The forces of nature appear intent on reversing mankind’s progress toward better health.   An example is the ever-increasing resistance of bacteria to antibiotics.  A timeline of the existence of humans and bacteria shows that bacteria have been around for a very long time— much longer than mammals, and much, much longer than humans.  In fact by the dawn mankind, bacteria had been thriving, relatively uninhibited, for over 2 billion years.

Modern humans have been around for 40,000-200,000 years or so, depending on the definition of ’modern.’  Bacteria have had the upper hand during all of mans’ existence, save for the past 100 years after penicillin and other antibiotics were discovered. Only the most self-centered of species would look at a timeline and conclude that humans have won the battle with bacterial diseases.  There are always reasons for optimism, but a fair assessment of our current struggle with antibiotic resistance suggests that someday, people will look back on the current sliver of time, when humans can treat most bacterial infections, as a golden era of medicine that wasn’t appreciated as such at the time.

Viruses adapt to mankind’s health efforts too, with new variants arising from the sludge at the bottom of the food chain to infect birds, swine, or other creatures before moving on to human hosts.  The CDC and other scientists work to predict the vulnerabilities of the next super-virus, hoping to reduce the severity of the next pandemic.  As with bacteria, we are enjoying an era without smallpox, polio, or other dreaded viral diseases that used to kill otherwise-healthy people.  We take the victor’s position for granted to the point that our children don’t know why chlorine was first added to swimming pools.  Gone with the last generation are the fears associated with iron lungs, orange window-signs, and leg braces.

Even the Human Immunodeficiency Virus, an agent of certain death in the 1980’s was transformed into a chronic, treatable illness.  I was new to medicine when ‘universal precautions’ were first instituted (can our children even imagine having their teeth examined by someone not wearing latex gloves?!)  Researchers don’t celebrate, though, since medication-resistant strains of HIV were expected …

I generally write positive articles about the use of buprenorphine for treating opioid dependence, and my articles have been reflective of my attitude toward the medication. The field of psychiatry encompasses more conditions than it does effective treatments for those conditions, and my initial experiences treating people with buprenorphine were strikingly positive.

My first buprenorphine patients were extremely desperate after multiple treatment failures, and they responded to buprenorphine the way a person with strep throat responds to penicillin.  Their lives improved so dramatically that I wondered if we needed a new understanding of ‘character defects’; whether the shortcomings should be seen not as semi-permanent flaws, but rather as dynamic, maladaptive personality traits, fueled and sustained by active obsession for opioids— and lessened when that obsession was reduced, using buprenorphine.

I still have a number of those patients in my practice, people who have done very well on buprenorphine and have little interest in discontinuing the medication.  As much as I would like to take on a few new patients, I won’t force these people off buprenorphine in order to make room under the cap.  They have worked hard, done well, and have earned the right to a medication that helps keep their illness in remission.

But I’ve noticed a change over the past couple years in the attitudes of patients coming for treatment.  I’ve been slow to specifically identify the change, but when I do an honest assessment, a clear pattern emerges.  To be blunt, young people don’t do as well on Suboxone or buprenorphine as their older counterparts. Maybe they have a harder time accepting the limits to their own mortality; maybe insight requires a longer time to accumulate life experiences.  Maybe they haven’t suffered enough consequences.   But after starting buprenorphine, instead of tearfully expressing disbelief over the lifting of cravings for opioids, younger patients are more likely to take the effects from buprenorphine in stride and continue to engage in addictive behaviors.

I always consider each new patient’s history of ‘consequences’.  I believe that consequences are what eventually spur recovery, providing the patient lives long enough for that to happen—which is certainly not a given with …

A local District Attorney wrote to me last week to express his concern about the increased diversion of buprenorphine.  I often sense an undercurrent of tension when I cross paths with attorneys, aware of the different attitudes that we hold that arise from our different roles in society.

The DA wrote about the dramatic increase in overdose deaths in the Midwest.   Overdose scenes are often littered with a variety of substances, ranging from bags of heroin to the orange plastic vials used by pharmacies to dispense medications.  If the overdose victim was on Suboxone or buprenorphine, the prescribing doctor is often contacted about the death and the ensuing investigation.  Doctors notified about patient deaths have reactions beyond the grief over the loss of someone they cared about, including guilt that they couldn’t save the patient, and even fear of being blamed for doing something wrong. Every doctor has seen headlines featuring peers accused of reckless prescribing, and the addiction world is somewhat unique from other specialties in the way that patient deaths cause a sense of ‘guilt by association.’  Oncologists, for example, are not viewed with the same degree of suspicion when their patients succumb to cancer.

I felt a bit defensive about the DA’s letter.   I know that buprenorphine saves lives, beyond a doubt.  I also notice that the positive actions of medications are often taken for granted, while the risks are cited as scapegoats.  I notice how quickly people complain about others ‘on buprenorphine’, without taking the time to ponder what would likely happen were buprenorphine not available.

Some physicians’ fears stem from dilemmas faced in treating addiction that are difficult or even impossible to resolve.  For example, a DA may point out that the doctor’s patients are not behaving like ideal citizens, not realizing that the doctor is every bit as aware of the problem, yet unable to make things better.  In some cases doctors do the very best they can (or that anybody could do, yet their patients struggle to maintain sobriety.  Doctors may be tempted to abandon the problem patients altogether, to avoid being seen …

A late post tonight, since my new exercise program has pushed my blogging back by an hour or so each night.  My suspicions about exercise were correct, by the way; it is much easier to suggest exercise to other people than it is to actually exercise.  I’ve been at it since the beginning of the year, and I at least feel a bit less hypocritical.

While I’m on the topic…  I’ve received many comments over the years from people complaining that they’ve been taking Suboxone or buprenorphine for X many years, and they have no energy, they feel stressed, they have gained weight, they don’t sleep well or they sleep TOO well… and concluding that all of the problems are from Suboxone.

They aren’t.

The problems are the result of other things, including things that tend to occur naturally as our lives become less chaotic and more outwardly-secure.  The problems I mentioned above, for example, come from inactivity.  They come from thinking that we’ve ‘paid our dues’ at the age of 30, and it’s time to coast in life.  They come from failing to seek out challenges, and from failing to do our best to tackle those challenges.  They come from letting out minds be idle, smoking pot or watching American Idol  instead of responding to the naggings sense of boredom that ideally pushes people to join basketball, tennis, or bowling leagues.

Our minds and bodies are capable of SO much.  I (honestly) am not a network TV viewer, but I love the contrast of ‘before and after’ scenes on ‘Biggest Loser.’  People magazine (it sits in my waiting room) had a section a while back about people who lost half their body size, by exercise and dieting.  The part I found most interesting was the deeply personal answer that each person had to the question, ‘what was your turning point?’  Each cited an episode of humiliation or shame that lifted the veil of denial, and helped them do what they knew, all along, needed to be done.

We are not all capable of ‘Biggest Loser’ comebacks. But it is important for people to understand that feeling good, physically or …

A recent exchange with a reader:

I have been on buprenorphine for 5 yrs.  Recently my doctor stated that my u/a t looked like I have been ‘loading my meds.’  He said my levels where ‘backwards’ and that would happen if I took just a few doses just before my appt.   My doc had me come back in two weeks to go over my next u/a, and again it came back funky.  So my doc starts having me take my meds in front of the nurses on a daily basis.  Two weeks later with supervised u/a’s, my urine comes back the same.  My doc looked perplexed but kind of ignored the results like I was still doing something to mess with the results.  I had to come in again for another urine test and it finally came back normal.  My numbers were fine after that, and all was good until last week.

I went to my normal monthly check up and the u/a showed NO buprenorphine in my system.  My doc looked at me like I am the biggest liar.  I am perplexed.  I am taking my meds daily.  I don’t know what is going on and I need to figure it out soon before my doc kicks me out of the program. What could be wrong with the test, that is says that I have no buprenorphine in my body?

My response:

There are several directions we could go with this issue.  One aspect is whether it is always fair to believe the results of drug tests over the word of our patients.  I understand the reasons for testing, but I think that doctors sometimes lose the forest (the patient’s addiction problem) on account of the trees (quantitative testing).  This patient has been on buprenorphine for five years; I would hope to have sufficient trust established with patients after that period of time, such that the lab results wouldn’t be seen as the only answer.  There can be problems with any laboratory test.  Drug tests are one tool– not the ultimate arbiter of truth.

Most people metabolize buprenorphine a certain way, …

In a recent Google search about Suboxone and pregnancy, one of the top links included the frightening statement that Suboxone and buprenorphine have been linked to SIDS or sudden infant death syndrome, commonly called ‘crib death.’

The statement was from a health forum where a woman wrote about taking Suboxone during pregnancy.  She wrote that her child went through opioid withdrawal after delivery, recovered, and then died two months later from SIDS.  She then claims that her doctors told her that Suboxone was a possible reason for her child’s death.

I don’t know if the woman’s story is true. If it is, I hope my comments do not cause her pain, and I’m sorry for her loss.  But someone should comment on the information, given the number of young women on Suboxone who become pregnant and frantically search the internet for reassurance that their baby will be OK.  I know that pregnant women in my practice lose a great deal of sleep because of guilt over taking buprenorphine.  I am not a SIDS specialist, obstetrician, or pediatrician, and I do not actively follow the SIDS literature.  But I have done some reading to prepare for this post, and I’ll do my best to address the issue.

While the causes of SIDS are not completely understood, a number of factors have been associated with sudden infant death, including maternal age and socioeconomic status (higher rates in infants of poorer, younger mothers), maternal smoking, air pollution, low birth weight, season of birth (higher in infants born in the winter), too high or too low room temperature, male sex, history of premature birth, and bottle feeding (instead of breastfeeding).

One of the biggest risk factors is the easiest to correct: sleeping position. The incidence of SIDS is thought to be about twice as high for babies who are placed prone (face-down).  Since 1992, when 4895 deaths were attributed to SIDS in the US, a public relations campaign to encourage parents to place infants on their backs may have reduced the incidence of SIDS by 50%.  I write ‘may …

We can now leave naloxone out of the discussion, and focus on the side effects of Suboxone that are caused by buprenorphine.

Side effects are symptoms caused by a given medication that are not part of the therapeutic benefit of that medication.  Whether a symptom is a side effect depends on the reason for taking the medication.  For example, decreased intestinal motility is the desired effect of opioids used to treat diarrhea, but a bothersome side effect when taking opioids for pain.  The term ‘side effect’ is not on the package insert for medication, the symptoms and actions instead referred to as ‘adverse reactions.’  Package inserts also have a section entitled ‘warnings and precautions’ where the most dangerous adverse reactions are listed.

Some medications have a ‘black box warning’ for adverse reactions that are particularly common or particularly dangerous, consisting of a frightening statement at the start of the package insert (enclosed, naturally, by a black box). Black box warnings in psychiatry include the warning for increased suicidal ideation in children and adolescents treated with antidepressants, and the increased risk of death in people with dementia treated with atypical antipsychotics.

Increased risk of cancer or mutations, and effects on fertility or fetal development, are listed in yet another section entitled ‘nonclinical toxicology.’  They are listed as ‘nonclinical’ because the events do not involve the intended physiologic system or pathway targeted by the medication.  For example, slowing of intestinal activity by opium is either treatment of diarrhea or unwanted constipation, but in either case the outcome is caused by actions of opioids at opioid receptors.  If the opium molecule happened to bind to DNA and cause cancer, the cancer would be nonclinical toxicology, not a side effect.  Carbamazepine decreases the excitability of neurons to prevent seizures, and the sedation caused by the slowing of neurons is considered an adverse reaction. Carbamazepine impairs fetal development through different actions, considered nonclinical toxicology.

All of these divisions can be picked apart so that division of symptoms to one category or another will appear arbitrary.  The system …

People who read this blog are aware of the shortage of physicians who can prescribe buprenorphine to treat people addicted to pain pills, even as an epidemic of addiction to heroin and pain pills devastates the heartland of the country.  In order to prescribe buprenorphine, physicians take a short course and obtain special certification.  To obtain certification, physicians must promise to treat no more than 30 patients at one time, a number that can be increased to 100 patients after one year.

If you only have a few minutes, please take the time to go to the White House web site and add you name to a petition to allow individual doctors to treat more than 100 patients using buprenorphine.  The whole process is fast and easy, and only requires your name and email address through this link: http://wh.gov/QR6K

If you have more time, need convincing, or just like hearing a 52-y-o rage against the machine, continue reading my thoughts about limiting treatment for this one health condition.

The reason for the patient cap, according to cap proponents, is to prevent pill-mill practices where patients could obtain narcotic medications without adequate care for their underlying addiction.  That concern is reasonable, I suppose, but I often discover that proponents of the cap have other motives to keep the limits in place.  For example, one person at a ‘linked in’ group argued that individual physicians don’t provide the all-encompassing care that he provides… to the 800+ patients he ‘counsels’ at the methadone clinic where he works!  According to that counselor, all people addicted to opioids need years of counseling—largely from other people with addictions, who after a couple years of school have all the answers.

He would be surprised to see just how well people can do on buprenorphine, a medication that selectively removes craving for opioids.  After years of treating and knowing patients on buprenorphine I realized that ‘character defects’ are largely maintained by active craving.  Yes– people with antisocial tendencies before and during active addiction have the same antisocial tendencies on buprenorphine.  But people who …

In my last post, I wrote about the work-up of a patient who experiences symptoms similar to opioid withdrawal that start about an hour after each dose of Suboxone.  We decided that the symptoms were signs of withdrawal—i.e. reduced activity of mu-opioid pathways—and that the symptoms were triggered by taking a daily dose of Suboxone (buprenorphine/naloxone).

Note that I wrote that the symptoms seemed to be caused by reduced mu activity, i.e. not necessarily by reduced mu-receptor binding. Endogenous opioid pathways are very complex.  Decreased activity in opioid pathways may arise from decreased binding of agonist at the receptor, or from changes in a number of other chemical or neuronal pathways.

This diagram shows the processes that are triggered by mu-receptor binding in humans before and after opioid tolerance.  The diagram only shows the complexity of processes within the neuron with opioid receptors; realize that each neuron 1. Has receptors for many other neurotransmitters as well, and 2. Receives input from thousands of other neurons.  As we sort through possible causes of our patient’s symptoms, keep in mind the complexity of neural pathways.

While we are on the subject of complexity, the web site linked above is an incredible resource for those interested in biochemistry.  The site includes diagrams of a number of metabolic pathways that describe how different molecules, including neurotransmitters, are manufactured by the human body.  I encourage people to browse the site.  You will gain insight into why the actions of substances are difficult to fully predict.

The withdrawal symptoms experienced by our patient might arise from dysfunction in any one of the many chemical pathways that affect opioid tone. But since a dose of Suboxone contains naloxone, a mu-receptor inverse agonist, it is possible, maybe even likely, that the naloxone is related to symptoms.

Naloxone is less lipid-soluble than buprenorphine and so only a small portion—about 3%– of a dose is absorbed through mucous membranes.  The rest of the naloxone is swallowed, consciously or inadvertently, and eventually absorbed from the small intestine, to pass to the liver via the portal vein.  …

I struggle with the length of my posts. I shoot for 1000 words—an amount of reading that most people can knock off in a typical trip to the bathroom— but I find it difficult to limit posts to that size. So as I have done in the past, I will break this post into a couple of sections. In the first, I’ll lay the groundwork for investigating symptoms of withdrawal in a patient taking buprenorphine. The second post will go into greater detail.

A patient recently contacted me to complain that he was experiencing withdrawal symptoms for several hours after each dose of Suboxone. I will describe my thought process, in case the description helps someone else experiencing similar symptoms.

My first decision point is whether or not the person is truly experiencing symptoms of withdrawal. Some people will misinterpret symptoms from excess opioid stimulation as withdrawal symptoms, for example. Nausea is a not-uncommon complaint among people taking buprenorphine, and patients often assume that nausea is the result of insufficient opioid activity, and so take higher doses of buprenorphine. But nausea is actually more common in opioid overdose than during opioid withdrawal, along with constipation, whereas withdrawal primarily causes diarrhea.

Pupil diameter is a good indicator of withdrawal vs. overdose; small or ‘pinpoint’ pupils suggest an excess of opioid activity, whereas withdrawal is associated with very large pupil diameter.

Other symptoms are also misinterpreted as withdrawal. Many opioid addicts develop a strong fear of withdrawal over years of using, and so ‘withdrawal’ is often the first thing to come to mind, during unpleasant symptoms. I also believe that the experience of withdrawal becomes learned in a way that allows the symptoms to re-occur after certain triggers. I remember an experience years ago, when I awoke from a dream experiencing significant withdrawal symptoms, even though I had not taken an opioid agent for years. I feel back asleep, and was grateful to find that the symptoms were gone, when I woke the second time.

People are angered by the notion that their symptoms have ‘psychological’ origins. But as …