syndrome, a disorder marked by muscle tics and uncontrollable blurting of sounds. Many researchers believe this suggests a linkage between OCD and brain disturbances.

There is a tendency for OCD to run in families, and many people with OCD also suffer from depression. The exact relationship between OCD and depression has not been established.

Treatment

There have been great strides in the treatment of OCD in recent years, and many people with the disorder report that their symptoms have been brought under control or eliminated. Traditional psychotherapy, which works by helping an individual analyze his problem, is generally of little value in OCD. But many people with OCD benefit from a form of behavior therapy in which they are gradually exposed to circumstances that trigger their compulsive behavior.

For example, a hand washer might be urged to touch an object she fears is contaminated, and then be discouraged form washing her hands for several hours. The goal is to eliminate or cut down on anxiety and compulsive behavior by convincing the individual with OCD that nothing will happen if she fails to perform the compulsive ritual.

Behavior therapy works best when the feared situation can be easily simulated. It is more difficult if the anxiety-producing situation is hard to create.

Medication can play a prominent role in the treatment of OCD, and is particularly helpful for patients who are bothered by obsessions.

In some cases family therapy can be a valuable supplement to behavior therapy. Family counseling sessions can help both the individual with OCD and his family by increasing understanding and establishing shared goals and expectations.

next: OCD Self-Help Resources for Home
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The following OCD questionnaire will help you identify the types of problems that most trouble you.

Read through the statements listed and note the ones that are true for you. If you note two or more items in any group, this is an indication that you should specifically address those concerns in your self-help program. Don't be surprised if you check more than one item in several groups. Many people have more than one type of OCD symptoms.

(you can't actually write on this page unless you print it out.)

A. What Symptoms Bother You? Note each item that has troubled you in the last month.

Washing and Cleaning

___ 1. I avoid touching certain things because of possible contamination.

___ 2. I have difficulty picking up items that have dropped on the floor.

___ 3. I clean my household excessively.

___ 4. I wash my hands excessively.

___ 5. I often take extremely long showers or baths.

___ 6. I'm overly concerned with germs and diseases.

Checking and Repeating

___ 1. I frequently have to check things over and over again.

___ 2. I have difficulty finishing things because I repeat actions.

___ 3. I often repeat actions in order to prevent something bad from happening.

___ 4. I worry excessively about making mistakes.

___ 5. I worry excessively that someone will get harmed because of me.

___ 6. Certain thoughts that come into my mind make me do things over and over again.

Ordering

___ 1. I must have certain things around me set in a specific order.

___ 2. I spend much time making sure that things are in the right place.

___ 3. I notice immediately when my things are out of place.

___ 4. It is important that my bed is straightened out impeccably.

___ 5. I need to arrange certain things in special patterns.

___ 6. When my things are rearranged by other, I get extremely upset.

Hoarding

___ 1. I have difficulty throwing things away.

___ 2. I find myself bringing home seemingly useless materials.

___ 3. Over the years my home has become cluttered with collections.

___ 4. I do not like other people to touch my possessions.

___ 5. I find myself unable to get rid of things.

___ 6. Other people think my collections are useless.

Thinking Rituals

___ 1. Repeating certain words or numbers in my head makes me feel good.

___ 2. I often have to say certain things to myself again and again in order to feel safe.

___ 3. I find myself spending a lot of time praying for non-religious purposes.

___ 4. "Bad" thoughts force me to think about "good" thoughts.

___ 5. I try to remember events in detail or make mental lists to prevent unpleasant consequences.

___ 6. The only way I can stay calm at times is by thinking the "right" things.

Worries and Pure Obsessions

While I do not engage in any behavioral or thinking rituals:

___ 1. I often get upset by unpleasant thoughts that come into my mind against my will.

___ 2. I usually have doubts about the simple everyday things I do.

___ 3. I have no control over my thoughts.

___ 4. Frequently the things that pop into my mind are shameful, frightening, violent, or bizarre.

___ 5. I'm afraid that my bad thoughts will come true.

___ 6. When I start to worry I cannot easily stop.

___ 7. Little, insignificant events make me worry excessively.

B. In the past month, how much time have you spent, on an average day, engaged in these symptoms. Note the hours or minutes for each.

	Hours	Minutes
Washing and Cleaning
Checking and Repeating
Ordering
Hoarding
Thinking Rituals
Worrying or Obsessing

Now total up the number of hours and minutes you listed in part B. If you spend more than two hours each day obsessing or ritualizing in any type of symptoms, you may need professional help in guiding you through this program. Please contact us if you need a referral.

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Important information about Depakote for women who could become pregnant

See Full Depakote Prescribing Information

About the use of DEPAKOTE® (divalproex sodium) Tablets

Please read this leaflet carefully before you take DEPAKOTE® (divalproex sodium) tablets. This leaflet provides a summary of important information about taking DEPAKOTE to women who could become pregnant. If you have any questions or concerns, or want more information about DEPAKOTE, contact your doctor or pharmacist.

Information For Women Who Could Become Pregnant
DEPAKOTE can be obtained only by prescription from your doctor. The decision to use DEPAKOTE is one that you and your doctor should make together, taking into account your individual needs and medical condition.

Before using DEPAKOTE, women who can become pregnant should consider the fact that DEPAKOTE has been associated with birth defects, in particular, with spina bifida and other defects related to failure of the spinal canal to close normally. Approximately 1 to 2% of children born to women with epilepsy taking DEPAKOTE in the first 12 weeks of pregnancy had these defects (based on data from the Centers for Disease Control, a U.S. agency based in Atlanta). The incidence in the general population is 0.1 to 0.2%.

Information For Women Who Are Planning to Get Pregnant

• Women taking DEPAKOTE who are planning to get pregnant should discuss the treatment options with their doctor.

Information For Women Who Become Pregnant While Taking DEPAKOTE

• If you become pregnant while taking DEPAKOTE you should contact your doctor immediately.

Other Important Information About DEPAKOTE Tablets

• DEPAKOTE tablets should be taken exactly as it is prescribed by your doctor to get the most benefits from DEPAKOTE and reduce the risk of side effects.
• If you have taken more than the prescribed dose of DEPAKOTE, contact your hospital emergency room or local poison center immediately.
• This medication was prescribed for your particular condition. Do not use it for another condition or give the drug to others.

Facts About Birth Defects
It is important to know that birth defects may occur even in children of individuals not taking any medications or without any additional risk factors.

 

This summary provides important information about the use of DEPAKOTE to women who could become pregnant. If you would like more information about the other potential risks and benefits of DEPAKOTE, ask your doctor or pharmacist to let you read the professional labeling and then discuss it with them. If you have any questions or concerns about taking DEPAKOTE, you should discuss them with your doctor.

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Manufactured by Abbott Pharmaceuticals PR Ltd. Barceloneta, PR 00617
Revised 09/2004

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See Full Depakote Prescribing Information

Detailed Info on Signs, Symptoms, Causes, Treatments of Bipolar Disorder

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The information in this monograph is not intended to cover all possible uses, directions, precautions, drug interactions or adverse effects. This information is generalized and is not intended as specific medical advice. If you have questions about the medicines you are taking or would like more information, check with your doctor, pharmacist, or nurse. Last updated 09/2004.

Copyright © 2007 Healthyplace Inc. All rights reserved.

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• Cybersexual Addiction Quiz - A quiz to determine if you are addicted to cybersex or viewing cyberporn.
• Internet Addiction Test - A test for on-line users to determine if they may be addicted to the Internet.
• Test for Obsessive Online Stock Traders - If you think you may spend too much time trading stocks over the Internet, then take this quiz.
• Test for Compulsive Online Gamblers - If you spend too much time at the virtual casinos, then take this quiz to see if you're hooked.
• Test for Online Auction Addiction - Do you spend too much time at eBay or uBid? Does winning the bid mean more than getting the actual item? Then take this quiz to see if you may be addicted to online auction houses.
• The Partner's Addiction Test - A test for spouses or partners of potential Internet addicts.
• The Parent-Child Internet Addiction Test - A guide for parents to evaluate if their son or daughter may be dealing with an addiction to the Internet.

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next:  Are You Addicted to Cybersex?
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Jeffrey Beadle wrote:

Why do you choose to overlook that the disease model of Alcoholism began in the 1700s? It was declared a disease by Dr. Benjamin Rush in Philadelphia, PA and by other doctors in Europe during the same period.

Is it true that Alcoholic's digest and break down Alcohol differently from non Alcoholic's?

Is it controversial that there are some things that science may never fully understand?

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Dear Jeff:

Indeed, Benjamin Rush originated the disease theory of alcoholism in the latter part of the eighteenth century. Do you know that, in his disease theory, it was necessary only to abstain from ardent spirits but not cider or wine? On the downside, do you know that Benjamin Rush conceived of minority political group dissent, lying, and murder as mental illnesses (in the latter cases, at least, anticipating modern developments in psychiatry), and he also defined "negritude" as a special type of leprosy. So, the fact the disease theory was "declared" a disease by the Colonial physician—although not really widely adopted in the U.S. until the Temperance movement promoted Rush's views of the inevitable progression of alcoholism in the middle of the next century—proves. . . . (Incidentally, I maintained your capitalization of "Alcohol" and "Alcoholic" because these remind me of Colonial writings.)

Jeff, the acetaldehyde theory of alcohol breakdown, advanced by James Milam in his widely popular book, Under the Influence, is now not well accepted, even by those who assert a large role for genes in alcoholism. I deal with this in any number of places: see the genetics index of my library, an overview of which I provide in one of my FAQs. I debated Milam at an NIAAA conference in 1988, and it was an eye-opening experience. Mr. Milam, who now calls me a liar, was not well-focused and spent most of his time engaging in ad hominem attacks of Herb Fingarette, who Milam claimed was supposed to be his opponent (after the debate, Enoch Gordis joked to me about Milam's mental state).

Milam's piece de resistance was an impassioned description of the plight of alcoholic Native Americans. However, Native Americans do seem to support well the notion of acetaldehyde explanations for alcoholism, since Asian groups which share the Native American trait of the quick breakdown of alcohol do not share a ready susceptibility to alcoholism.

Your question about things that "science may never fully understand" is very intriguing. I might also say that when people don't really understand something, they seek answers in many places. To me, the resort to half-baked genetic explanations is actually very parallel to the search for angels, psychic revelations, and belief in the afterlife—magical solutions for irresolvable human problems which it depresses people to think we cannot solve.

Very best,
Stanton

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Brand Name: Strattera
Generic Name: Atomoxetine HCI

Strattera is a non-amphetamine medication for treatment of ADHD in children, adolescents and adults. Usage, dosage, side effects of Strattera.

Strattera Medication Guide
Strattera Patient Information

Contents:

Box Warning
Description
Clinical Pharmacology
Indications and Usage
Contraindications
Warnings
Precautions
Drug Interactions
Adverse Reactions
Drug Abuse and Dependence
Overdose
Dosage and Administration
Supplied

Strattera Patient Information (in plain English)

Warning

Suicidal Ideation in Children and Adolescents - STRATTERA (atomoxetine) increased the risk of suicidal ideation in short-term studies in children or adolescents with Attention-Deficit/Hyperactivity Disorder (ADHD). Anyone considering the use of STRATTERA in a child or adolescent must balance this risk with the clinical need. Patients who are started on therapy should be monitored closely for suicidality (suicidal thinking and behavior), clinical worsening, or unusual changes in behavior. Families and caregivers should be advised of the need for close observation and communication with the prescriber. STRATTERA is approved for ADHD in pediatric and adult patients. STRATTERA is not approved for major depressive disorder. Pooled analyses of short-term (6 to 18 weeks) placebo-controlled trials of STRATTERA in children and adolescents (a total of 12 trials involving over 2200 patients, including 11 trials in ADHD and 1 trial in enuresis) have revealed a greater risk of suicidal ideation early during treatment in those receiving STRATTERA compared to placebo. The average risk of suicidal ideation in patients receiving STRATTERA was 0.4% (5/1357 patients), compared to none in placebo-treated patients (851 patients). No suicides occurred in these trials. (See WARNINGS and PRECAUTIONS, Pediatric Use).

 

Description

STRATTERA® (atomoxetine HCl) is a selective norepinephrine reuptake inhibitor. Atomoxetine HCl is the R(-) isomer as determined by x-ray diffraction. The chemical designation is (-)-N-Methyl-3-phenyl-3-(o-tolyloxy)-propylamine hydrochloride. The molecular formula is C17H21NO-HCl, which corresponds to a molecular weight of 291.82. The chemical structure is:

Atomoxetine HCl is a white to practically white solid, which has a solubility of 27.8 mg/mL in water. OCH3NHCH3-HCl

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STRATTERA capsules are intended for oral administration only.

Each capsule contains atomoxetine HCl equivalent to 10, 18, 25, 40, 60, 80, or 100 mg of atomoxetine. The capsules also contain pregelatinized starch and dimethicone. The capsule shells contain gelatin, sodium lauryl sulfate, and other inactive ingredients. The capsule shells also contain one or more of the following: FD&C Blue No. 2, synthetic yellow iron oxide, titanium dioxide, red iron oxide. The capsules are imprinted with edible black ink.

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Clinical Pharmacology

Pharmacodynamics and Mechanism of Action

The precise mechanism by which atomoxetine produces its therapeutic effects in Attention-Deficit/Hyperactivity Disorder (ADHD) is unknown, but is thought to be related to selective inhibition of the pre-synaptic norepinephrine transporter, as determined in ex vivo uptake and neurotransmitter depletion studies.

Human Pharmacokinetics

Atomoxetine is well-absorbed after oral administration and is minimally affected by food. It is eliminated primarily by oxidative metabolism through the cytochrome P450 2D6 (CYP2D6) enzymatic pathway and subsequent glucuronidation. Atomoxetine has a half-life of about 5 hours. A fraction of the population (about 7% of Caucasians and 2% of African Americans) are poor metabolizers (PMs) of CYP2D6 metabolized drugs. These individuals have reduced activity in this pathway resulting in 10-fold higher AUCs, 5-fold higher peak plasma concentrations, and slower elimination (plasma half-life of about 24 hours) of atomoxetine compared with people with normal activity [extensive metabolizers (EMs)]. Drugs that inhibit CYP2D6, such as fluoxetine, paroxetine, and quinidine, cause similar increases in exposure.

The pharmacokinetics of atomoxetine have been evaluated in more than 400 children and adolescents in selected clinical trials, primarily using population pharmacokinetic studies. Single-dose and steady-state individual pharmacokinetic data were also obtained in children, adolescents, and adults. When doses were normalized to a mg/kg basis, similar half-life, Cmax, and AUC values were observed in children, adolescents, and adults. Clearance and volume of distribution after adjustment for body weight were also similar.

Absorption and distribution - Atomoxetine is rapidly absorbed after oral administration, with absolute bioavailability of about 63% in EMs and 94% in PMs. Maximal plasma concentrations (C_max) are reached approximately 1 to 2 hours after dosing.

STRATTERA can be administered with or without food. Administration of STRATTERA with a standard high-fat meal in adults did not affect the extent of oral absorption of atomoxetine (AUC), but did decrease the rate of absorption, resulting in a 37% lower C_max, and delayed Tmax by 3 hours. In clinical trials with children and adolescents, administration of STRATTERA with food resulted in a 9% lower C_max.

The steady-state volume of distribution after intravenous administration is 0.85 L/kg indicating that atomoxetine distributes primarily into total body water. Volume of distribution is similar across the patient weight range after normalizing for body weight.

At therapeutic concentrations, 98% of atomoxetine in plasma is bound to protein, primarily albumin.

Metabolism and elimination - Atomoxetine is metabolized primarily through the CYP2D6 enzymatic pathway. People with reduced activity in this pathway (PMs) have higher plasma concentrations of atomoxetine compared with people with normal activity (EMs). For PMs, AUC of atomoxetine is approximately 10-fold and Css,max is about 5-fold greater than EMs. Laboratory tests are available to identify CYP2D6 PMs. Coadministration of STRATTERA with potent inhibitors of CYP2D6, such as fluoxetine, paroxetine, or quinidine, results in a substantial increase in atomoxetine plasma exposure, and dosing adjustment may be necessary (see Drug-Drug Interactions). Atomoxetine did not inhibit or induce the CYP2D6 pathway.

The major oxidative metabolite formed, regardless of CYP2D6 status, is 4-hydroxyatomoxetine, which is glucuronidated. 4-Hydroxyatomoxetine is equipotent to atomoxetine as an inhibitor of the norepinephrine transporter but circulates in plasma at much lower concentrations (1% of atomoxetine concentration in EMs and 0.1% of atomoxetine concentration in PMs). 4-Hydroxyatomoxetine is primarily formed by CYP2D6, but in PMs, 4-hydroxyatomoxetine is formed at a slower rate by several other cytochrome P450 enzymes. N-Desmethylatomoxetine is formed by CYP2C19 and other cytochrome P450 enzymes, but has substantially less pharmacological activity compared with atomoxetine and circulates in plasma at lower concentrations (5% of atomoxetine concentration in EMs and 45% of atomoxetine concentration in PMs).

Mean apparent plasma clearance of atomoxetine after oral administration in adult EMs is 0.35 L/hr/kg and the mean half-life is 5.2 hours. Following oral administration of atomoxetine to PMs, mean apparent plasma clearance is 0.03 L/hr/kg and mean half-life is 21.6 hours. For PMs, AUC of atomoxetine is approximately 10-fold and Css,max is about 5-fold greater than EMs. The elimination half-life of 4-hydroxyatomoxetine is similar to that of N-desmethylatomoxetine (6 to 8 hours) in EM subjects, while the half-life of N-desmethylatomoxetine is much longer in PM subjects (34 to 40 hours).

Atomoxetine is excreted primarily as 4-hydroxyatomoxetine-O-glucuronide, mainly in the urine (greater than 80% of the dose) and to a lesser extent in the feces (less than 17% of the dose). Only a small fraction of the STRATTERA dose is excreted as unchanged atomoxetine (less than 3% of the dose), indicating extensive biotransformation.

Special Populations

Hepatic insufficiency - Atomoxetine exposure (AUC) is increased, compared with normal subjects, in EM subjects with moderate (Child-Pugh Class B) (2-fold increase) and severe (Child-Pugh Class C) (4-fold increase) hepatic insufficiency. Dosage adjustment is recommended for patients with moderate or severe hepatic insufficiency (see DOSAGE AND ADMINISTRATION).

Renal insufficiency - EM subjects with end stage renal disease had higher systemic exposure to atomoxetine than healthy subjects (about a 65% increase), but there was no difference when exposure was corrected for mg/kg dose. STRATTERA can therefore be administered to ADHD patients with end stage renal disease or lesser degrees of renal insufficiency using the normal dosing regimen.

Geriatric - The pharmacokinetics of atomoxetine have not been evaluated in the geriatric population.

Pediatric - The pharmacokinetics of atomoxetine in children and adolescents are similar to those in adults. The pharmacokinetics of atomoxetine have not been evaluated in children under 6 years of age.

Gender - Gender did not influence atomoxetine disposition.

Ethnic origin - Ethnic origin did not influence atomoxetine disposition (except that PMs are more common in Caucasians).

Drug-Drug Interactions

CYP2D6 activity and atomoxetine plasma concentration - Atomoxetine is primarily metabolized by the CYP2D6 pathway to 4-hydroxyatomoxetine. In EMs, inhibitors of CYP2D6 increase atomoxetine steady-state plasma concentrations to exposures similar to those observed in PMs. Dosage adjustment of STRATTERA in EMs may be necessary when coadministered with CYP2D6 inhibitors, e.g., paroxetine, fluoxetine, and quinidine (see Drug-Drug Interactions under PRECAUTIONS). In vitro studies suggest that coadministration of cytochrome P450 inhibitors to PMs will not increase the plasma concentrations of atomoxetine.

Effect of atomoxetine on P450 enzymes - Atomoxetine did not cause clinically important inhibition or induction of cytochrome P450 enzymes, including CYP1A2, CYP3A, CYP2D6, and CYP2C9.

Albuterol - Albuterol (600 mcg iv over 2 hours) induced increases in heart rate and blood pressure. These effects were potentiated by atomoxetine (60 mg BID for 5 days) and were most marked after the initial coadministration of albuterol and atomoxetine (see Drug-Drug Interactions under PRECAUTIONS).

Alcohol - Consumption of ethanol with STRATTERA did not change the intoxicating effects of ethanol.

Desipramine - Coadministration of STRATTERA (40 or 60 mg BID for 13 days) with desipramine, a model compound for CYP2D6 metabolized drugs (single dose of 50 mg), did not alter the pharmacokinetics of desipramine. No dose adjustment is recommended for drugs metabolized by CYP2D6.

Methylphenidate - Coadministration of methylphenidate with STRATTERA did not increase cardiovascular effects beyond those seen with methylphenidate alone.

Midazolam - Coadministration of STRATTERA (60 mg BID for 12 days) with midazolam, a model compound for CYP3A4 metabolized drugs (single dose of 5 mg), resulted in 15% increase in AUC of midazolam. No dose adjustment is recommended for drugs metabolized by CYP3A.

Drugs highly bound to plasma protein - In vitro drug-displacement studies were conducted with atomoxetine and other highly-bound drugs at therapeutic concentrations. Atomoxetine did not affect the binding of warfarin, acetylsalicylic acid, phenytoin, or diazepam to human albumin. Similarly, these compounds did not affect the binding of atomoxetine to human albumin.

Drugs that affect gastric pH - Drugs that elevate gastric pH (magnesium hydroxide/aluminum hydroxide, omeprazole) had no effect on STRATTERA bioavailability.

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Clinical Studies

The effectiveness of STRATTERA in the treatment of ADHD was established in 6 randomized, double-blind, placebo-controlled studies in children, adolescents, and adults who met Diagnostic and Statistical Manual 4th edition (DSM-IV) criteria for ADHD (see INDICATIONS AND USAGE).

Children and Adolescents

The effectiveness of STRATTERA in the treatment of ADHD was established in 4 randomized, double-blind, placebo-controlled studies of pediatric patients (ages 6 to 18). Approximately one-third of the patients met DSM-IV criteria for inattentive subtype and two-thirds met criteria for both inattentive and hyperactive/impulsive subtypes (see INDICATIONS AND USAGE).

Signs and symptoms of ADHD were evaluated by a comparison of mean change from baseline to endpoint for STRATTERA- and placebo-treated patients using an intent-to-treat analysis of the primary outcome measure, the investigator administered and scored ADHD Rating Scale-IV-Parent Version (ADHDRS) total score including hyperactive/impulsive and inattentive subscales. Each item on the ADHDRS maps directly to one symptom criterion for ADHD in the DSM-IV.

In Study 1, an 8-week randomized, double-blind, placebo-controlled, dose-response, acute treatment study of children and adolescents aged 8 to 18 (N=297), patients received either a fixed dose of STRATTERA (0.5, 1.2, or 1.8 mg/kg/day) or placebo. STRATTERA was administered as a divided dose in the early morning and late afternoon/early evening. At the 2 higher doses, improvements in ADHD symptoms were statistically significantly superior in STRATTERA-treated patients compared with placebo-treated patients as measured on the ADHDRS scale. The 1.8-mg/kg/day STRATTERA dose did not provide any additional benefit over that observed with the 1.2-mg/kg/day dose. The 0.5-mg/kg/day STRATTERA dose was not superior to placebo.

In Study 2, a 6-week randomized, double-blind, placebo-controlled, acute treatment study of children and adolescents aged 6 to 16 (N=171), patients received either STRATTERA or placebo. STRATTERA was administered as a single dose in the early morning and titrated on a weight-adjusted basis according to clinical response, up to a maximum dose of 1.5 mg/kg/day. The mean final dose of STRATTERA was approximately 1.3 mg/kg/day. ADHD symptoms were statistically significantly improved on STRATTERA compared with placebo, as measured on the ADHDRS scale. This study shows that STRATTERA is effective when administered once daily in the morning.

In 2 identical, 9-week, acute, randomized, double-blind, placebo-controlled studies of children aged 7 to 13 (Study 3, N=147; Study 4, N=144), STRATTERA and methylphenidate were compared with placebo. STRATTERA was administered as a divided dose in the early morning and late afternoon (after school) and titrated on a weight-adjusted basis according to clinical response. The maximum recommended STRATTERA dose was 2.0 mg/kg/day. The mean final dose of STRATTERA for both studies was approximately 1.6 mg/kg/day. In both studies, ADHD symptoms statistically significantly improved more on STRATTERA than on placebo, as measured on the ADHDRS scale.

In 2 identical, 9-week, acute, randomized, double-blind, placebo-controlled studies of children aged 7 to 13 (Study 3, N=147; Study 4, N=144), STRATTERA and methylphenidate were compared with placebo. STRATTERA was administered as a divided dose in the early morning and late afternoon (after school) and titrated on a weight-adjusted basis according to clinical response. The maximum recommended STRATTERA dose was 2.0 mg/kg/day. The mean final dose of STRATTERA for both studies was approximately 1.6 mg/kg/day. In both studies, ADHD symptoms statistically significantly improved more on STRATTERA than on placebo, as measured on the ADHDRS scale.

Adults

The effectiveness of STRATTERA in the treatment of ADHD was established in 2 randomized, double-blind, placebo-controlled clinical studies of adult patients, age 18 and older, who met DSM-IV criteria for ADHD.

Signs and symptoms of ADHD were evaluated using the investigator-administered Conners Adult ADHD Rating Scale Screening Version (CAARS), a 30-item scale. The primary effectiveness measure was the 18-item Total ADHD Symptom score (the sum of the inattentive and hyperactivity/impulsivity subscales from the CAARS) evaluated by a comparison of mean change from baseline to endpoint using an intent-to-treat analysis.

In 2 identical, 10-week, randomized, double-blind, placebo-controlled acute treatment studies (Study 5, N=280; Study 6, N=256), patients received either STRATTERA or placebo.

STRATTERA was administered as a divided dose in the early morning and late afternoon/early evening and titrated according to clinical response in a range of 60 to 120 mg/day. The mean final dose of STRATTERA for both studies was approximately 95 mg/day. In both studies, ADHD symptoms were statistically significantly improved on STRATTERA, as measured on the ADHD Symptom score from the CAARS scale.

Examination of population subsets based on gender and age (<42 and ≥42) did not reveal any differential responsiveness on the basis of these subgroupings. There was not sufficient exposure of ethnic groups other than Caucasian to allow exploration of differences in these subgroups.

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Indications and Usage

STRATTERA is indicated for the treatment of Attention-Deficit/Hyperactivity Disorder (ADHD).

The effectiveness of STRATTERA in the treatment of ADHD was established in 2 placebo-controlled trials in children, 2 placebo-controlled trials in children and adolescents, and 2 placebo-controlled trials in adults who met DSM-IV criteria for ADHD (see CLINICAL STUDIES).

A diagnosis of ADHD (DSM-IV) implies the presence of hyperactive-impulsive or inattentive symptoms that cause impairment and that were present before age 7 years. The symptoms must be persistent, must be more severe than is typically observed in individuals at a comparable level of development, must cause clinically significant impairment, e.g., in social, academic, or occupational functioning, and must be present in 2 or more settings, e.g., school (or work) and at home. The symptoms must not be better accounted for by another mental disorder. For the Inattentive Type, at least 6 of the following symptoms must have persisted for at least 6 months: lack of attention to details/careless mistakes, lack of sustained attention, poor listener, failure to follow through on tasks, poor organization, avoids tasks requiring sustained mental effort, loses things, easily distracted, forgetful. For the Hyperactive-Impulsive Type, at least 6 of the following symptoms must have persisted for at least 6 months: fidgeting/squirming, leaving seat, inappropriate running/climbing, difficulty with quiet activities, "on the go," excessive talking, blurting answers, can't wait turn, intrusive. For a Combined Type diagnosis, both inattentive and hyperactive-impulsive criteria must be met.

Special Diagnostic Considerations

The specific etiology of ADHD is unknown, and there is no single diagnostic test. Adequate diagnosis requires the use not only of medical but also of special psychological, educational, and social resources. Learning may or may not be impaired. The diagnosis must be based upon a complete history and evaluation of the patient and not solely on the presence of the required number of DSM-IV characteristics.

Need for Comprehensive Treatment Program

STRATTERA is indicated as an integral part of a total treatment program for ADHD that may include other measures (psychological, educational, social) for patients with this syndrome. Drug treatment may not be indicated for all patients with this syndrome. Drug treatment is not intended for use in the patient who exhibits symptoms secondary to environmental factors and/or other primary psychiatric disorders, including psychosis. Appropriate educational placement is essential in children and adolescents with this diagnosis and psychosocial intervention is often helpful. When remedial measures alone are insufficient, the decision to prescribe drug treatment medication will depend upon the physician's assessment of the chronicity and severity of the patient's symptoms.

Long-Term Use

The effectiveness of STRATTERA for long-term use, i.e., for more than 9 weeks in child and adolescent patients and 10 weeks in adult patients, has not been systematically evaluated in controlled trials. Therefore, the physician who elects to use STRATTERA for extended periods should periodically reevaluate the long-term usefulness of the drug for the individual patient (see DOSAGE AND ADMINISTRATION).

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Contraindications

Hypersensitivity

STRATTERA is contraindicated in patients known to be hypersensitive to atomoxetine or other constituents of the product (see WARNINGS).

Monoamine Oxidase Inhibitors (MAOI) STRATTERA should not be taken with an MAOI, or within 2 weeks after discontinuing an MAOI. Treatment with an MAOI should not be initiated within 2 weeks after discontinuing STRATTERA. With other drugs that affect brain monoamine concentrations, there have been reports of serious, sometimes fatal reactions (including hyperthermia, rigidity, myoclonus, autonomic instability with possible rapid fluctuations of vital signs, and mental status changes that include extreme agitation progressing to delirium and coma) when taken in combination with an MAOI. Some cases presented with features resembling neuroleptic malignant syndrome. Such reactions may occur when these drugs are given concurrently or in close proximity.

Narrow Angle Glaucoma

In clinical trials, STRATTERA use was associated with an increased risk of mydriasis and therefore its use is not recommended in patients with narrow angle glaucoma.

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Warnings

Suicidal Ideation

STRATTERA increased the risk of suicidal ideation in short-term studies in children and adolescents with Attention-Deficit/Hyperactivity Disorder (ADHD). Pooled analyses of short-term (6 to 18 weeks) placebo-controlled trials of STRATTERA in children and adolescents have revealed a greater risk of suicidal ideation early during treatment in those receiving STRATTERA. There were a total of 12 trials (11 in ADHD and 1 in enuresis) involving over 2200 patients (including 1357 patients receiving STRATTERA and 851 receiving placebo). The average risk of suicidal ideation in patients receiving STRATTERA was 0.4% (5/1357 patients), compared to none in placebo-treated patients. There was 1 suicide attempt among these approximately 2200 patients, occurring in a patient treated with STRATTERA. No suicides occurred in these trials. All events occurred in children 12 years of age or younger. All events occurred during the first month of treatment. It is unknown whether the risk of suicidal ideation in pediatric patients extends to longer-term use. A similar analysis in adult patients treated with STRATTERA for either ADHD or major depressive disorder (MDD) did not reveal an increased risk of suicidal ideation or behavior in association with the use of STRATTERA.

All pediatric patients being treated with STRATTERA should be monitored closely for suicidality, clinical worsening, and unusual changes in behavior, especially during the initial few months of a course of drug therapy, or at times of dose changes. Such monitoring would generally include at least weekly face-to-face contact with patients or their family members or caregivers during the first 4 weeks of treatment, then every other week visits for the next 4 weeks, then at 12 weeks, and as clinically indicated beyond 12 weeks. Additional contact by telephone may be appropriate between face-to-face visits.

The following symptoms have been reported with STRATTERA: anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hypomania and mania. Although a causal link between the emergence of such symptoms and the emergence of suicidal impulses has not been established, there is a concern that such symptoms may represent precursors to emerging suicidality. Thus, patients being treated with STRATTERA should be observed for the emergence of such symptoms.

Consideration should be given to changing the therapeutic regimen, including possibly discontinuing the medication, in patients who are experiencing emergent suicidality or symptoms that might be precursors to emerging suicidality, especially if these symptoms are severe or abrupt in onset, or were not part of the patient's presenting symptoms.

Families and caregivers of pediatric patients being treated with STRATTERA should be alerted about the need to monitor patients for the emergence of agitation, irritability, unusual changes in behavior, and the other symptoms described above, as well as the emergence of suicidality, and to report such symptoms immediately to healthcare providers. Such monitoring should include daily observation by families and caregivers.

Screening Patients for Bipolar Disorder - In general, particular care should be taken in treating ADHD in patients with comorbid bipolar disorder because of concern for possible induction of a mixed/manic episode in patients at risk for bipolar disorder. Whether any of the symptoms described above represent such a conversion is unknown. However, prior to initiating treatment with STRATTERA, patients with comorbid depressive symptoms should be adequately screened to determine if they are at risk for bipolar disorder; such screening should include a detailed psychiatric history, including a family history of suicide, bipolar disorder, and depression.

Severe Liver Injury

Postmarketing reports indicate that STRATTERA can cause severe liver injury in rare cases. Although no evidence of liver injury was detected in clinical trials of about 6000 patients, there have been two reported cases of markedly elevated hepatic enzymes and bilirubin, in the absence of other obvious explanatory factors, out of more than 2 million patients during the first two years of postmarketing experience. In one patient, liver injury, manifested by elevated hepatic enzymes (up to 40 X upper limit of normal (ULN)) and jaundice (bilirubin up to 12 X ULN), recurred upon rechallenge, and was followed by recovery upon drug discontinuation providing evidence that STRATTERA caused the liver injury. Such reactions may occur several months after therapy is started, but laboratory abnormalities may continue to worsen for several weeks after drug is stopped. Because of probable underreporting, it is impossible to provide an accurate estimate of the true incidence of these events. The patients described above recovered from their liver injury, and did not require a liver transplant. However, in a small percentage of patients, severe drug-related liver injury may progress to acute liver failure resulting in death or the need for a liver transplant.

STRATTERA should be discontinued in patients with jaundice or laboratory evidence of liver injury, and should not be restarted. Laboratory testing to determine liver enzyme levels should be done upon the first symptom or sign of liver dysfunction (e.g., pruritus, dark urine, jaundice, right upper quadrant tenderness, or unexplained "flu-like" symptoms). (See also Information for Patients under PRECAUTIONS.)

Allergic Events

Although uncommon, allergic reactions, including angioneurotic edema, urticaria, and rash, have been reported in patients taking STRATTERA.

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Precautions

General

Effects on blood pressure and heart rate - STRATTERA should be used with caution in patients with hypertension, tachycardia, or cardiovascular or cerebrovascular disease because it can increase blood pressure and heart rate. Pulse and blood pressure should be measured at baseline, following STRATTERA dose increases, and periodically while on therapy.

In pediatric placebo-controlled trials, STRATTERA-treated subjects experienced a mean increase in heart rate of about 6 beats/minute compared with placebo subjects. At the final study visit before drug discontinuation, 3.6% (12/335) of STRATTERA-treated subjects had heart rate increases of at least 25 beats/minute and a heart rate of at least 110 beats/minute, compared with 0.5% (1/204) of placebo subjects. No pediatric subject had a heart rate increase of at least 25 beats/minute and a heart rate of at least 110 beats/minute on more than one occasion. Tachycardia was identified as an adverse event for 1.5% (5/340) of these pediatric subjects compared with 0.5% (1/207) of placebo subjects. The mean heart rate increase in extensive metabolizer (EM) patients was 6.7 beats/minute, and in poor metabolizer (PM) patients 10.4 beats/minute.

STRATTERA-treated pediatric subjects experienced mean increases of about 1.5 mm Hg in systolic and diastolic blood pressures compared with placebo. At the final study visit before drug discontinuation, 6.8% (22/324) of STRATTERA-treated pediatric subjects had high systolic blood pressure measurements compared with 3.0% (6/197) of placebo subjects. High systolic blood pressures were measured on 2 or more occasions in 8.6% (28/324) of STRATTERA-treated subjects and 3.6% (7/197) of placebo subjects. At the final study visit before drug discontinuation, 2.8% (9/326) of STRATTERA-treated pediatric subjects had high diastolic blood pressure measurements compared with 0.5% (1/200) of placebo subjects. High diastolic blood pressures were measured on 2 or more occasions in 5.2% (17/326) of STRATTERA-treated subjects and 1.5% (3/200) of placebo subjects. (High systolic and diastolic blood pressure measurements were defined as those exceeding the 95th percentile, stratified by age, gender, and height percentile - National High Blood Pressure Education Working Group on Hypertension Control in Children and Adolescents.)

In adult placebo-controlled trials, STRATTERA-treated subjects experienced a mean increase in heart rate of 5 beats/minute compared with placebo subjects. Tachycardia was identified as an adverse event for 3% (8/269) of these adult atomoxetine subjects compared with 0.8% (2/263) of placebo subjects.

STRATTERA-treated adult subjects experienced mean increases in systolic (about 3 mm Hg) and diastolic (about 1 mm Hg) blood pressures compared with placebo. At the final study visit before drug discontinuation, 1.9% (5/258) of STRATTERA-treated adult subjects had systolic blood pressure measurements ≥150 mm Hg compared with 1.2% (3/256) of placebo subjects. At the final study visit before drug discontinuation, 0.8% (2/257) of STRATTERA-treated adult subjects had diastolic blood pressure measurements ≥100 mm Hg compared with 0.4% (1/257) of placebo subjects. No adult subject had a high systolic or diastolic blood pressure detected on more than one occasion.

Orthostatic hypotension has been reported in subjects taking STRATTERA. In short-term, child- and adolescent-controlled trials, 1.8% (6/340) of STRATTERA-treated subjects experienced symptoms of postural hypotension compared with 0.5% (1/207) of placebo-treated subjects. STRATTERA should be used with caution in any condition that may predispose patients to hypotension.

Effects on urine outflow from the bladder - In adult ADHD controlled trials, the rates of urinary retention (3%, 7/269) and urinary hesitation (3%, 7/269) were increased among atomoxetine subjects compared with placebo subjects (0%, 0/263). Two adult atomoxetine subjects and no placebo subjects discontinued from controlled clinical trials because of urinary retention. A complaint of urinary retention or urinary hesitancy should be considered potentially related to atomoxetine.

Effects on Growth - Data on the long-term effects of STRATTERA on growth come from open-label studies, and weight and height changes are compared to normative population data. In general, the weight and height gain of pediatric patients treated with STRATTERA lags behind that predicted by normative population data for about the first 9-12 months of treatment. Subsequently, weight gain rebounds and at about 3 years of treatment, patients treated with STRATTERA have gained 17.9 kg on average, 0.5 kg more than predicted by their baseline data. After about 12 months, gain in height stabilizes, and at 3 years, patients treated with STRATTERA have gained 19.4 cm on average, 0.4 cm less than predicted by their baseline data (see Figure 1 below).

Figure 1: Mean Weight and Height Percentiles Over Time for Patients With Three Years of STRATTERA Treatment

This growth pattern was generally similar regardless of pubertal status at the time of treatment initiation. Patients who were pre-pubertal at the start of treatment (girls ≤8 years old, boys ≤9 years old) gained an average of 2.1 kg and 1.2 cm less than predicted after three years. Patients who were pubertal (girls >8 to ≤13 years old, boys >9 to ≤14 years old) or late pubertal (girls >13 years old, boys >14 years old) had average weight and height gains that were close to or exceeded those predicted after three years of treatment.

Growth followed a similar pattern in both extensive and poor metabolizers (EMs, PMs). PMs treated for at least two years gained an average of 2.4 kg and 1.1 cm less than predicted, while EMs gained an average of 0.2 kg and 0.4 cm less than predicted.

In short-term controlled studies (up to 9 weeks), STRATTERA-treated patients lost an average of 0.4 kg and gained an average of 0.9 cm, compared to a gain of 1.5 kg and 1.1 cm in the placebo-treated patients. In a fixed-dose controlled trial, 1.3%, 7.1%, 19.3%, and 29.1% of patients lost at least 3.5% of their body weight in the placebo, 0.5, 1.2, and 1.8 mg/kg/day dose groups.

Growth should be monitored during treatment with STRATTERA.

Aggressive Behavior or Hostility - Aggressive behavior or hostility is often observed in children and adolescents with ADHD, and has been reported in clinical trials and the postmarketing experience of some medications indicated for the treatment of ADHD. Although there is no conclusive evidence that STRATTERA causes aggressive behavior or hostility, aggressive behavior or hostility was more frequently observed in clinical trials among children and adolescents treated with STRATTERA compared to placebo (overall risk ratio of 1.33 - not statistically significant). Patients beginning treatment for ADHD should be monitored for the appearance of or worsening of aggressive behavior or hostility.

Information for Patients

Prescribers or other health professionals should inform patients, their families, and their caregivers about the benefits and risks associated with treatment with STRATTERA and should counsel them in its appropriate use. A patient Medication Guide about using STRATTERA is available. The prescriber or health professional should instruct patients, their families, and their caregivers to read the Medication Guide and should assist them in understanding its contents. Patients should be given the opportunity to discuss the contents of the Medication Guide and to obtain answers to any questions they may have. The complete text of the Medication Guide is reprinted at the end of this document.

Patients should be advised of the following issues and asked to alert their prescriber if these occur while taking STRATTERA.

Suicide Risk - Patients, their families, and their caregivers should be encouraged to be alert to the emergence of anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hypomania, mania, other unusual changes in behavior, depression, and suicidal ideation, especially early during STRATTERA treatment and when the dose is adjusted. Families and caregivers of patients should be advised to observe for the emergence of such symptoms on a day-to-day basis, since changes may be abrupt. Such symptoms should be reported to the patient's prescriber or health professional, especially if they are severe, abrupt in onset, or were not part of the patient's presenting symptoms. Symptoms such as these may be associated with an increased risk for suicidal thinking and behavior and indicate a need for very close monitoring and possibly changes in the medication.

Patients initiating STRATTERA should be cautioned that liver dysfunction may develop rarely. Patients should be instructed to contact their physician immediately should they develop pruritus, dark urine, jaundice, right upper quadrant tenderness, or unexplained "flu-like" symptoms.

Patients should be instructed to call their doctor as soon as possible should they notice an increase in aggression or hostility.

STRATTERA is an ocular irritant. STRATTERA capsules are not intended to be opened. In the event of capsule content coming in contact with the eye, the affected eye should be flushed immediately with water, and medical advice obtained. Hands and any potentially contaminated surfaces should be washed as soon as possible.

Patients should consult a physician if they are taking or plan to take any prescription or over-the-counter medicines, dietary supplements, or herbal remedies.

Patients should consult a physician if they are nursing, pregnant, or thinking of becoming pregnant while taking STRATTERA.

Patients may take STRATTERA with or without food.

If patients miss a dose, they should take it as soon as possible, but should not take more than the prescribed total daily amount of STRATTERA in any 24-hour period.

Patients should use caution when driving a car or operating hazardous machinery until they are reasonably certain that their performance is not affected by atomoxetine.

Laboratory Tests

Routine laboratory tests are not required.

CYP2D6 metabolism - Poor metabolizers (PMs) of CYP2D6 have a 10-fold higher AUC and a 5-fold higher peak concentration to a given dose of STRATTERA compared with extensive metabolizers (EMs). Approximately 7% of a Caucasian population are PMs. Laboratory tests are available to identify CYP2D6 PMs. The blood levels in PMs are similar to those attained by taking strong inhibitors of CYP2D6. The higher blood levels in PMs lead to a higher rate of some adverse effects of STRATTERA (see ADVERSE REACTIONS).

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Drug Interactions

Albuterol - STRATTERA should be administered with caution to patients being treated with systemically-administered (oral or intravenous) albuterol (or other beta2 agonists) because the action of albuterol on the cardiovascular system can be potentiated resulting in increases in heart rate and blood pressure.

CYP2D6 inhibitors - Atomoxetine is primarily metabolized by the CYP2D6 pathway to 4-hydroxyatomoxetine. In EMs, selective inhibitors of CYP2D6 increase atomoxetine steady-state plasma concentrations to exposures similar to those observed in PMs. Dosage adjustment of STRATTERA may be necessary when coadministered with CYP2D6 inhibitors, e.g., paroxetine, fluoxetine, and quinidine (see DOSAGE AND ADMINISTRATION). In EM individuals treated with paroxetine or fluoxetine, the AUC of atomoxetine is approximately 6- to 8-fold and Css,max is about 3- to 4-fold greater than atomoxetine alone.

In vitro studies suggest that coadministration of cytochrome P450 inhibitors to PMs will not increase the plasma concentrations of atomoxetine.

Monoamine oxidase inhibitors - See CONTRAINDICATIONS.

Pressor agents - Because of possible effects on blood pressure, STRATTERA should be used cautiously with pressor agents.

Carcinogenesis, Mutagenesis, Impairment of Fertility

Carcinogenesis -Atomoxetine HCl was not carcinogenic in rats and mice when given in the diet for 2 years at time-weighted average doses up to 47 and 458 mg/kg/day, respectively. The highest dose used in rats is approximately 8 and 5 times the maximum human dose in children and adults, respectively, on a mg/m2 basis. Plasma levels (AUC) of atomoxetine at this dose in rats are estimated to be 1.8 times (extensive metabolizers) or 0.2 times (poor metabolizers) those in humans receiving the maximum human dose. The highest dose used in mice is approximately 39 and 26 times the maximum human dose in children and adults, respectively, on a mg/m2 basis.

Mutagenesis - Atomoxetine HCl was negative in a battery of genotoxicity studies that included a reverse point mutation assay (Ames Test), an in vitro mouse lymphoma assay, a chromosomal aberration test in Chinese hamster ovary cells, an unscheduled DNA synthesis test in rat hepatocytes, and an in vivo micronucleus test in mice. However, there was a slight increase in the percentage of Chinese hamster ovary cells with diplochromosomes, suggesting endoreduplication (numerical aberration).

The metabolite N-desmethylatomoxetine HCl was negative in the Ames Test, mouse lymphoma assay, and unscheduled DNA synthesis test.

Impairment of fertility - Atomoxetine HCl did not impair fertility in rats when given in the diet at doses of up to 57 mg/kg/day, which is approximately 6 times the maximum human dose on a mg/m2 basis.

Pregnancy

Pregnancy Category C - Pregnant rabbits were treated with up to 100 mg/kg/day of atomoxetine by gavage throughout the period of organogenesis. At this dose, in 1 of 3 studies, a decrease in live fetuses and an increase in early resorptions was observed. Slight increases in the incidences of atypical origin of carotid artery and absent subclavian artery were observed. These findings were observed at doses that caused slight maternal toxicity. The no-effect dose for these findings was 30 mg/kg/day. The 100-mg/kg dose is approximately 23 times the maximum human dose on a mg/m2 basis; plasma levels (AUC) of atomoxetine at this dose in rabbits are estimated to be 3.3 times (extensive metabolizers) or 0.4 times (poor metabolizers) those in humans receiving the maximum human dose.

Rats were treated with up to approximately 50 mg/kg/day of atomoxetine (approximately 6 times the maximum human dose on a mg/m2 basis) in the diet from 2 weeks (females) or 10 weeks (males) prior to mating through the periods of organogenesis and lactation. In 1 of 2 studies, decreases in pup weight and pup survival were observed. The decreased pup survival was also seen at 25 mg/kg (but not at 13 mg/kg). In a study in which rats were treated with atomoxetine in the diet from 2 weeks (females) or 10 weeks (males) prior to mating throughout the period of organogenesis, a decrease in fetal weight (female only) and an increase in the incidence of incomplete ossification of the vertebral arch in fetuses were observed at 40 mg/kg/day (approximately 5 times the maximum human dose on a mg/m2 basis) but not at 20 mg/kg/day.

No adverse fetal effects were seen when pregnant rats were treated with up to 150 mg/kg/day (approximately 17 times the maximum human dose on a mg/m2 basis) by gavage throughout the period of organogenesis.

No adequate and well-controlled studies have been conducted in pregnant women. STRATTERA should not be used during pregnancy unless the potential benefit justifies the potential risk to the fetus.

Labor and Delivery

Parturition in rats was not affected by atomoxetine. The effect of STRATTERA on labor and delivery in humans is unknown.

Nursing Mothers

Atomoxetine and/or its metabolites were excreted in the milk of rats. It is not known if atomoxetine is excreted in human milk. Caution should be exercised if STRATTERA is administered to a nursing woman.

Pediatric Use

Anyone considering the use of STRATTERA in a child or adolescent must balance the potential risks with the clinical need (see BOX WARNING and WARNINGS, Suicidal Ideation).

The safety and efficacy of STRATTERA in pediatric patients less than 6 years of age have not been established. The efficacy of STRATTERA beyond 9 weeks and safety of STRATTERA beyond 1 year of treatment have not been systematically evaluated.

A study was conducted in young rats to evaluate the effects of atomoxetine on growth and neurobehavioral and sexual development. Rats were treated with 1, 10, or 50 mg/kg/day (approximately 0.2, 2, and 8 times, respectively, the maximum human dose on a mg/m2 basis) of atomoxetine given by gavage from the early postnatal period (Day 10 of age) through adulthood. Slight delays in onset of vaginal patency (all doses) and preputial separation (10 and 50 mg/kg), slight decreases in epididymal weight and sperm number (10 and 50 mg/kg), and a slight decrease in corpora lutea (50 mg/kg) were seen, but there were no effects on fertility or reproductive performance. A slight delay in onset of incisor eruption was seen at 50 mg/kg. A slight increase in motor activity was seen on Day 15 (males at 10 and 50 mg/kg and females at 50 mg/kg) and on Day 30 (females at 50 mg/kg) but not on Day 60 of age. There were no effects on learning and memory tests. The significance of these findings to humans is unknown.

Geriatric Use

The safety and efficacy of STRATTERA in geriatric patients have not been established.

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Adverse Reactions

STRATTERA was administered to 2067 children or adolescent patients with ADHD and 270 adults with ADHD in clinical studies. During the ADHD clinical trials, 169 patients were treated for longer than 1 year and 526 patients were treated for over 6 months.

The data in the following tables and text cannot be used to predict the incidence of side effects in the course of usual medical practice where patient characteristics and other factors differ from those that prevailed in the clinical trials. Similarly, the cited frequencies cannot be compared with data obtained from other clinical investigations involving different treatments, uses, or investigators. The cited data provide the prescribing physician with some basis for estimating the relative contribution of drug and non-drug factors to the adverse event incidence in the population studied.

Child and Adolescent Clinical Trials

Reasons for discontinuation of treatment due to adverse events in child and adolescent clinical trials - In acute child and adolescent placebo-controlled trials, 3.5% (15/427) of atomoxetine subjects and 1.4% (4/294) placebo subjects discontinued for adverse events. For all studies, (including open-label and long-term studies), 5% of extensive metabolizer (EM) patients and 7% of poor metabolizer (PM) patients discontinued because of an adverse event. Among STRATTERA-treated patients, aggression (0.5%, N=2); irritability (0.5%, N=2); somnolence (0.5%, N=2); and vomiting (0.5%, N=2) were the reasons for discontinuation reported by more than 1 patient.

Commonly observed adverse events in acute child and adolescent, placebo-controlled trials- Commonly observed adverse events associated with the use of STRATTERA (incidence of 2% or greater) and not observed at an equivalent incidence among placebo-treated patients (STRATTERA incidence greater than placebo) are listed in Table 1 for the BID trials. Results were similar in the QD trial except as shown in Table 2, which shows both BID and QD results for selected adverse events. The most commonly observed adverse events in patients treated with STRATTERA (incidence of 5% or greater and at least twice the incidence in placebo patients, for either BID or QD dosing) were: dyspepsia, nausea, vomiting, fatigue, appetite decreased, dizziness, and mood swings (see Tables 1 and 2).

¹ Events reported by at least 2% of patients treated with atomoxetine, and greater than placebo. The following events did not meet this criterion but were reported by more atomoxetine-treated patients than placebo-treated patients and are possibly related to atomoxetine treatment: anorexia, blood pressure increased, early morning awakening, flushing, mydriasis, sinus tachycardia, tearfulness. The following events were reported by at least 2% of patients treated with atomoxetine, and equal to or less than placebo: arthralgia, gastroenteritis viral, insomnia, sore throat, nasal congestion, nasopharyngitis, pruritus, sinus congestion, upper respiratory tract infection.

Table 2: Common Treatment-Emergent Adverse Events Associated with the Use of STRATTERA in Acute (up to 9 weeks) Child and Adolescent Trials
Adverse Event	Percentage of Patients Reporting Events from BID Trials					Percentage of Patients Reporting Events from QD Trials
STRATTERA (N=340)		Placebo (N=207)		STRATTERA (N=85)			Placebo (N=85)
Gastrointestinal Disorders
Abdominal pain upper	20		16		16			9
Constipation	3		1		0			0
Diarrhea	3		6		4			1
Dry mouth	1		2		4			1
Dyspepsia	4		2		8			0
Nausea	7		8		12			2
Vomiting	11		9		15			1
General Disorders
Fatigue	4		5		9			1
Psychiatric Disorders
Mood swings	2		0		5			2

The following adverse events occurred in at least 2% of PM patients and were either twice as frequent or statistically significantly more frequent in PM patients compared with EM patients: decreased appetite (23% of PMs, 16% of EMs); insomnia (13% of PMs, 7% of EMs); sedation (4% of PMs, 2% of EMs); depression (6% of PMs, 2% of EMs); tremor (4% of PMs, 1% of EMs); early morning awakening (3% of PMs, 1% of EMs); pruritus (2% of PMs, 1% of EMs); mydriasis (2% of PMs, 1% of EMs).

Adult Clinical Trials

Reasons for discontinuation of treatment due to adverse events in acute adult placebo-controlled trials - In the acute adult placebo-controlled trials, 8.5% (23/270) atomoxetine subjects and 3.4% (9/266) placebo subjects discontinued for adverse events. Among STRATTERA-treated patients, insomnia (1.1%, N=3); chest pain (0.7%, N=2); palpitations (0.7%, N=2); and urinary retention (0.7%, N=2) were the reasons for discontinuation reported by more than 1 patient.

Commonly observed adverse events in acute adult placebo-controlled trials - Commonly observed adverse events associated with the use of STRATTERA (incidence of 2% or greater) and not observed at an equivalent incidence among placebo-treated patients (STRATTERA incidence greater than placebo) are listed in Table 3. The most commonly observed adverse events in patients treated with STRATTERA (incidence of 5% or greater and at least twice the incidence in placebo patients) were: constipation, dry mouth, nausea, appetite decreased, dizziness, insomnia, decreased libido, ejaculatory problems, impotence, urinary hesitation and/or urinary retention and/or difficulty in micturition, and dysmenorrhea (see Table 3).

¹ Events reported by at least 2% of patients treated with atomoxetine, and greater than placebo. The following events did not meet this criterion but were reported by more atomoxetine-treated patients than placebo-treated patients and are possibly related to atomoxetine treatment: early morning awakening, peripheral coldness, tachycardia. The following events were reported by at least 2% of patients treated with atomoxetine, and equal to or less than placebo: abdominal pain upper, arthralgia, back pain, cough, diarrhea, influenza, irritability, nasopharyngitis, sore throat, upper respiratory tract infection, vomiting.

² Based on total number of males (STRATTERA, N=174; placebo, N=172).

³ Based on total number of females (STRATTERA, N=95; placebo, N=91).

Male and female sexual dysfunction - Atomoxetine appears to impair sexual function in some patients. Changes in sexual desire, sexual performance, and sexual satisfaction are not well assessed in most clinical trials because they need special attention and because patients and physicians may be reluctant to discuss them. Accordingly, estimates of the incidence of untoward sexual experience and performance cited in product labeling are likely to underestimate the actual incidence. The table below displays the incidence of sexual side effects reported by at least 2% of adult patients taking STRATTERA in placebo-controlled trials.

¹ Males only.

There are no adequate and well-controlled studies examining sexual dysfunction with STRATTERA treatment. While it is difficult to know the precise risk of sexual dysfunction associated with the use of STRATTERA, physicians should routinely inquire about such possible side effects.

Postmarketing Spontaneous Reports

The following list of undesirable effects (adverse drug reactions) is based on post-marketing spontaneous reports, and corresponding reporting rates have been provided.

Vascular disorders - Very rare (<0.01%): Peripheral vascular instability and/or Raynaud's phenomenon (new onset and exacerbation of preexisting condition).

Drug Abuse and Dependence

Controlled Substance

Class STRATTERA is not a controlled substance.

Physical and Psychological Dependence

In a randomized, double-blind, placebo-controlled, abuse-potential study in adults comparing effects of STRATTERA and placebo, STRATTERA was not associated with a pattern of response that suggested stimulant or euphoriant properties.

Clinical study data in over 2000 children, adolescents, and adults with ADHD and over 1200 adults with depression showed only isolated incidents of drug diversion or inappropriate self-administration associated with STRATTERA. There was no evidence of symptom rebound or adverse events suggesting a drug-discontinuation or withdrawal syndrome.

Animal Experience

Drug discrimination studies in rats and monkeys showed inconsistent stimulus generalization between atomoxetine and cocaine.

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Overdose

Human Experience

There is limited clinical trial experience with STRATTERA overdose and no fatalities were observed. During postmarketing, there have been reports of acute and chronic overdoses of STRATTERA. No fatal overdoses of STRATTERA alone have been reported. The most commonly reported symptoms accompanying acute and chronic overdoses were somnolence, agitation, hyperactivity, abnormal behavior, and gastrointestinal symptoms. Signs and symptoms consistent with sympathetic nervous system activation (e.g., mydriasis, tachycardia, dry mouth) have also been observed.

Management of Overdose

An airway should be established. Monitoring of cardiac and vital signs is recommended, along with appropriate symptomatic and supportive measures. Gastric lavage may be indicated if performed soon after ingestion. Activated charcoal may be useful in limiting absorption. Because atomoxetine is highly protein-bound, dialysis is not likely to be useful in the treatment of overdose.

Dosage and Administration

Initial Treatment

Dosing of children and adolescents up to 70 kg body weight - STRATTERA should be initiated at a total daily dose of approximately 0.5 mg/kg and increased after a minimum of 3 days to a target total daily dose of approximately 1.2 mg/kg administered either as a single daily dose in the morning or as evenly divided doses in the morning and late afternoon/early evening. No additional benefit has been demonstrated for doses higher than 1.2 mg/kg/day (see CLINICAL STUDIES).

The total daily dose in children and adolescents should not exceed 1.4 mg/kg or 100 mg, whichever is less.

Dosing of children and adolescents over 70 kg body weight and adults - STRATTERA should be initiated at a total daily dose of 40 mg and increased after a minimum of 3 days to a target total daily dose of approximately 80 mg administered either as a single daily dose in the morning or as evenly divided doses in the morning and late afternoon/early evening. After 2 to 4 additional weeks, the dose may be increased to a maximum of 100 mg in patients who have not achieved an optimal response. There are no data that support increased effectiveness at higher doses (see CLINICAL STUDIES).

The maximum recommended total daily dose in children and adolescents over 70 kg and adults is 100 mg.

Maintenance/Extended Treatment

There is no evidence available from controlled trials to indicate how long the patient with ADHD should be treated with STRATTERA. It is generally agreed, however, that pharmacological treatment of ADHD may be needed for extended periods. Nevertheless, the physician who elects to use STRATTERA for extended periods should periodically reevaluate the long-term usefulness of the drug for the individual patient.

General Dosing Information

STRATTERA may be taken with or without food. The safety of single doses over 120 mg and total daily doses above 150 mg have not been systematically evaluated.

Dosing adjustment for hepatically impaired patients - For those ADHD patients who have hepatic insufficiency (HI), dosage adjustment is recommended as follows: For patients with moderate HI (Child-Pugh Class B), initial and target doses should be reduced to 50% of the normal dose (for patients without HI). For patients with severe HI (Child-Pugh Class C), initial dose and target doses should be reduced to 25% of normal (see Special Populations under CLINICAL PHARMACOLOGY).

Dosing adjustment for use with a strong CYP2D6 inhibitor - In children and adolescents up to 70 kg body weight administered strong CYP2D6 inhibitors, e.g., paroxetine, fluoxetine, and quinidine, STRATTERA should be initiated at 0.5 mg/kg/day and only increased to the usual target dose of 1.2 mg/kg/day if symptoms fail to improve after 4 weeks and the initial dose is well tolerated.

In children and adolescents over 70 kg body weight and adults administered strong CYP2D6 inhibitors, e.g., paroxetine, fluoxetine, and quinidine, STRATTERA should be initiated at 40 mg/day and only increased to the usual target dose of 80 mg/day if symptoms fail to improve after 4 weeks and the initial dose is well tolerated.

Atomoxetine can be discontinued without being tapered.

Instructions for Use/Handling STRATTERA capsules are not intended to be opened, they should be taken whole. (See also Information for Patients under PRECAUTIONS.)

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How Supplied

STRATTERA® (atomoxetine HCl) capsules are supplied in 10-, 18-, 25-, 40-, 60-, 80-, and 100-mg strengths.

* Atomoxetine base equivalent.

Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F) [see USP Controlled Room Temperature].

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Strattera Medication Guide
Strattera Patient Information

Detailed Info on Signs, Symptoms, Causes, Treatments of ADHD

Last updated: 11/2005

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The information in this monograph is not intended to cover all possible uses, directions, precautions, drug interactions or adverse effects. This information is generalized and is not intended as specific medical advice. If you have questions about the medicines you are taking or would like more information, check with your doctor, pharmacist, or nurse.

Copyright © 2007 Healthyplace Inc. All rights reserved.

back to: Psychiatric Medications Pharmacology Homepage

Read articles about alternative treatments for addiction, including nutrition therapy for alcoholism, hynotherapy, and more.

• Alternative Treatments for Alcoholism and Addiction
• Nutrition Therapy for Treating Alcoholism
• Alternative Treatments for Addiction

 

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next: Alternative Treatments for Alcoholism and Addiction

Parents share stories of how a low phosphate diet and magnet therapy work to help their child's ADHD symptoms.

Low Phosphate Diet

Richard from Australia wrote saying:
"My colleague and I have recently launched an important new ADD web site. It is about German research into ADD which goes back some twenty years but has until now been almost completely unknown in the English-speaking world.

The information has benefited thousands of families in Europe. Very many have found it makes the use of stimulant medication unnecessary and gives better results. More than 70,000 copies of the book we introduce have been sold in German - which makes it a 'best seller' many times over.

Full and carefully targeted information is available on our new web site at: http://www.phosadd.com/."

Here is an extract from the site:

"We describe the important discovery of German research pharmacist Hertha Hafer, largely unknown in the English-speaking world. She discovered that excess dietary phosphate triggered her son's ADD. Phosphate is a very common and versatile food additive today; its use by food manufacturers and processors has increased enormously over the last fifty years, in parallel with the explosion of ADD/ADHD in the developed countries.

A low phosphate diet led to dramatic improvements in her son's behaviour, well-being and school performance, making medication unnecessary. Her family's ADD problem was resolved and her son had no further problems as long as he avoided high phosphate foods.

For over twenty years thousands of families in Europe have been following her recommendations and have been rewarded with normal, manageable, lovable, sometimes highly performing children. This site is for adults affected by ADD/ADHD too."

Magnets and Far Infar Red

Simone from Florida USA wrote saying....
"Dear Simon,

I have got an ADHD child 9 years of age. I've read through your article and I have to say that I agree with you that not a lot is known about the side effects of these drugs given to these kids. My experience with them are limited to Ritalin and Adderall. I have to tell you I was not impressed with either.

Against the wishes of my husband, to the point of having very HEATED arguments with him, I got our son these meds hoping they would work. I was desparate to try anything to have my son function at "normal" level. While my son is not destructive, he was being disruptive to his peers because he was always moving and wanting to play. I found these drugs did no more than just what they are; drug him. This, while calming his physical symptoms, had no effect on his ability to focus. I took him off the meds and was to the point of home schooling. I was fortunate enough to have been directed to a charter school in his school district that teaches only children with ADHD.

Since being there, our son was chosen as one of 3 kids to participate in an experiment involving Magnets and Far Infar Red. We were so pleased with the results, my husband and I have become distributors and are busy telling all who are willing to listen about these non-invasive and drugless products that can help others. While we are not claiming these products to be medical devices, we believe them to be an alternative to these drugs.

As you stated in your article, sleep deprivation has been shown to have an effect and even more pronouncement of these symptoms expressed by these children.

One of these magnetic products I mentioned is a sleep system. It is a mattress pad with magnets that are dispersed and secured. There is also a comforter that is made with the FIR ceramics which is floated into the fabric of the comforter. It was to my delight that I found these products had a very positive effect on my son.

My objective is to introduce you to a product that has been my experience and that of others to be helpful to those children.

E-mail:SimoneC777@aol.com

Ed. Note: Please remember, we do not endorse any treatments and strongly advise you to check with your doctor before using, stopping or changing any treatment

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next: Making ADHD-Friendly Career Choices
~ back to adders.org homepage
~ adhd library articles
~ all add/adhd articles

Journal Articles and Book Chapters

• Peele, S. (1996), Assumptions about drugs and the marketing of drug policies. In W.K. Bickel & R.J. DeGrandpre (Eds.), Drug policy and human nature. New York: Plenum, pp. 199-220.
• Peele, S. (1998), The results for drug reform goals of shifting from interdiction/punishment to treatment. International Journal of Drug Policy,9, 43-56.
• Peele, S. & Brodsky, A. (1998), Gateway to nowhere: How alcohol came to be scapegoated for drug abuse. Addiction Research, 5, 419-426.
• Husak, D., & Peele, S. (1998), "One of the major problems of our society": Symbolism and evidence of drug harms in U.S. Supreme Court decisions. Contemporary Drug Problems, 25, 191-233.
• Peele, S. (1999), The fix is in. A Commentary on "The Fix" (Massing, 1998) and "An Informed Approach to Substance Abuse" (Kleiman, 1998). International Journal of Drug Policy, 10, 9-16.
• Peele, S. (2000), The road to hell. Review of 'Mental Hygiene: Classroom Films — 1945-1970'. International Journal of Drug Policy, 11, 245-250.
• Peele, S. (2001), Court-ordered treatment for drug offenders is much better than prison: Or is it? Reconsider Quarterly, Winter 2000-1001, pp. 20-23.
• Peele, S. (2001), The new consensus—"Treat 'em or jail 'em" —is worse than the old. DPFT News (newsletter of the Drug Policy Forum of Texas), February, pp. 1; 3-4.
• Peele, S. (2001), Whose spirits have been broken anyway? Review of 'Broken Spirits: Power and Ideas in Nordic Alcohol Control'. Nordisk alkohol- & narkotikatidskrift, 18(1), 2001, 106-110.
• Peele, S. (2001), Will the Internet encourage or combat addiction? Review of 'Telematic Drug and Alcohol Prevention: Guidelines and Experience from Prevnet Euro'. Nordisk alkohol- & narkotikatidskrift, 18(1), 2001, 114-118.
• Peele, S. (2001, July/August), The world as addict. Review of "Forces of Habit: Drugs and the Making of the Modern World," by David E. Courtwright. Psychology Today, p. 72.

Magazine Articles

• Peele, S. (2001, May), Drunk with power. The case against court-imposed 12-step treatments. Reason, pp. 34-38.
• Peele, S. (2003, Spring), The best and the worst of 2002. SMART Recovery News & Views, Vol. 9, pp. 6-8.

Newspaper Articles

• Peele, S. (1990, March 14), Cures depend on attitudes, not programs. Los Angeles Times.
• Peele, S. (1997, April 14), Should we continue to wage the drug war? Chasing the dragon. New York Times (Letters), p. A16.
• Peele, S. (1998, August 9), A drug-users' advocate. Washington Post (Letters), p. C6.
• Peele, S. (2000, February 14), McCain has two standards on drug abuse. The GOP candidate is a hawk in the drug war, yet his wife got no penalty. Los Angeles Times, p. B5.

Internet Publications

• Peele, S., & Brodsky, A. (1997), The Great Zinberg/McCaffrey Debate. The Stanton Peele Addiction Website.
• Peele, S. (2000), On being Jewish, a communist, and a drug legalizer. The Stanton Peele Addiction Website.
• Peele, S. (2000), Little drunken rats. The Stanton Peele Addiction Website.
• Peele, S. (2000), Eliminate bad crops — rent hell. The Stanton Peele Addiction Website.
• Peele, S. (2000), The drug reform movement is doing the wrong thing. The Stanton Peele Addiction Website.
• Peele, S., & Archie Brodsky (2000), Guidelines for sensible cannabis use. Prepared for, and with the assistance of, Cannabis Action Network, Berkeley, CA. Morristown, NJ: The Stanton Peele Addiction Website.
• Peele, S. (2006), Marijuana Is Addictive - So What? The Stanton Peele Addiction Website.
• Peele, S. (2006, March), I Know - Let's Really Scare Kids About Drugs! The Stanton Peele Addiction Website.

next: How Do I Get My Boyfriend To Quit Drugs/Drinking?
~ all Stanton Peele articles
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Find out why Campral is prescribed, side effects of Campral, and Campral's role in helping people who are alcohol-dependent - in plain English.

Campral (acamprosate calcium) Full Prescribing Information

Campral Patient FAQs

Q - Is there a difference between alcohol dependence and alcohol abuse?

A -Yes. The difference is in the degree of symptoms. People who are alcohol-dependent may have a physical addiction and have lost the ability to control their drinking. With physical dependence, their bodies need alcohol and without it, they go into withdrawal. People who abuse alcohol are able to control the amount of alcohol they consume, are not physically dependent on it, and will not experience withdrawal symptoms when they do not drink.

Q - Is there a difference between alcoholism and alcohol dependence?

A - Alcohol dependence is the medical term for alcoholism.

Q - How can I tell if I or someone I'm close to is alcohol dependent?

A - That is not always a simple thing to do. But, on this Campral website, you will find a questionnaire that can help you answer this question. Download the questionnaire, fill it out, and discuss it with your doctor or the person you are trying to help.

Q - What is the best way to bring up the subject of drinking with a friend or family member?

A - There's no easy answer to this question because every situation is different. Begin by discussing the problem with your family physician. Your physician can steer you to local resources that you and your family member or friend may want to explore together.

Q - How do I know if I am a candidate for Campral (acamprosate calcium) Delayed-Release Tablets?

A - Campral is for people who are alcohol-dependent, not for those who abuse alcohol. Candidates must be committed to abstaining from alcohol and abstinent when they begin treatment with Campral. Campral must be prescribed by a physician. If you think you or someone you know is a candidate for Campral, speak to your physician.

 

Q - How is Campral different from other medicines for alcohol dependence?

A - Campral is the first new medical treatment approved for alcoholism in in a decade. It works differently from other treatments. Antabuse (disulfiram) works by making you nauseous when you drink. ReVia (naltrexone) reduces the pleasure of drinking. Campral helps reduce both the physical and emotional discomfort (e.g. sweating, anxiety, sleep disturbances) many people feel in the weeks and months after they've stopped drinking. This makes it easier for them not to drink after the immediate withdrawal period. It is the first medication thought to impact the biological and medical processes of the disease.

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Q - Is Campral addictive?

A - No. Campral is not addictive and is not listed by the FDA as a controlled substance.

Q - Will Campral make me stop drinking?

A - Campral will not prevent you from drinking. Only you can do that. But it will make it easier for you to resist drinking and get yourself moving along the road to recovery. Campral works best when it is part of a comprehensive treatment program that includes counseling and support.

Q - How does Campral help me maintain abstinence?

A - As is true of many medicines, we do not know exactly how Campral works. Currently, researchers believe that Campral acts on the complex processes of the nervous system by restoring a balance that was altered by continued alcohol consumption.

Q - Does Campral prevent withdrawal symptoms?

A - No. None of the alcohol dependence therapies will prevent acute withdrawal symptoms. Speak to your doctor about what to expect during withdrawal and how to deal with it.

Q - Does Campral have side effects?

A - Campral is well tolerated. As is often the case with many medications, Campral does have side effects but does not pose any serious safety problems. In clinical trials patients reported a range of side effects, including asthenia, diarrhea, flatulence, nausea, and itching. Side effects were generally mild and few patients discontinued treatment due to them. In fact, in trials lasting longer than 6 months, the same percentage of patients discontinued treatment due to side effects in both the Campral and placebo groups.

Q - How do I take Campral?

A - Campral is a tablet. The recommended dose is two 333 mg tablets 3 times per day.

Q - Can I take Campral with food?

A - Yes. You can take your Campral dose with food. Some people find that coordinating their Campral with meals makes it easier to keep on schedule.

Q - If I relapse while I'm taking Campral, does that mean Campral is not for me?

A - Not necessarily. If you relapse, you should continue taking your Campral as prescribed by your doctor. Speak to your doctor about relapse problems.

Q - How long do I need to take Campral?

A - Clinical trials have shown Campral is effective and safe for one year. You and your doctor will decide the best course of treatment for you.

Q - What is a "Standard Drink"?

A - While alcohol dependence is not defined by how much alcohol a person consumes, it may be useful to estimate alcohol consumption to determine health risks and other potential problems. Currently, there is no universally accepted definition of a standard drink. However, the National Institute on Alcohol Abuse and Alcoholism (NIAAA, NIH) has published a guideline that establishes the relative amounts of alcohol in different drinks (Dawson, 2003).

12 oz. of beer or cooler	8-9 oz. of malt liquor	5 oz. of table wine	3-4 oz. of fortified wine (such as sherry or port) 3.5oz.	2-3 oz. of cordial liqueur or aperitif	1.5 oz. of brandy (a single jigger)	1.5 oz. of spirits (a single jigger of 80-proof gin, vodka, whisky, etc.
Note: People buy many of these drinks in containers that hold multiple standard drinks. For example, malt liquor is often sold in 16, 22 or 40 oz. containers that hold between two and five standard drinks, and table wine is typically sold in 25 oz. (750ml.) bottles that hold five standard drinks.

Q - What is "At Risk" drinking?

A - Physicians use terms such as "heavy," "chronic heavy," "harmful," "hazardous," and "at risk" drinking interchangeably to describe alcohol consumption that meets or exceeds the following limits:

• For men: more than 14 drinks per week or more than 4 drinks per occasion
• For women: more than 7 drinks per week or more than 3 drinks per occasion

People whose drinking exceeds these levels should be assessed for alcohol-related problems.

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Campral (acamprosate calcium) Full Prescribing Information

back to: Psychiatric Medication Patient Information Index