Online Courses and CE: We offer a series of online educational programs for professionals and the public. Visit us here for previews and discounts on our online programs.

Follow PsychologySalon on Facebook: Become a fan of the PsychologySalon page; updates will appear in your news feed.

Looking for a therapist? We have eleven registered psychologists in our clinic, and we are accepting new clients. For information, visit

Friday, 30 December 2011

PsychologySalon 2012: A 100% Discount

Library Square in Vancouver
PsychologySalon has allied with Vancouver Public Library to present our monthly talks at Library Square on Robson Street downtown in 2012.

This new relationship allows us to eliminate all fees for our talks, which henceforth will be free! It has been our goal to make these talks as accessible as we can, and VPL is helping us reach this goal. No more tickets, no more reservations, no more costs.

We'll be in the VPL Central Branch's Alma VanDusen & Peter Kaye Room, beneath the concourse at Library Square. I'll be away for part of early 2012, so the first talk will be in March.  Here's the lineup:

Monday March 26. Out of the Blue: The Nature and Treatment of Clinical Depression. Speaker: Dr Randy Paterson.

Tuesday April 24. Learning to Love Your Emotions. Speaker: Dr Lindsey Thomas.

Beneath the concourse, stairs at left.

Tuesday May 22. Overload! Create a Less Pressured Life. Speaker: Dr Randy Paterson.

Tuesday June 26. Put Off Procrastinating! Speaker: Dr Ekin Blackwell.

All talks run 7 pm to 8:30.  Come and join us.

And  Happy New Year, everyone!

Tuesday, 27 December 2011

New Year's: Not Just for Getting Drunk Any More

Someone has to steer.

End of the year. Christmas has passed, and it’s time to think about the next holiday. So what do you do?

One option, indulged in by millions, is a drunken blowout with champagne and cardboard horns. What better way of beginning the new year than being unable to recall the last night of the previous one?

New Years parties have a thread of dissatisfaction that goes beyond the overconsumption. It’s possible to detect more than a hint of artificiality in the date, and if it truly is the end of one year and the beginning of the next, then surely something of greater import should take place.

It’s like standing in a crowded, tinsel-filled room, chatting about the weather, our jobs, our last holiday - and attempting to stave off the boredom that such conversations eventually bring. We look down and see that the floor is made of thick glass; and in the depths beneath there are more significant events taking place, interesting currents, candlelight, silence, clarity. But at this party there doesn’t seem to be a staircase leading down there. It’s inaccessible.

Perhaps rather than a loud, shouting revel, we should spend at least part of the time thinking. We should sit quietly on the border, gazing back over the year just finished, then swing our legs over the fence and look forward at the year to come.

Many such rituals are best done with paper and pen, and time to think, and solitude. Find a quiet space where you will be undisturbed for at least half an hour, preferably more. But if all you have is half an hour, you can still spend it well.

First, the year just past. Write the year at the top. Answer these questions:

  1. What were the most personally significant events of the year? Emphasize the things you chose to do, not just the things that happened to you.
  2. How satisfying a year was that? Would you rate it as one of your life’s best years? One of the worst?
  3. If an observer sat watching your actions for the entire year, what would he or she say were your top priorities – regardless of what you think they should have been?
  4. If there are dissatisfactions with how you spent the year, what are they and what would you like to have done instead?

Next, on a separate sheet, write the number of the year to come. Spend most of your time on a single task.

  • What do I want to do this year?  What would make me look back at the end of the year and rate it as one of my best?

Let your mind roam freely, and don’t edit. Don’t try to categorize or, if you do, have only two or three headings (like “Work” and “Life”).  Don’t worry if your ideas seem to be of various magnitudes (“Visit India”, “Finally watch ‘The Seven Samurai’”, “Clean out hall closet”).  Emphasize things that are under your control; that you might be able to bring about.  “Buy pencils” is better than “Win the lottery” or “Have a more romantic spouse.”

If you find yourself running dry, sit back. Consciously relax. Breathe deeply. Repeat the word “Anything” as you exhale. Don’t grab at ideas; let them come to you.

When the flow slows again, place your mind gently in the various rooms, or realms, of your life.  Some common ones include: Work, Family, Social, Romantic, Avocation/Hobbies, Creative, Learning, Home, Read/Watch/Buy, Daily Routine, Health, Finances, and Spiritual. There are others. Even if a room seems empty, stay there with the emptiness for at least a few minutes. Ideas may begin to emerge from the walls.

Give it time, and consider carrying your page around with you for a few days. Having stirred up your mind, new thoughts will pop into your head when you are on the bus, or in the bath, or waking up. Add them to your list.

Finally, remind yourself that the new year has begun. Ask yourself what you will do this week to begin the process of living the year you want. Don’t wait for the impulse. Don’t wait to want to exercise, or to call your estranged sibling, or to clean out the attic. The goal is to do these things, not to wait until they seem fun. You won’t act on everything on your list this week, but if you don’t act on any of them ask yourself why not. What are you waiting for? Who are you hoping will take charge of your life, if not you?

Our lives are like sailboats. It’s fun to sit back and look up at the sky, chat with friends, and even break out some wine (or a cardboard horn). But every now and then, we need to put a hand back on the tiller and steer.

Friday, 23 December 2011

Are You Unsafe or Just Uncomfortable?

A recent workshop by a fellow psychologist reminded me of a useful principle in working with the emotions.

Nothing to worry about.
As humans, we routinely feel the full range of emotions, some of them enjoyable and others less so. When we experience sadness, anxiety, fear, or general unease, the temptation is generally to withdraw.  Fear, for example, almost always shouts the same thing in our ear: get away, get away, get away.

So what should we do? To a great extent, the answer depends on the situation in which we find ourselves.

If we are actually in physical danger, then we should probably obey the temptation and retreat.  The apartment balcony really is shaking as though it is about to collapse, so perhaps we should step inside.

If we know from past experience or from the magnitude of the feeling that we are in some very real psychological danger, then we can sometimes do the same. For example, if I know that the situation is definitely beyond my coping ability, or will put me into a week of emotional recovery that I can’t afford, then I can ease away. If being at a drunken party will put your long-fought-for abstinence at risk, then leave.

But if, as is more often the case, I am simply uncomfortable, but not unsafe, then I need to think more carefully. The route to an expanded life is almost always in the direction of our fears. If I am uncomfortable but not really in any objective danger, then the choice to stay and sit out the discomfort will probably be a more productive one.

If, since being caught in crossfire during a robbery, I have been fearful of shopping malls, then I will almost certainly feel uncomfortable when I enter a mall. I need to examine my fear. Am I really in danger? Is there any reason to think that the mall will once again be robbed today? Will I really lose my mind if I become anxious in the mall? Or will I simply be uncomfortable and unhappy? If I will just be unhappy, then the best course of action is to go to the mall and to stay there for an extended time – long enough for the anxiety to fade.

If I dislike speaking in public, I might ask myself “Am I unsafe, or just uncomfortable?” If it is simply discomfort, then perhaps I can use this as my cue to move toward my fear, volunteering to give talks and pushing myself to ask questions in meetings or propose toasts at dinners.

It has become a part of the cultural vernacular of late for people to say things like “I don’t do that – not in my comfort zone.” But perhaps if something is not in our comfort zone it is where we need to go – or can benefit from going.

We also hear “I didn’t feel safe there” when what is really meant is “I didn’t feel comfortable there.” We have misconstrued comfort with safety. In fact, there are situations that are safe and comfortable, safe and uncomfortable, and unsafe and uncomfortable (as well as a few that feel comfortable but aren’t really safe).

If we confuse safety and comfort we will, almost inevitably, live smaller and more restricted lives.  We will use our discomfort as a cue to close yet another door to larger experience.

So: Am I unsafe, or just uncomfortable? The distinction is important. They point me in opposite directions.

Thank you to Steve S.

Tuesday, 20 December 2011

Resources: The single best thing you can do for your health

Staying healthy can seem a bit overwhelming. I have to work on my diet, boost my social network, meditate, find my passion, manipulate my sleep schedule, drink less coffee, drink more coffee (depending on the study), and on and on.  

Maybe you worry about your weight. You have bad knees. You want to avoid age-related cognitive decline. Uncle Frank had heart disease and you want to avoid it.

To avoid all of these different hazards seems like a full-time job. It's easier just to give up and let the fates do their worst.

But what if you didn't have to do all those things? What if there was just ONE thing you could do that would reduce your risk of dying from most causes? And what if the same thing would reduce your risk of an anxiety disorder or clinical depression and boost your quality of life? 

And, damn, you're not a smoker, so just giving up cigarettes isn't an option for you.

Well, actually, there IS one thing that can help prevent the most common emotional problems and chronic illnesses, as well as age-related cognitive decline. And you can guess what it is.

But here's a short video that makes the point clearly, concisely, with reference to the research:

It'll take you 9 minutes, and you already know what it's going to tell you.

But it really puts the ball back in our own court. Something we've wanted, something we might have wished for, has been discovered. So: Are we willing to make use of it?

You can extend your life, and have more fun living it. Want to? If not, why not?

Friday, 16 December 2011

Medications: What Would a Selective Serotonin Reuptake ENHANCER Do?

In recent years there has been considerable controversy about the Selective Serotonin Reuptake Inhibitors (SSRIs) like citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac), and the like.
These drugs are widely thought to operate by reducing the reuptake of serotonin into the sending neuron, thereby leaving more serotonin available in the gap between neurons so that enough can get across and cause the next neuron in line to fire.

Irving Kirsch and others have called this explanation into question, acknowledging that about 60% of people taking SSRIs seem to improve, but questioning whether the popularly-accepted explanation is correct.

If an SSRI helps mood by inhibiting serotonin reuptake, then what if we had a drug that promotes reuptake? Such a drug would open the reuptake pumps wider, reduce the amount of serotonin in the gap between neurons, and reduce the likelihood that the next neuron in line would fire. Presumably, such a drug would increase depression or, at minimum, have no antidepressant effect.

Fine. But is there such a drug?

Yes. It’s called tianeptine. It is a selective serotonin reuptake enhancer (an SSRE). It has been used in Europe and elsewhere for over ten years, and has been the subject of considerable study, including a number of double-blind trials.

Oddly enough, it’s sold as an antidepressant.

In 2002, a meta-analysis (a statistical reanalysis of multiple previous trials) examined five studies of tianeptine versus SSRI. The SSRI was fluoxetine (Prozac) in two cases, paroxetine (Paxil) in two cases, and sertraline (Zoloft) in one (Kasper & Olie, 2002).

The results indicated that there were no significant differences in effectiveness between SSRE and SSRI, except for one measure that leaned in favour of tianeptine. Most studies and reviews considering tianeptine concur that there is ample evidence that tianeptine is approximately as effective as SSRIs (eg., McEwan & Olie, 2005, Brink et al., 2006) and there are scattered reports that it is better tolerated with fewer side effects.

What’s missing from this picture?

What's missing is a nice medication crossover trial. Perhaps people who are given an SSRI and do not respond well will respond better to an SSRE than to another SSRI. As far as I can tell, this hasn’t yet been done.

So what’s up? 

How can tianeptine possibly work? One option is that both SSRI and SSRE are simply placebos, and that it doesn’t matter what you give people, some of them will get better – even if the drugs have opposite chemical effects.

Another option is that the reuptake effect doesn’t really explain the antidepressant effect, and that one or both of these medications works against depression at some other level. And indeed, there are hints that in addition to the SSRE effect, tianeptine operates elsewhere in the brain: on glutamate transmission, on the hippocampus, and possibly by reducing the damaging effects of stress (Kasper & McEwan, 2008).

What the tianeptine data does do is cast the popular explanation of antidepressant action into serious question. It’s hard to claim that antidepressants work by reducing reuptake when an equally effective drug increases reuptake. This is just one line of evidence nailing down the coffin lid of the monoamine hypothesis of depression.

It will be interesting to see what comes of the research into tianeptine. What we can already conclude is that our traditional explanation to patients about how SSRIs work is simply not supported - not by this data, nor by other lines of evidence. To the extent that we continue to give out the story, we are spinning fairy tales.

The truth is: We just don’t know how these medications work on depression – apart from the action of expectancy (the belief that one is receiving an active treatment), which seems to account for a large proportion of the effect.

Is there an additional biochemical margin, an organic benefit to these medications? Perhaps. But at this point there is no consensus about what it is.


Brink, CB, Harvey, BH, & Brand, L (2006).  Tianeptine: A novel atypical antidepressant that may provide new insights into the biomolecular basis of depression.  Recent Patents on CNS Drug Discovery, 1, 29-41.

Kasper, S, & McEwan, BS (2008).  Neurobiological and clinical effects of the antidepressant tianeptine.  CNS Drugs, 22, 15-26.

Kasper, S, & Olie, JP (2002).  A meta-analysis of randomized controlled trials of tianeptine versus SSRI in the short-term treatment of depression.  European Psychiatry, 17, 331-340.

Kirsch, I, et al., (2008).  Initial severity and antidepressant benefits: A meta-analysis of data submitted to the Food and Drug Administration.  PLoS Medicine, 5(2), e45.

McEwan, BS, & Olie, JP (2005).  Neurobiology of mood, anxiety, and emotions as revealed by studies of a unique antidepressant:  Tianeptine.  Molecular Psychiatry, 10, 525-537.

Online Course

Is there an alternative to a medication-based approach? If someone takes medication, is there more they can do in order to maximize the effect? Consider seeking the help of a qualified psychotherapist trained in cognitive behaviour therapy.

In addition, our clinic has developed a cognitive behavioral guide to self-care for depression. Though not a substitute for professional face-to-face care, UnDoing Depression may be a useful adjunct to your efforts.  The preview is below. For 50% off the regular fee of $140 USD, use coupon code “changeways70” when you visit our host site, here.

We also have courses for professionals and for the public entitled What Is Depression, What Causes Depression, Diagnosing Depression, Cognitive Behavioral Group Treatment of Depression, How to Buy Happiness, and Breathing Made Easy. For the full list with previews and substantial discounts, visit us at the Courses page of the Changeways Clinic website.

Tuesday, 13 December 2011

Gifts For The Needless

"Everything is better in Gears of War 3... Four player co-op, new multiplayer modes, bajillions of unlockables, retrolancers, stuff that blows up, and perfect controls make this a top pick for the holiday season." - Metro News, Nov 25-27 2011, written with no apparent sense of irony.

Last week I posted some survival strategies for the holidays, and I mentioned that one of the biggest stresses for some people is trying to decide what to get for the person who has everything they need.
How about giving a mountain?

People often tell me they like the parties, the dinners, the decorations, and even the weather at Christmas. They just don’t like the shopping. They don’t know what to get, the people on their list don’t really need anything, and they’re uncomfortably aware of the discrepancy between the supposed point of Christmas and what it has become. We are one of the wealthiest societies the planet has ever known. The last thing most of us need is more stuff.

So stop buying people objects they do not need or, in most cases, want.

“Oh, but I have to give them something,” you say.

Fine. Give them eye surgery.

Not on them. On someone who needs it.

It’s possible to give great gifts to people who already have everything. Because the one thing they don’t have is a world in which others aren’t suffering.

What if you could give someone an HIV clinic, or an urban greenbelt, or a passport for a border-crossing bear, or eye exams for an entire village, or an acre of Canadian habitat, or an elementary school education, or a microfinance bank? Wouldn’t that be better than yet another sweater they won’t wear?

An increasing number of people are taking the opportunity of Christmas to give gifts that fit with their values and that have greater meaning than a new cordless drill.

Here are just a few suggestions. Your values and preferences may vary, so investigate your favourite organizations to see what they offer.

The Nature Conservancy

When you give a gift they send the recipient a calendar and certificate.  For $40 you can give a gift representing an acre of habitat. Larger donations represent habitat areas for more wide-roaming species ranging from owls ($55) to caribou ($400). You can also give any amount of money to support the activities of the Conservancy.

Trans-Himalayan Aid Society

TRAS, a local Vancouver charity, funds projects in India, Nepal, and Tibet, including child education sponsorships at a variety of schools in the region.

Seva Canada

SEVA focuses on the prevention and cure of blindness in the third world. They conduct educational, preventive, and surgical programs to deal with treatable blindness (the most common cause of which is cataract).  For $25 you can provide eye exams for 25 children, for $50 you can pay for cataract surgery, and for $150 you can pay for eye surgery for a child.

The Stephen Lewis Foundation

SLF supports community-level organizations focused on HIV/AIDS in Africa by providing care and support to women, orphans, grandmothers, and people living with HIV/AIDS.  Stephen Lewis is the former Special Envoy for HIV/AIDS in Africa for the United Nations.  You can gifts of any amount and you can order Christmas cards from the organization.

David Suzuki Foundation

An environmental organization, DSF engages in scientific, educational, and advocacy related activities to highlight a wide variety of issues.  This year they have a tongue-in-cheek set of symbolic gifts based on the idea that the North Pole (site of a certain workshop) is melting. You can buy water wings for reindeer ($20), elf-sized hockey sticks ($20), an abominable snowmaker ($50), and a variety of e-Cards (ranging from Critter Passports to Green Belts) that help fund the organization’s activities.


You’ve heard about microcredit in developing countries. You may not know that you can be a microcredit bank yourself. Kiva allows you to deposit money with them, and then issue loans of $25 or more to projects and individuals of your own choosing. You look through the photographs and stories of people seeking funding, and simply click to loan a specific amount to the projects you want to support. Kiva sends you updates on the repayment of these loans. When your loan is repaid, you can lend the money to another project. This is a perpetual gift that allows you to help any number of people over time.

Canada Helps

Want to contribute to a group not on the list? The website makes it easy to contribute to any registered charity in Canada. You can browse the available charities and donate right on the site. You can also create your own “Cause Wish List” that others can look at when they want to give you a gift – kind of like a wedding registry.

*     *     *

Don’t like any of these options? No problem. They’re just examples. There are thousands of ways of giving gifts to those who have no real needs – gifts that can benefit people and causes that fit with your values and those of your recipient.

What easier last-minute gift can you think of?

Friday, 9 December 2011

Medications. Comparing Antidepressants to Placebo

Listening Closely to Prozac…

In the mid-1990s, psychologist Irving Kirsch (and his colleague Guy Sapirstein) wanted to determine the size of the placebo effect in clinical depression. The result was an explosion of literature that has been calling some of our most widely-accepted practices into question.

Recently Kirsch published a book, The Emperor's New Drugs, that summarizes the work from his perspective (which is unabashedly skeptical about the antidepressants, as the title suggests).

In his original study, Kirsch collected published studies of depression treatment that included a pill placebo condition – studies originally intended to examine antidepressant medication effectiveness.

Once you get a lot of similar studies on a subject, you can combine them and perform a meta-analysis.  In effect, this is like treating the participants in all of these separate studies as though they were in one giant study. A meta-analysis has a tendency to smooth over irregularities between trials and can show the general trend of results. On the other hand, they can also obscure some of the nuances of individual trials.

Fortunately, some of the trials included a no-treatment condition. This allowed Kirsch to compare the response to placebo to the response associated with just the passage of time. Some people get better on their own, after all, and there are a few other factors (reviewed in a recent post, here) that can otherwise inflate an apparent placebo effect.

Sure enough, Kirsch found that no-treatment groups had a small tendency to improve (Kirsch & Sapirstein, 1998). The placebo groups improved much more, however, indicating that the belief that one was receiving an active treatment had a significant therapeutic effect.

The surprise for Kirsch was that patients receiving antidepressant medications did not improve much more than those receiving placebo. In fact, the placebo group improved about 75% as much as the medication group. Put another way, about ¾ of the medication effect could be accounted for by expectancy or by spontaneous recovery with the passage of time. The active ingredient in the medication didn’t seem to add much potency.

In addition, Kirsch knew about the problem discussed a few weeks back: antidepressants have side effects and placebos do not, so patients receiving the antidepressants in such studies often figure out which study condition they are in. Suspecting they are getting the active drug, their expectancy effect may be greater. Kirsch raised the possibility that even the small difference between placebo conditions and active antidepressant conditions may be partly an expectancy effect rather than being attributable to the medication’s active ingredient.

This study created quite a stir when it was published, as it called the effectiveness of antidepressants into question. These are some of the most widely prescribed medications in North America, and it has been generally accepted that they work.

But what about the unpublished studies?

Kirsch had easy access to all of the published placebo-controlled antidepressant studies. But he knew that some of these studies never see the light of day. It’s easier to get a study published if it shows positive results than if it shows no difference between conditions. And perhaps the companies funding the studies would be less than enthusiastic about publishing data suggesting that their medications weren’t very effective.

The US Food and Drug Administration requires that all of the existing studies, published or not, be submitted to them before a drug can be approved. So Kirsch knew the FDA had them. He used a Freedom of Information request to obtain the complete data set and conducted another meta-analysis.

The results were even more discouraging than in his previous study. Response to the placebo condition was 82% as great as to the active medications. Only 18% of the response in medication conditions could be attributed to the chemical effect of the drug. And there was still the problem of unblinding of the study, because subjects could guess whether they were getting the placebo or the antidepressant.

The difference between placebo and antidepressant was still statistically significant. But Kirsch asked whether it was clinically significant. It amounted to an average difference of 1.8 points on the 51-point Hamilton Rating Scale for Depression.

I’ve treated depression for many years, and I can usually hazard a guess about where a client will score on the depression scales I use. But I wouldn’t be able to reliably guess within 1.8 points of their score – the difference is simply too slight. So even if there was a genuine chemical effect, it's questionable whether it was important from a patient's perspective.

Is there a publication bias favouring positive studies?

A subsequent study (Turner, Matthews, Linardatos, Tell, & Rosenthal, 2008) looked at whether there was a systematic difference between the published and unpublished drug trials. Of the 69% of studies that were published, 94% showed a positive result favouring the antidepressant being tested.

Of all the studies judged to exhibit a superiority of antidepressant over placebo, 37 were published and just one was not. Of those judged to have negative or equivocal results, 22 were not published, 3 were published with the negative result made explicit, and 11 were judged by Turner et al to have been interpreted in a misleadingly positive light.

A scrupulous reader evaluating the published literature would conclude that 94% of studies supported the effectiveness of antidepressants. One able to read all of the studies would find that only 51% were positive.

Whether or not a given trial supports a difference between drug and placebo is one thing; the size of that difference is another. Turner et al examined the difference in effect size between antidepressant and placebo for the total data set, and compared this to the difference found in the published studies. On average, the effect size was 32% higher in the published data than in the complete set of FDA-submitted studies.

This points to a serious problem. Clinicians are expected to follow the published literature and guide their practices accordingly. But a publication bias in favour of positive studies skews the picture.

Imagine a dutiful clinician asking each researcher whether antidepressant medications outperformed placebo in a given trial.  “Yes, no, no, yes, yes, no, yes, no, no…”

Then imagine the same clinician looking at the published literature.  “Yes, yes, yes, yes, yes, no, yes, yes, yes…” The resulting treatment decisions would likely differ markedly.

So do antidepressants work?

Let’s be clear. People who received antidepressants improved a great deal, on average. So yes, the medications work.

The question is why. Patients receiving placebos improved a great deal as well, though not quite as much as the patients receiving antidepressants. It is certain that much of the improvement we see in patients prescribed antidepressants is the result of expectancy rather than chemistry.

But is there a chemical effect too?

That remains unclear. It seems likely that there is, but we know that it is somewhat unreliable. We know that people who suddenly stop taking antidepressants will often experience a rebound depression, which suggests the medications must be doing something, even if we aren’t sure just what.

At this point I’m not willing to declare that antidepressants are placebos. I’ve seen too many remarkable effects in too many clients to dismiss the effectiveness of these medications out of hand.

My suspicion is that depression, like fever, is a symptom of many possible conditions, and that antidepressants may well help with some of these ailments but not others. I would guess that in 20 years we will look back and see that these weak effects were obtained by including a very diverse group of problems in the medication trials. (I've advanced this idea before on this blog, and I suspect that some of the more aggressive medication critics would snort at me for my timidity on this issue.)

Kirsch, who argues forcefully that there is no convincing evidence in favour of the antidepressants, would disagree with me. And his grasp of the literature is unquestionably better than mine. Others with expertise in this area have significant reservations about Kirsch’s work. At this point, a consensus has yet to emerge.

So: Is there a chemical antidepressant effect? At this point the answer remains unclear and unsettled in the research community.


Kirsch, I (2009) The Emperor's New Drugs: Exploding the antidepressant myth. London: Bodley Head.
Kirsch, I, Moore, TJ, Scoboria, A, & Nicholls, SS (2002).  The emperor’s new drugs: An analysis of antidepressant medication data submitted to the US Food and Drug Administration.  Prevention and Treatment, Vol 5, Article 23.
Kirsch, I, & Sapirstein, G (1998) Listening to Prozac but hearing placebo: A meta-analysis of antidepressant medication. Prevention and Treatment, Vol. 1, Article 2a.
Turner, EH, Matthews, AM, Linardatos, E., Tell, RA, & Rosenthal R. (2008). Selective publication of antidepressant trials and its influence on apparent efficacy. New England Journal of Medicine, 358, 252-260.

Tuesday, 6 December 2011

A Christmas Tradition: The Survival Guide

Is it over yet?
Ahhh, December again. Time to dust the mall decorations that have been out since October. Time to check the credit limit twice. Time to practice the diaphragmatic breathing.

And for psychologists, time for the most hallowed tradition of them all. In newsrooms across the nation, reporters are drawing straws. The one who gets the shortest straw has to write the obligatory “how to cope with Christmas” article without make it sound like a retread from last year – and the year before, and…

'Twas the month before Christmas and all through the land, psychologists’ phones are ringing, interviews to be had.

The truth is, Christmas does not cause significant psychological problems. Anxiety, stress, disappointment, and sadness are not disorders, as therapists everywhere keep saying. They are part of being human. 

But for a holiday allegedly about joy, it’s surprising how much stress people can feel in the lead-up to it. So: here’s a dozen tips to help you make it to New Year’s.

1.  Remember: Christmas is voluntary.

People stare at me when I tell them this, but it’s true. December the 25th will come whether you like it or not. Christmas, however, is optional. If you don’t like it, you don’t have to do it. You can just announce that you won’t be celebrating it. And then don’t. Yes, this is possible. People everywhere are skipping the holiday altogether. Easter used to be mandatory as well; now only a minority actually observe the holiday. If you’re worried you will feel bereft, plan the day ahead of time. A pair of movies separated by a long walk, plus an hour of work on a pet project can fill the time.

2. Give up.

Disappointment is produced not by your experiences, but by your expectations. If you have no fantasy you cannot be disappointed. Popular media will attempt to ratchet your expectations up to a Victorian dinner with Tiny Tim and the late arrival of a reformed Scrooge – or at least a holiday with the Waltons. Recognize that this will not happen and has not happened in your recent past, so let it go.

3. Dice the holiday.

Christmas isn’t a monolithic structure. It’s a collection of bits. Chop it into pieces, preferably on paper: decorations, tree, family gift-giving, friend gift-giving, Christmas Eve get-together, Christmas dinner, whatever. Then ask yourself which bits you like and which bits you hate. Some (visiting Aunt Kate at the nursing home) may not be fun but you’ll decide to do them anyway. Some (risking your neck on the roof stringing lights) might be optional. Stop these ones.

4.  Compete with your worst, not your best.

If you must set a mark for yourself, don’t make it your ‘best-ever’ Christmas. Think back over your life, and try to remember what you did every holiday season. Sure, there was a great one here and there. But look for the very worst of the bunch – the one with the screaming fight, the trip to the Emergency Room, the deep depression, the house fire. And strive to make this year just a bit better than that one. Don’t try to push the brackets upward; just try not to set a new all-time low. It’s easier.

5.  Stop the arms race.

Arms races bankrupt the competitors. Much of the stress of Christmas comes from the “bigger and better” idea. Last year you gave gifts to X people and spent Y dollars. And some of those people outdid you. This year you feel you have to ramp it up a bit. But why? Take your foot off the gas a bit and start ramping it down. Pull back on the expense and let everyone breathe a little easier.

6. Fly.

The airport is a nightmare during the holidays, right? Yes, but there is an eye in the storm: Christmas Day. Almost no one flies, the airport is quiet, the flight crew is happy and relaxed, and you’re not at Aunt Mabel’s with your sister-in-law. An Air Canada bagged sandwich may be the best Christmas dinner you’ve ever had. (Yes, I’ve done this myself. It was blissful.)

7. Leave.

If it seems impossible to extract yourself from the trap of Christmas-as-usual if you stay home, then don’t stay home. Skip town. Go to a cheap cabin in the woods or get out of the country altogether. Spending the time with other Christmas refugees will make it even better.

'Tis the season to shoot your enemies, apparently.
8. Don’t buy gifts you don’t approve of.

I’ve noticed that one of the biggest stresses for people is doing things that are against their better judgment out of a misplaced sense of obligation. Maybe the only thing your nephew wants is a Call of Duty shoot-em-up video game (the top recommendation for holiday gift-giving in a recent article in Metro News) so he can practice slaughtering people with machine guns. Tough. Don’t buy it. If he doesn’t like what you give him, it ultimately doesn’t matter. If a package isn’t an expression of yourself to at least some extent, then it’s a bribe, not a gift.

9. Push experience.

Christmas memories are seldom of the gifts, the elaborateness of decorations, or the amount spent. They are about time spent with people. Make this the priority, not a slavish attempt to make your home mimic a magazine photo. Seven hours of labour may indeed produce a handmade wreath that Martha Stewart would declare a “good thing,” but seven hours spent with friends will be a better thing.

10. Cut an escape hatch.

Some families convene in large numbers for the holidays. Even if you generally get along, the close quarters can grate after a while. Plan breaks. Forget to pack enough underwear so you have an excuse to go shopping by yourself for a few hours. Plan to do things alone or with other friends after a few days with family. Remember that they probably don’t want to be around you 24 hours a day either.

11. Pick and choose.

When I was a child, Christmas streets were quiet. It almost seemed wrong to be driving in a car on that day. Somehow our culture morphed along the way, and now people spent half the day driving from place to place as though they are in a demented car rally, trying to hit all the checkpoints on their lists. The sense of futile pointlessness of this (“Is this any fun? Really?”) gets added to the stress of travel, and contributes to the sense of being trapped by the holiday. Instead, choose what you’re going to do and stick with it. My rule of thumb is that if you spend the day in more than two places you’ve made an error in planning.

12. Make someone else’s holiday.

“If you want others to be happy, practice compassion. If you want to be happy, practice compassion.” – The Dalai Lama. If you don’t have much to do, or if you don’t like the way you’ve spent the holiday the last few years, then make a change. Volunteer for a charity on Christmas Day. There are few guarantees associated with the holidays, but this one comes as close as you can get: It will almost certainly be one of the best Christmases you’ve had, and it will certainly be better than any alternative.

*    *    *

So, do I sound like Scrooge yet? I shouldn’t. I recognized years ago that my own dissatisfaction with the holidays was created in large part by a feeling that I was acting out a script written by someone else; a script I didn’t like, written by commercial authors I did not respect. Sometime in my 30’s I threw most of the script away, and I’ve been discarding pages ever since. I can heartily recommend this approach.

If you want a holiday script at all, then write it yourself. You’ll be happier, you’ll have more fun, and you’ll be more enjoyable to be around.

“Mm,” you say. “Nice try. But I still want to give gifts to a few people, and have no idea what to get them. They don’t actually need anything. That’s what stresses me out.”

Next week: Gift-giving for the needless.

Friday, 2 December 2011

Medications: Is Placebo Response a Placebo Effect?

For the last month or so I've been posting about medications, the proposed mechanism of action of SSRI antidepressants, and the monoamine hypothesis.

Running through all of this has been a discussion of the placebo effect, which seems like a fairly straightforward idea, but like many such concepts it quickly morphs into something more complicated the more you look at it.

So: It seems obvious that the placebo effect is the amount of improvement that we see in people who are given a placebo (an inactive treatment). In fact, this seems so obvious that researchers themselves often report results as though this was true.

Well, it isn't.

In fact, the improvement due to expectancy (the true placebo effect) – is only one of several factors contributing to the apparent efficacy of placebos. Let’s look at a few others.

Regression toward the mean

How do you get into a drug trial?  You have to meet a number of criteria, one of which is to have a disorder of a minimum level of intensity.  So if the trial is on depression, you have to have a depression score of X or more.

Every measure has a degree of error. Imagine that right now your “true” level of depression could be quantified as a score of 20. If we give you a test to find this out, you might get a score of 16, or 21, or 24. You’d get a score of around 20, but seldom would the test peg you perfectly. This is just like your old math tests. Sometimes you’d luck out and look a bit smarter than you really were; sometimes the test would make you look worse than you really were.

Now imagine that we’ll only let people into the study if they get a test score of 21 or higher. People with a “true” score of 10 are unlikely to get a test score wrong enough to be over 21, so they’ll all be denied entry to the study. People with a true score of 35 probably won’t get a test score lower than 21, so they’ll all be admitted.

But think of what happens to people who score close to the cutoff of 21.  Some people with a “true” score of 18 will score 22, and they’ll get into the study group. Some people with a “true” score of 23 will score 19, and they’ll be tossed out. All the people with a true score of 21 and who score a bit too high will be included. Those who score a bit too low will be omitted.

In other words, we have a bias: People close to the cutoff who test a bit high will get into the study, and those who test a bit low won’t.

Imagine that neither the drug nor the placebo does anything at all. We test all of our study participants again. Our extremely depressed folks scored high the first time, and they score high again. The second test is a few points higher for some and lower for others due to the random error in the tests. They average out the same.

But think about our group who started out near the cutoff. We have dropped people who randomly tested low from the study, and included those who randomly tested high. When we retest them, about half will score higher than their “true” score, just like they did before; and about half will score too low. But this time we won’t dump the ones who score too low. It will look as though this group of people got a little bit better.

The result: If we use a cutoff score, and if there is any measurement error at all (and there always is), we will always get a little bit of improvement when we retest the subgroup of people we let into the study. We’ll get that improvement in the real drug condition, and in the placebo condition. And we’ll call it a placebo effect, but it isn’t.  It’s a statistical anomaly.

Passage of Time

Again, think of how people get into a medication study for a problem like depression. They’re depressed!

What is the natural history of depression? It gets a bit worse and it gets a bit better. Later on, it can get worse again.

Now: When are you going to seek treatment, or volunteer for an experimental drug trial? Probably not when you’re feeling better. You’d only seek help if you were feeling somewhat worse lately.

So if we conduct a drug trial for depression, we’re going to get a lot of volunteers who have a mood problem that spontaneously gets worse and gets better. And most of them will be at the “worse” phase. If we admit them to the study and give them a medication, or a sugar pill, or just have them wait around, what will happen?

A few of them, who felt fairly lousy, will get even worse. But many of them, who volunteered precisely because they felt unusually bad, will feel somewhat better. If we test everyone and average out the scores, we’ll discover that the average depression score is a bit lower than when the study started. It’ll look like being a part of our study was therapeutic, but it wasn’t. It was the simple passage of time, plus an anomaly caused by people seeking help at the worst part of their mood cycle.

The Hawthorne Effect

Just being part of a study can help you feel better. In the late 1920s and early 1930s a series of studies was carried out at an American electrical plant to see whether light levels would influence productivity. It turned out that productivity improved when changes were made, regardless of whether the light was increased or decreased.

Since 1950, when the Hawthorne effect (named for the factory) was first described, it has routinely been noticed that simply being a part of a study creates changes in the people being examined. People in a placebo-controlled drug trial are likely to improve regardless of what treatment they are given, simply because they are in a trial.

Care and Support

When you are in a drug trial you go through a long series of intake measures, you see clinicians regularly, and people monitor your condition. In some ways the care you receive is much more attentive than you would get in the average physician's office.

During depression people often feel isolated and insignificant, and they usually have difficulty getting out of the house. We know that if we can help people become more active, if we can have them interact with people more often, and if we can help them to feel (rightly) that they are deserving of care and support, this often works against the depression.

In effect, just having appointments and talking with a professional (or for that matter any warm human being) can be a genuine and effective treatment for depression - even if the medication taken as a part of that relationship does nothing.

For people who are away from work, I have often found that doing volunteer work is one of the most potent strategies to help people recover from depression. It provides structure during the day. It provides a reason to get out (and once out it is easier to stay out a bit longer and do some errands or buy groceries). It provides human contact. It gives the person a sense that they have something to contribute. And the person is genuinely participating in outside life. Participating in a drug trial does all of these things as well.

So in addition to whatever the capsules contain, being in a study is therapy itself.

*     *     *

These are just some of the effects that can contribute to improvement in a person who takes a placebo in a drug trial. And, of course, all of the same effects can likewise contribute to those who are given the active drug.

Some of these effects - regression to the mean and the passage of time - would also appear in a group given no treatment at all. Some (the Hawthorne effect; care and support) would be much weaker in a group that only came in for pretest and post-test screening.

So we might wonder whether a group of depressed clients given no treatment at all would improve, and by how much. This has been examined and yes, people given no treatment do tend to improve - but not a great deal. The effect size in studies of antidepressants have averaged just under 0.4 (Kirsch & Sapirstein, 1998), beneath a commonly-used cutoff of 0.5 to describe a moderate effect. Placebo groups average over 1.1, by contrast.

Who cares?

There are two main reasons to care about this issue.

First, if we carelessly combine a variety of influences into the placebo effect, we make placebos look much more effective than they really are. If we want to think carefully about the placebo effect, we need to separate it from the other effects that sometimes inflate it.

Second, all of the effects above, PLUS the placebo effect, also apply to people given active medications in these trials. It is arguably a little oversimplified to say this, but the actual drug effect is usually taken to be the magnitude of response for patients in the active drug condition, minus the response of those in the placebo condition.

Sometimes the difference between drug and placebo is so minimal that a genuine chemical effect of the drug cannot be found.

And some studies suggest that the effects we attribute to the medication may just be more powerful placebo effects, brought on by the presence of medication side effects: Study participants experience side effects and conclude that they are on the real drug, thus developing greater expectation than those in the placebo condition.

Well, fine.  But what's the actual difference between people given antidepressant medication and those given placebos?  Stay tuned.

Tuesday, 29 November 2011

You Too Can Be Mentally Ill!

Please indulge me in a simulated interview for this post; it's a paraphrase of some conversations we've been having around the clinic. 

Why do we bother diagnosing illnesses?

There are several reasons, some of them a bit cynical. The most important one, from a public health perspective, is to guide treatment. We can take a variety of signs and symptoms, use these as clues to find the common problem producing all of them, and then target that problem. The label guides the treatment.

But why do we treat illnesses?

So that people can be healthier, happier, and (perhaps) more productive.

That’s what I thought.

Yes. But in the field of mental health there are significant controversies about diagnosis.

For one thing, psychiatric diagnosis often fails the treatment specificity test. Knowing a person’s diagnosis is supposed to be useful mainly as a way of informing treatment selection. It does that to an extent, and more for some disorders (e.g., bipolar 1 disorder) than others (e.g., dysthymia), but, on the whole, diagnosis does not help treatment selection nearly as much as it does in many other fields of medicine.

In my own work training clinicians in the treatment of depression, people often become obsessed with determining whether a client fully meets the diagnostic criteria for major depressive disorder, or whether they fall just short of the line. Although of some interest, from a practical perspective for the cognitive behavioural therapist the issue can be almost irrelevant.

Further, knowing that someone has major depressive disorder doesn’t help much with treatment selection. Having packed our client’s individuality into a diagnostic box, we need to unpack it all again and have a look at the person’s life circumstances, triggers, ways of thinking, lifestyle variables, life goals, and activity level. Then we can build a treatment approach.

You can only do this so many times before a still small voice begins to ask “What was the point of spending all that time coming up with the label, when the label doesn’t help you?”

That sounds a bit farcical.

It can be.

You mentioned more than one controversy.

The other big one at the moment is the proliferation of diagnoses, and the watering down of the diagnostic criteria, widening the categories so that more and more people are diagnosable.

In North America, and increasingly around the world, the Bible of diagnosis is the Diagnostic and Statistical Manual of Mental Disorders (or DSM), now in its fourth edition, hence DSM-IV.  (The other is the International Classification of Disease, ICD-10, which includes both mental and physical problems.)

DSM-I, released in 1952, contained 106 disorders.  DSM-II, 1968, contained 185. DSM-III in 1980 had 265, and DSM-IV, released in 1994, has 357. In 42 years the number of mental disorders more than trebled.

Some of this makes sense. Problems that were not recognized in 1952 were added, and some disorders were split into two or more related problems. But the number of people who could find themselves described in the DSM expanded markedly from DSM-I to DSM-IV. As well, the boundary between normal-range experience and disorder was moved in many cases to include more people. In effect, by shifting the definition of abnormality, and hence normality, we created millions of additional cases of “mental illness.”

Currently the American Psychiatric Association is developing DSM-V, scheduled to be released in 2013. Once again, vast swathes of normality are being redefined as mental illness.

Well, vast swathes of normality can still be pretty miserable. If it can be treated, what’s the problem?

Much of the treatment used for mental conditions is pharmacological, and most pharmacological approaches have their downsides as well as potential benefits. The data supporting the treatment of milder conditions is typically much weaker than for their more severe counterparts. So we may be encouraging more and more people to see themselves as mentally ill, and to accept treatments that may or may not be helpful for them.

As well, the boundaries of what it is to be normal are steadily shrinking. Many of us in the field believe we are pathologizing much of the human experience. It is as though we are saying “Pinkie fingers are cancerous growths, and you should seek treatment if you have them.” Sadness, bereavement, shyness, anxiety, anger, and much more are increasingly being viewed as symptoms of mental illness rather than natural elements of being human.

So what’s motivating all this?

Some of it is well-intentioned altruism. If we can help more people to feel better, why not? And in order to treat them, it seems reasonable to try to define what might be going wrong. Critics might say, though, that nothing is going wrong in most people: Life is challenging, and if you find it occasionally difficult this does not mean that there is anything the matter with you.

Some of this widening of mental illness definitions appears to be motivated by profit. If we can convince you that you are ill, we can sell you products. Many of the people on advisory panels for DSM-V also receive funding from pharmaceutical firms. This is no great surprise – pharmaceutical firms and the APA both want good people, and they often settle on the same ones. But the potential for a significant conflict of interest is too great to ignore. The more people we can call mentally ill, the more we can market to them – and the products we market tend not to be curative. So we can have them continue to purchase the product (or have insurers purchase it for them) for many years.

Even the lead developer of past versions of the DSM, Robert Spitzer, has expressed his concerns about the new edition. (This is putting it a bit mildly.) Here is one of his writings on the subject of proposed changes to the description of post-traumatic stress disorder (PTSD):

Can I read more?

Easily. Just google DSM-V and see what comes up. The Society for Humanistic Psychology has been particularly vociferous on the subject.  Here is their blog:

Here is an editorial on, of all things, the Psychology Today blog, by physician Allen Francis:

The problem is not limited to the mental health field, however.  Here is a similar red flag raised for medicine as a whole by health journalist Ray Moynihan, published in the respected British Medical Journal:

And here’s Moynihan’s website:

And where do you sit on all this?

I share the concerns about overdiagnosis and the narrowing definition of normal experience. I do believe that much of the broadening of disease categories is well-intentioned if naïve, but I also believe that much of it is motivated by the desire for profit.

I believe that if we take normal reactions and reclassify them as illnesses, we remove their usefulness to the person experiencing them. So rather than viewing a sense of ennui and anxious sleeplessness as cues to look at my life, I can begin to see them as a resurgence of a mental illness. I will become even more alarmed, and far from taking constructive measures to take charge of my life, I will see myself as more damaged.

In effect, I believe that classifying experiences as pathology can actually create pathology. Overdiagnosis isn’t just misdiagnosis.  It creates distress and, potentially, the very illnesses it predicts. By broadening disease categories we may not be helping anyone; we may be creating additional misery in the world.

Thanks to Johanna Trimble for sparking this post.

Friday, 25 November 2011

Medications: Are Blind Trials Really Blind?

We've been talking about psychopharmacology and the testing of medications.  In the last post on this subject, we considered the idea of the placebo control trial. But what about this "blind" business?

As you'll recall, the point of a double-blind placebo-controlled trial is that neither the treating clinician nor the patient knows which condition the patient is in. 

Why is this important? 

Patients’ belief that they are being treated with a medication can cause them to expect to get better. As a result, they may notice signs of improvement, even if the drug doesn’t really do anything. So if we give one group the “brand new drug” and the other group nothing, then the treated group will almost always do better.

Instead, we give both groups something that looks like a treatment. In fact, it must look identical (because some research suggests that certain pill colours and sizes are seen as more potent than others). If there is an expectancy effect, then it should appear equally in the groups getting the placebo and the active medication. Any differences in the effect between the groups would have to be due to the active ingredient in the pill.

Remind me why the clinician has to be blind.

We all communicate nonverbally. A physician who hands us a prescription confidently will produce more of an expectancy effect (“This’ll clear up your problem!”) than one who exhibits shame, anxiety, or an apologetic manner (“Sorry I don’t have anything more effective to offer you”). If the clinician knows which medication a patient is receiving, he or she might behave differently with clients receiving the real thing than with those receiving the fake. So it’s vital the clinician not know.

Similarly, it’s important that whoever is doing the evaluation of the patient (whether that is the treating clinician or someone else) not know which group the patient is in. If the evaluator really hopes that the test drug works, people who got the drug may be scored as more improved than those who got the placebo – even if the evaluator is trying hard to be even-handed.

So with all these precautions, patients must not know what drug they’re getting, right?

You’d think so. But no. The problem is that there are no perfect medications that change the target symptom (depression, psoriasis, heart rate) and nothing else. Virtually every medication has side effects.  

If you are in a drug trial and you notice that your hair is dry, you have a metallic taste in your mouth, and your libido is gone, you might very easily guess that the pill you are taking isn’t just a jelly bean. In fact, in antidepressant trials patients are sometimes asked at the end of the study “So, any guesses whether you got the test drug or the placebo?” Antidepressants are notoriously “buggy” with side effects, so patients tend to get the right answer. As a result, the supposedly blind trial isn’t blind at all. 

If patients are getting all kinds of side effects they will strongly suspect they are on the active medication, and they may experience a stronger expectancy effect as a result. “I must be getting the real thing so maybe I really will get better.”

There is a problem even if the drug has no side effects. Imagine a stunningly effective drug that eradicates the problem symptom completely. Patients in the medication condition will notice the vast improvement in their condition and will realize that they must be on the real thing, effectively unblinding the study. But this will be a result of the real effectiveness of the drug. A bigger problem is when the side effects give the story away – potentially making an ineffective medication look better than it really is.

So what?

So even in a well-designed placebo control trial, the study may not actually be blind. As a result, patients may have a greater expectancy effect in the genuine-drug condition than in the placebo condition. The study will show that the drug is more effective than placebo, when in reality the drug condition only had a stronger placebo effect than the sugar pill.

How big a problem is this?

No one knows.

Is there any solution?

Yes. Use a placebo that has side effects. Instead of a sugar pill, we can use an existing medication that is not thought to have an effect on the condition that is being studied. So if we are looking at, say, depression, we could compare our new antidepressant with a drug that produces similar side effects but that has never been shown to be effective against depression. These are called “active placebos.”

Does anyone do this?

It's not done often. In 2004, the Cochrane Collaboration (an organization that conducts reasonably rigourous analyses of the general trend of medical data) published a review of studies in which antidepressants were compared to active placebos (Moncrieff, Wessely, & Hardy, 2004). They found nine such studies - not a particularly impressive number.  

Only two of the nine demonstrated a consistent statistically significant difference between the antidepressant and the active placebo. When the studies were combined, the overall effect size (the difference between drug and active placebo) was 0.39 standard deviations - a relatively weak treatment effect. When one particularly positive trial was not included, the effect size dwindled to 0.17 standard deviations. These differences are smaller than the differences that are usually found when antidepressants are compared to inactive placebo. 

The United Kingdom's National Institute for Health and Clinical Excellence recently chose an effect size of 0.50 as a lower cutoff to represent an effect large enough to be considered clinically (as opposed to statistically) significant. Not everyone agrees with the cutoff, which is somewhat arbitrary, but these findings for antidepressants fall below it. 

Unlike some reviews that find more powerful drug-placebo differences in severely depressed populations, the studies of inpatient populations produced weaker effects than those of outpatient populations.  

This review of a few studies should not be used to conclude that antidepressants are nothing more than active placebo. But it’s not exactly a ringing endorsement, either. The authors concluded that standard drug trials using inactive placebos ("sugar pills") might overestimate drug effects because subjects often figure out which condition they are in and develop higher expectations when they have side effects than when they do not.  

It would be nice to see more studies comparing antidepressant medication with active placebo, to see if we can demonstrate a genuine drug effect that isn't based on patient expectations. Until we do this, some of our former optimism about the antidepressant drug class must be tempered with a bit of skepticism.


Moncrieff, J, Wessely, S, & Hardy, R Active placebos versus antidepressants for depression. Cochrane Database of Systematic Reviews 2004, Issue 1. Art. No.: CD003012.

Tuesday, 22 November 2011

Smoking and overeating: Ways of reducing healthcare costs?

Do smoking and obesity result in higher healthcare costs? Of course they do. This is trivially easy to document. Just take, for example, some smokers and some nonsmokers and compare healthcare-related billings to government and extended-health plans. Studies that do this routinely find differences in the direction you would expect. Smokers cost more.

For example, the rate ratio found in one study for smokers to nonsmokers is 3-1 for heart disease, 10-1 for lung cancer, 2-1 for stroke, 2-1 for a subgroup of other cancers, and 20-1 for chronic obstructive pulmonary disease (Barendregt, Bonneux, & van der Maas, 1997).

It follows that if we were to reduce the rates of smoking and obesity in our culture, we would have lower healthcare costs overall. Obviously.

Sometimes what seems obvious is untrue, however, and this is one of those instances. In fact, smoking and obesity may save healthcare dollars overall.

The key to this apparent contradiction is that smoking and obesity not only affect health status, they also affect mortality. Smokers die earlier – on average, over 7 years earlier for men and 6 years earlier for women.

When you’re dead, your healthcare costs are zero.

So take a pair of 45 year old men, one a smoker and the other a nonsmoker. Sure enough, the smoker has more colds, more early heart disease, more chest symptoms, and his healthcare costs are higher than his clean-living twin. Over time, healthcare costs rise for both of them, because as people age they make more use of the health system.

At age 67 our smoker is incurring much higher costs than our nonsmoker, but at age 68 he dies of a heart attack. Many of the illnesses that finish off smokers are relatively quick and don’t create too many costs.

Upon his death his healthcare costs vanish, whereas the nonsmoker lives into the years associated with more chronic illness, more health problems, and much greater usage of the healthcare system. The moment our smoker passes away, the nonsmoker’s lifetime costs begin to catch up. Eventually, of course, he dies too. But by the time he does, his lifetime healthcare costs have leapt beyond the smoker’s costs.

Barendregt et al (1997) calculated lifetime healthcare costs among Dutch male smokers at $72,700 and nonsmokers at $83,400, and among women smokers at $94,700 versus nonsmokers at $111,000.

So what would happen if everyone suddenly quit smoking? There would be a short-term reduction in healthcare costs as the smokers reaped the benefits of nonsmoking. But eventually the former smokers would live as long as the nonsmokers and the benefit would be wiped out. In fact, healthcare costs would rise.

What about obesity? A similar phenomenon is observed. Obesity is associated with higher year by year health costs, but also with premature death. In a simulation study based on existing risk factors associated with obesity (van Baal et al, 2008), a cohort of obese individuals would be expected to have higher health care costs each year until age 56 than similar groups of smokers or nonsmoking nonobese individuals. At age 57, smokers began costing more. Lifetime health costs, however, would be highest among the nonsmoking nonobese group, lower for the obese group, and lowest for the smoking group.

This intriguing study is only a simulation, and it would be nice to see it borne out in a large-scale epidemiological study. Nevertheless, it offers support for the idea that smokers have lower healthcare costs overall, and it provides a hint that the same may be true for people who are overweight.

People often hate research like this and wonder if those who report on it support obesity and smoking, or are in thrall to the tobacco companies. So does this mean that I am opposed to smoking reduction efforts or the idea of healthy eating? Of course not. I think that the benefits of longevity strongly outweigh the costs. I am no more in favour of people smoking than I am of handing out cyanide-laced lemonade at retirement parties (which would reduce healthcare costs in about the same way), and I work with many clients on developing healthier lifestyles.

In recent years, many governments have attempted to sue cigarette manufacturers for the “additional healthcare costs” associated with smoking. I’ve heard rumblings that we should be doing the same with fast food suppliers.

But if this research on costs is accurate, such additional costs may not exist. I’ve paid attention to these debates, and it appears that the tobacco companies never seem to defend themselves using this data.  Perhaps we shouldn’t be surprised. “Actually, we kill our customers so they wind up costing the healthcare system less” probably wouldn’t make a good sound bite.


Barendregt, JJ, Bonneux, L, & van der Maas, PJ (1997). The health care costs of smoking.  New England Journal of Medicine, 337, 1052-1057.

Van Baal, et al.  (2008).  Lifetime medical costs of obesity: Prevention no cure for increasing health expenditure.  PLoS Medicine, 5(2): e29.

Friday, 18 November 2011

Medications: The Double-Blind Trial

(This post is part of a series on psychopharmacology and medication.)

We've been talking about neuronal signal transmission, the monoamine hypothesis, and the theory of how SSRIs work. Much of the recent controversy about medication rests on the examination of medication outcome trials. So let's take a time out and consider the nature of these studies.

The double-blind placebo control trial has, for better or worse, become the gold standard for the evaluation of healthcare interventions – in the areas of both mental and physical health. These studies sound straightforward enough, but like most subjects in science, things get more complicated the closer we look.

The nature of placebos

A placebo is an inactive treatment - one that no theory would suggest should work from its physical effects alone. Placebos are often referred to as sugar pills, but in fact they might be made of almost anything, so long as the substance is not believed to have any effect on the disorder being examined.

Placebos may not even be pills. Placebo surgery (in which an incision is made but nothing else is done), placebo psychotherapy (in which a clinician meets with a person but doesn't do anything believed to be effective), and placebo light therapy (in which people sit before a light box that doesn't really give off enough light to be helpful) have all been used.

Usually the placebo treatment is made to seem as similar as possible to the other (hopefully active) treatment being tested. So when you're testing the effectiveness of a medication in pill form, your placebo comparison would be a pill of the same colour, size, and shape.

The Confirmatory Bias

Why not just compare a new medication with doing nothing? That, after all, is the usual alternative in healthcare: Treat the person with something thought to be effective, or watch and wait to see whether the problem resolves itself. Why bother with a placebo control?

Human beings are prone to a powerful confirmatory bias. This means that when we develop a theory about something, we automatically assign greater significance to information that conforms to our theory than to information that contradicts it.

If I develop a conviction that rain tends always to fall on my days off, I will notice the sunny days when I am working and the rainy days on the weekend. I will tend to forget the rainy days when I am working, and the few sunny days when I am not. Over time, my theory will seem more and more true.

Similarly, if I think that life goes better when I wear blue socks, I will begin to notice that this seems more and more true. If I think that Vitamin Z cures colds, I will notice my recovery when I take it, and the persisting symptoms when I don't. When we look for evidence of almost anything (unusual behaviour at the full moon, personality types associated with star signs, mood changes associated with certain crystals), we tend to find it. Disconfirming evidence tends to be ignored.

There is a lot of uncertainty in healthcare, but we know this: the expectation of improvement will lead to a perception of improvement - in at least some symptoms, in some disorders, for some period of time. In general, the symptoms most affected will be subjective ones - things like mood, pain, and discomfort.

Placebos do not work with everything. If we give placebos to patients with high cholesterol, this does not seem to reduce their cholesterol over time. Objective measures like blood tests, tissue regrowth, and tooth decay do not seem to be nearly as affected by placebos as subjective indicators. There are exceptions to this principle, but let's leave those alone for the time being.

The Rationale for Placebo Trials

When we administer a treatment for a disorder, we can say (with a bit of oversimplification) that there are two effects:

  1. The genuine, measurable effect produced by the expectation of receiving a treatment for the problem.
  2. The physical impact of the treatment on the problem, regardless of what the client expected.

So if we violate all ethics and sneak pain medication into the food of a person with back pain (producing effect 2 but not effect 1), they should notice a reduction in pain even though they don't know why it is happening. And if we manufacture sugar pills that look like powerful pain medication (resulting in effect 1 but not effect 2), they should also reduce the pain to at least some extent.

And if we show the person the pill bottle, describe the predicted effects of the medication, and provide a pill containing the active ingredient, we will get both effects: expectation plus physical impact.

The question, obviously, is to what extent the improvements we see are attributable to Effect 1 versus Effect 2.

Perhaps our supposed miracle cure is actually no better than placebo, and all of the improvement we see is the product of expectancy. Or maybe we have made a real discovery, and the improvement is partly expectancy but partly physical impact.

Why do we care whether an effect is due to expectancy?

A placebo effect, after all, is still an effect. It's not imaginary, it's real. Do we care whether it is produced by expectancy or by the chemical ingredient?

Well, yes, for a number of reasons.

  1. Placebo effects tend to be somewhat time-limited in their action, and may make a disease process seem to improve while the underlying pathology continues. 
  2. Most medical treatments have disadvantages as well as advantages. A medication that alleviates cholesterol might strain the liver, for example. If the chemical ingredient of our medication does no good but causes harm, we need to know this.
  3. There's an ethical issue involved in charging large sums of money for inactive ingredients.

Plus, the healthcare professions pride themselves in having treatments that are more advanced than the superstitions of centuries past. If our new patented medication is no better than repeating an incantation three times, then why do we fund medical healers but not faith healers?

The double-blind trial

In a double-blind trial, neither the person taking the placebo (the patient) nor the person giving it (the clinician) knows which medication the person is receiving.

It's obvious by now why the patient shouldn't know which treatment they are getting: This controls for expectancy, or at least it should. (There are some problems with this reasoning, but I'll leave that for another post.) So people who receive Treatment A should have about the same expectation of improvement as those receiving Treatment B. If we have succeeded in keeping expectancy the same in both groups, then any differences we see should be attributable to the chemical ingredient in the pill.

But why do we need the caregiver to be blind as well?

We know that people communicate a great deal by their nonverbal behaviour. Presumably no one in a blind trial would announce to the patient, "You're in luck - you get the real drug!" But they might do so involuntarily. If they believe that the drug is effective, they might show more anxiety and less optimism when seeing people who are taking the placebo. The result could be that patients in the placebo group would develop less powerful expectancy effects than those in the active treatment group.

As well, some of the outcome measures are collected by the treating clinician. For example, one of the outcome measures for many depression trials is a physician-rated scale. If the clinician believes in the effectiveness of the medication, he or she might see greater improvement in people receiving the active treatment than in those receiving placebo - even if they are trying their hardest to be honest and even-handed. Similarly, if they believe the medication doesn't work, they may fail to see genuine effects in the drug condition.

Consequently, it's important that the clinician - and anyone else doing evaluations of patients - not know which treatment a given patient received (particularly if there is any subjective element whatsoever to the outcome measure).

Sounds great.  But...

The problem is that placebo control trials are not quite as simple as advertised. A lot of assumptions are made about how they work, and it is easy to make interpretations that aren’t warranted. In upcoming posts we’ll explore several of these:

  • In a double-blind trial, neither patient nor clinician knows which condition the patient is in.
  • Differences between placebo and medication can be attributed to the chemical effects of the medication.
  • The placebo effect is the degree of improvement seen in the group of patients given the inactive medication.
  • Expectancy is the only determinant of improvement in the placebo group.

In fact, none of these statements is necessarily true. Stay tuned.

Tuesday, 15 November 2011

PsychologySalon November 22 at UBC Robson Square: When Our Minds Play Tricks On Us

The Tuesday November 22 PsychologySalon presentation at UBC Robson Square (7-9 pm) will feature Dr Lindsey Thomas. For tickets, call Changeways Clinic at 604 871 0490 or buy online here.

Dr Thomas is a registered psychologist at Changeways Clinic who works with people experiencing a wide variety of difficulties – mainly using the perspectives of Cognitive Behaviour Therapy and Acceptance and Commitment Therapy. I spoke with her about her upcoming talk.

What is your talk about?

I’m going to be talking about some of the different distortions that can happen in our thinking – distortions that tend to become more pronounced in people when they are experiencing anxiety, depression, and anger.

Is this a talk that’s applicable for everyone?

Definitely. Cognitive distortions are things that we are all vulnerable to. I think that everyone will see themselves in at least some of what I talk about.

Can you give me an example of a distortion?

Sure. One of these is all or nothing thinking, which is a tendency to think in extremes. Things are either right or wrong, good or bad. The in-between or grey area gets missed. We see this particularly in people who have difficulties with depression and managing anger.

When might a person use all or nothing thinking?

One way would be to assume that we have all the answers. For example, I might assume that I have the right answer and that everyone else is wrong. As you can imagine, this can set people up for having difficulty relating to others.

I bet.  But why bother knowing our mistakes? Why is it useful to know how we distort things?

These thoughts are automatic; they often happen without our awareness. The goal is to slow the process down, learn to see the distortions as they occur, and work toward changing them if necessary.

Is this all about positive thinking?

Not at all. Although there is some value to seeing the positive side of things, this is more about looking for the evidence, and challenging the problematic thoughts that get us into trouble.

Is there anything wrong with positive thinking?

It’ll only take us so far. Cognitive distortions can shift us toward being either too positive or too negative; both of these can be a problem. This is more about coming into line with what’s really happening.

How do we make our thinking more realistic?

One of the main ways is to stop ourselves, look at what we are actually thinking, and then look at the evidence behind those thoughts. I’ll show some particular strategies in action at the talk.

What if I’m not depressed or anxious?

Again, this is something we all do, whether we are extreme enough to say we’re depressed or not. I’ll be giving a lot of examples, and demonstrating some strategies. I want the talk to be as practical as possible, so that people will take away useful ideas that they can use in their own lives.

*     *     *

This will be our final talk for 2012. We will start up again on March 27 with Out of the Blue: The Nature and Treatment of Clinical Depression with Dr Randy Paterson.

Information and online registration for all talks can be found here. Tickets can also be purchased at the door.

Friday, 11 November 2011

Medications: How are SSRI Antidepressants Supposed to Work?

(This is part of a series of posts on the basics of psychopharmacology that I’m posting so that I can refer people back to it. Here is the first in the series.)

The SSRI antidepressants include medications such as citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac), fluvoxamine (Luvox), paroxetine (Paxil), and sertraline (Zoloft).

SSRI stands for Selective Serotonin Reuptake Inhibitor, which summarizes how the drugs are supposed to work. Let’s consider these terms:

Selective. Unlike some of the older antidepressants (such as the tricyclics like amitriptyline and clomipramine), SSRIs are intended to act on a single neurotransmitter system. They are, thus, selective in the system they act upon.

Serotonin. The specific neurotransmitter affected by SSRIs is serotonin.

Reuptake. Reuptake (discussed at greater length here) is essentially a recycling process. The sending neuron dumps neurotransmitter into the gap between it and the receiving neuron, then opens its own ports and takes some of the transmitter back for use next time. If there is a problem with the pathway, however (not enough neurotransmitter, for example, or too few receptors), reuptake runs the risk of preventing signal transmission.

Inhibitor. The action of an SSRI is to inhibit the reuptake process. It closes the gates to the reabsorption, or reuptake, of serotonin by the sending neuron. As a result, more serotonin is left in the gap, increasing the likelihood that enough will get across to the receiving neuron’s receptors that it will fire.

So an SSRI should make serotonin systems work better by keeping released transmitter in the gap, rather than prematurely depleting it through reuptake.

Note what an SSRI does NOT do, contrary to what some people might believe:

  • It doesn’t create more serotonin in the brain.
  • It doesn’t correct any flaw in the system.
  • It doesn’t produce more serotonin receptors.
  • It doesn't "rebalance" the neurotransmitters.
  • It does not treat the cause of the depression, whatever that might be.

The last point is important. No one believes that the root cause of depression is excessive reuptake in serotonin systems. A reuptake inhibitor might help, just as a brace might help a person with a bad knee to get around, but it does not correct any known cause of depression.

What is an SNRI?

An SNRI is a Serotonin and Norepinephrine Reuptake Inhibitor. In other words, it is thought to work much the same as the SSRIs. But rather than being selective, it does the same thing on both serotonin and norepinephrine systems.

The SNRIs include venlafaxine (Effexor), desvenlafaxine (Pristiq), duloxetine (Cymbalta), and others. Pristiq is a remarkably similar drug to Effexor, and was introduced to the market in 2008, shortly before the patent (hence profitability) of Effexor ran out. This may have been coincidental. Or not.

A variant of the monoamine hypothesis suggests that some depressed people may have a problem in serotonin-based systems, some might have more of an issue with norepinephrine-based systems, and some might have problems in both.

This notion has some appeal, because depression looks very different in different people. Some people are agitated, others look very slow-moving. Some sleep all the time, others have insomnia. Some can’t stop eating, others have no appetite. Maybe the differences have to do with different chemical problems in the brain.

The test of this idea is probably obvious. If an SSRI treats only one subgroup of depressed people, and an SNRI treats two subgroups, then SNRIs should be more effective overall.

Yes, but the data in depression treatment tends not to match the theories. There is relatively little evidence for the superiority of SNRIs over SSRIs. Response rates are about the same.

Coming up:  Let's consider some of the ideas indicated by the monoamine hypothesis.