Dr. Qaadri

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Medical Post Depression Interview - 1

The media is often talking about the overuse and overmedication of depression, yet we as physicians are being taught that depression and mood disorders are under-diagnosed and under-managed. How do we reconcile this?

There are several stories that are simultaneously occurring. The scientific literature demonstrates that persons who suffer from mood disorders are largely underdetected and undiagnosed, and certainly do not receive guideline-concordant therapy. That is unambiguous and unequivocal.

My speculation about what might be happening is this—it is indeed true that there are people who are receiving psychiatric care who may not be receiving it for appropriate indications…For example, it’s not uncommon for me to meet someone who’s suffering from a mood disorder, such as major depressive disorder, who’s been receiving a benzodiazepine for years as the cornerstone of therapy. That’s an example of someone who has a bone fide illness and need for treatment, but who is receiving a medication that is inappropriate for the illness…

There’s also a larger issue: the majority of people who suffer from major depressive disorder are not seeking out appropriate care, and often rely on self-medication, and other sundry types of treatment. I think this partly explains the remarkable disconnect between the treatments available, and how inadequately many patients are being treated.

How should busy family physicians make the diagnosis of depression?
In family medicine, often the diagnosis is made in two ways—almost a gut diagnosis, relying on their clinical acumen and experience. The literature shows that family physicians do very well, and are able to make the diagnosis of depression quickly.

Perhaps the second, more traditional way, is to make a diagnosis of exclusion. For example, there will be lists of blood tests and medical disorders that have been ruled out, in a systematic way, and if everything comes back negative, that may lead to the diagnosis of depression.

It’s my sense that these two processes work together—the gut instinct with an algorithmic approach…The challenge is for family physicians to deal with patients who present with a complex myriad of somatic and psychosocial complaints, which may take considerable time to sort out.

What is the difference between clinical depression and the ‘blues’?
The blues would be a statistically common, and by definition, transitory and non-impairing condition, that most human beings will experience.

For example, when a child leaves home, the parents may feel a sense of loss, or when people lose out on a job, or a relationship, and so on. It’s not pathological insofar as it doesn’t significantly interfere with functioning, and does not in fact endure.

I would say that depression is differentiated on those two levels: one, it’s more enduring and persistent; and second, it’s more impairing. People are in fact unable to enter into relationships, socially they may not quite be themselves, and you begin to see an enduring dysfunction.

The DSM IV (Diagnostic and Statistical Manual for Mental Disorders) duration criteria for depression—the time for symptoms—is only two weeks. Is that not a little too short for a diagnosis of clinical depression?
I personally don’t find that to be too short, it’s a fair number, and we have refined our understanding of depression. It is an illness that clearly is chronic and recurrent, and it is also an illness that is quite fluid…The biostatisticians have to cut the bar somewhere, and I think two weeks meets the statistical requirement for validity and reliability.

I think we may have inadvertently promoted the story that many patients have episodes of depression which clear up after several weeks. I think that as disease models, hypertension and diabetes are much more analogous: symptoms that are more persistent, fluid, changeable, and chronic.

It’s also been my experience, that when patients are followed longitudinally with depression, they have episodes which last from a week to ten days, other episodes that last several weeks, others which last several months and beyond…There’s a waxing and waning both in the severity and duration.

Does anyone actually use the many depression rating scales that are available?
Yes, but very infrequently…I passionately believe that we should use scales more often: this will cut down on wasted time, allow a more focused assessment, lead to earlier therapy, and better outcomes.

There are two parts. For a rating scale or tool to be employed, it has to be validated—it has to be shown that it works. There is good scientific literature showing that this has been accomplished.

The second issue is what is the clinician’s motivation to use a particular scale? There are many scales that exist that meet the scientific threshold and criteria, but are not adopted in clinical practice, even though we know that they’re helpful. For example, clinicians may question how the use of the scale improves clinical practice, and how does it benefit patients.

Also, the dissemination of these rating tools has been an area of weakness. Similarly, depression treatment guidelines have also been shown to be effective, but their dissemination is weak, and clinicians don’t really use them.

Why is it that all roads lead to Serotonin—meaning that this neurotransmitter has been implicated in essentially every mood condition, whether it’s depression, anxiety, eating disorders, obsessions, and so on?
As life becomes more complex, the human need for simplicity has never changed.

Psychiatric illnesses by definition are complicated illnesses, which cover the full array of thinking, mood, behaviour, and social interaction. It is attractive, if you will, to bring parsimony to any explanation.

Serotonin remains an intriguing explanatory model, because it is integral to so many physiologic functions—sleep, energy, concentration, sexual function, mood, motivation, thinking, and so on.

Complex illnesses require complex models: if you want to keep it simple, than you want something that’s at the root of the matter. As a construct, the serotonin model does help to bring together many different conditions.

We are learning that there are many psychiatric illnesses such as depression, anxiety, eating disorders, impulsive disorders like alcohol abuse, and so on, that may be related. They have overlapping and similar neurobiological abnormalities, so medications that engage serotonin may be therapeutic for an array of conditions.

Do family doctors, along with patients, chase only isolated symptoms, like sleeplessness or anxiety?
I think clinicians do what they can. My sense is that we do, in fact, take a symptom-based approach. Not all dimensions of a depressive illness are equally severe or equally disabling to patients…Sleep and anxiety are always—not sometimes—but always an issue for patients.

We need to take a systematic approach to our treatments: which symptoms are most prominent, and what symptoms can we most effectively treat?

What is meant by “sleep architecture,” and have our previous first-line therapies such as the benzodiazepines been interfering with it?
Loosely stated, sleep architecture would be the electrophysiological signature, as measured with sophisticated laboratory instruments. The analogy would be the “electrocardiogram of your sleep,” looking at the sine waves and the electrical activity. It’s a proxy of the normality, or lack thereof, of the sleep pattern.

The medications that we currently have, such as the benzodiazepines, although clinically we know that they can be of assistance in putting somebody to sleep, actually interfere with the sleep architecture, the electrophysiologic reading…They do not appear to offer a health-promoting effect on the electrophysiology: patients get to sleep, but it’s not the most restorative sleep.

We see similar effects with alcohol. We know that alcohol puts people to sleep, but it actually has a deleterious effect on sleep architecture, the sleep rhythm.

What is the genetic and gender bias in depression?
The gender bias is an interesting one: female patients have a higher incidence of depression. They may have a slightly different symptom profile, perhaps with more anxiety-comorbidity, eating disorders, associated with premenstrual dysphoric disorders, the perimenopause, pregnancy, and physical and sexual abuse. Also, although not entirely certain, women seem to be at higher risk for recurrent episodes.

Men tend to have more problems with alcohol and substance abuse disorders.

The genetic bias is unclear. Genetics do play a role in depression, but we have not nailed down any gene or cluster of genes that give us a full explanation.

When considering the goals of treating depression, what is the difference between response and remission?
Response means that the patient is partially improved, whereas remission means the symptoms have fully abated. For example, a responder would be experiencing some symptoms, whereas a remitter would be experiencing no symptoms.

What are your thoughts about talk-therapy versus drug-therapy for depression?
Both are modalities of therapy that are effective—antidepressant pharmacotherapy, along with cognitive behavioural therapy and/or interpersonal psychotherapy.

We need to be clear as to which psychotherapy has been proven, with good science, to be of help, and those are the modalities that have been shown to be effective.

Larger questions are which type of therapy is most effective. For mild to moderate depression, which is the lion’s share, both drug therapy and psychotherapy have been shown to be equally effective.

For the more severe depressions, it appears that pharmacotherapy may have an edge. Part of this is just pragmatics: severely depressed patients can’t concentrate on their therapy, and are not motivated to participate.

In this post-Prozac era, are the newer drugs smarter—more targeted with less side effects? Are they designer drugs?
I would say largely no. The treatments that we have developed in the last fifteen years have advanced tolerability and safety. When it comes to their robustness and their depth of efficacy, there have been some gains, but that is not the primary advantage.

Now, having said that, some of the newer treatments such as duloxetine [Cymbalta], venlafaxine [Effexor], mirtazapine [Remeron]—these are drugs that may have a slight advantage in terms of efficacy. So the depth of the efficacy may have a higher octane, or they may have a slightly faster onset of action.
I must emphasize that this may be true, because I’m not certain that this is true for most patients, or only certain sub-populations.

What is your final message?
Diagnose early--depression that is undiagnosed not uncommonly progresses to a chronic, refractory illness. When initiating therapy, adhere to guidelines, and we’re recommending lengthier treatments as we’re learning more about this chronic disease state.

Dr. Shafiq Qaadri is a Toronto family physician and Continuing Medical Education (CME) lecturer. www.doctorQ.ca

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