Posts Tagged ‘depression’

Grief and Depression

March 16th, 2012

If you read the popular press, you are aware of the controversy about dropping the bereavement exclusion from the diagnosis of Major Depressive Disorder in DSM-V. The Lancet published an editorial in their February 18th issue decrying what they called the classification of grief as a mental illness. The same issue carried a moving Perspective by Dr. Arthur Kleinman, who described the recent death of his wife, his own bereavement, and his warning against “medicalizing” grief.

Freud struggled with the separation of grief and depression. His elegant monograph Mourning and Melancholia bears re-reading today.

The thought of turning natural grief into an illness and treating it with drugs is anathema to me. Grieving truly is a normal, personal, intimate process. It requires friends and loved ones and, as Freud describes, it is a gradual, healing path of saying good-bye and moving forward with the rest of one’s life.

But sometimes loss triggers the pathological mood state of depression. I have seen patients whose normal grief went off track and ground to a halt when the pall of depression descended on them. When they were treated with antidepressants or psychotherapy, they were able to resume the healing process, move forward in grieving, and find their place again in the world.

I am no expert in nosology. But as a clinical psychiatrist, I do hope the framers of the next DSM will find a path between the extremes—neither medicalizing a normal process, nor making it impossible for a grieving person who then develops depression to legitimately receive proper treatment.

-Alan J. Gelenberg, M.D.
Editor,
Biological Therapies in Psychiatry
Shively/Tan Professor and Chair, Psychiatry, Penn State University
Editor-in-Chief,
Journal of Clinical Psychiatry

 

Can Too Much Work Make You Depressed?

January 30th, 2012

Last week two reporters asked me to comment on an article in the open-access journal PLos ONE.

Citation: Virtanen M, Stansfeld SA, Fuhrer R, Ferrie JE, Kivima¨ki M (2012) Overtime Work as a Predictor of Major Depressive Episode: A 5-Year Follow-Up of the Whitehall II Study. PLoS ONE 7(1): e30719. doi:10.1371/journal.pone.0030719

http://www.cnn.com/2012/01/25/health/working-overtime-doubles-depression/index.html?hpt=he_c2

The study, by Virtanen and others, followed 2,123 British civil servants for 6 years. It found that workers who put in an average of at least 11 hours per day at the office had roughly two and a half times higher odds of developing depression than their colleagues who worked a standard 7 or 8 hours. The association of long workdays with depression persisted even after the researchers took into account potentially confounding factors such as job strain, the level of support in the workplace, alcohol use, smoking, and chronic physical diseases.

Psychiatrists know that many factors contribute to a person’s becoming depressed. These days we assume genetic and early-life variables set the stage for depression later in life. But immediate factors play a role too. Working long hours for an extended period takes away time to unwind, to seek comfort and pleasures in recreation, friends, and loved ones. Then there is the element of control. In the Virtanen study, the length of the workday didn’t have a perceptible impact on the mental health of higher-paid, top-level British civil servants —employees such as cabinet secretaries, directors, team leaders, and policy managers. I have the good fortune of choosing when I work extra and on what projects. It’s more fun and less adverse

When we consult to individuals or employers, we’ll want to keep this study in mind. Individuals at risk for depression should be cautious about long stretches of overtime work—if they have a realistic choice. And supervisors will want to take a long view: get extra work accomplished, but don’t burn out your most valuable workers.

-Alan J. Gelenberg, M.D.
Editor, Biological Therapies in Psychiatry
Shively/Tan Professor and Chair, Psychiatry, Penn State University
Editor-in-Chief, Journal of Clinical Psychiatry

 

 

 

 

The Best Laid Plans

April 8th, 2011

During the decades I have spent in academic medicine and psychiatry, I have read countless inspired theories and hypotheses concerning diseases and their treatments. Unfortunately, few have panned out. Scientists were going to cure schizophrenia with renal dialysis. Personally, I was going to alleviate tardive dyskinesia and depression with the dietary neurotransmitter precursors lecithin and tyrosine.

Fortunately, medical science is not a religious faith. The nature of empiricism allows for hypotheses to be proved—or more commonly, disproved. That’s been the story of my career and, sadly, most psychiatric science of the last century. But in our healing arts, it’s better to face the truth.

Doesn’t it stand to reason that if we inhibit both the norepinephrine and serotonin reuptake pumps, we should heal more depressed people than if we block only the serotonin transporter? A study called PREVENT showed that not to be the case.

And if we administer long-acting injectable antipsychotic medicines to patients with schizophrenia, shouldn’t we lower the relapse rate more than if we depend on their taking oral tablets? Again, no. An upcoming article in Biological Therapies in Psychiatry—“Does LAIR Beat Oral Antipsychotics?”—bursts this very logical bubble.

Someday, we’ll reach “personalized medicine” in psychiatry. Someday, more good theories will prove true than not. We’re not there yet.

-Alan J. Gelenberg, M.D.
Editor, Biological Therapies in Psychiatry
Shively/Tan Professor and Chair, Psychiatry, Penn State University
Editor-in-Chief, Journal of Clinical Psychiatry


 

Dandelions and Orchids

March 11th, 2011

Dandelions are hardy. Give them a crack on a city sidewalk, and they will thrive. The beautiful orchid, by contrast, is much more delicate. To thrive it needs conditions like those in Costa Rica: warm, sunny, and moist.

Increasingly, research on the human genome suggests that important gene-environment interactions may lead to psychiatric syndromes. An example is that two short alleles on the serotonin-transporter (5-HTT) gene may heighten vulnerability to depression under adverse circumstances.

Why would such vulnerability genes survive? Shouldn’t people who inherit them be adversely selected, so their genes would decrease and die out over generations? Or, might such genetic patterns give evolutionary advantage in selected environments—something like sickle-cell trait making people more resistant to malaria?

Emerging evidence, including data from studies by Penn State scientists, suggests that some genetic patterns, such as two short 5-HTT alleles, might confer behavioral advantages in an optimal environment. People with two short alleles who grow up in nurturing, intact families, with educational and economic privilege, may actually show greater resilience and creativity, while others with the same genetic pattern, who come from poverty and dysfunction, may do worse than average. If this theory is correct, the people with two short 5-HTT alleles are “orchids,” doing beautifully in ideal environments, but worse than average in bad environments. The majority of people, who have either a short and a long or two long alleles, are “dandelions,” doing moderately well in a broad range of environments.

As I write periodically in BTP, we stand on the threshold of dramatic and exciting breakthroughs in understanding the brain. In time, these discoveries should help people who suffer from psychiatric syndromes—including autism, ADHD, depression, and PTSD

Alan J. Gelenberg, M.D.
Editor,
Biological Therapies in Psychiatry
Professor and Chair, Psychiatry, Penn State University
Editor-in-Chief,
Journal of Clinical Psychiatry

Cognition and Depression

December 27th, 2010

Someday psychiatric diagnoses will entail biological tests. Today we rely on clinical knowledge.

Cognitive function can suffer when someone is depressed. Depressed patients often have trouble concentrating. Their minds wander. They are less productive, more distractible. But some elements of memory or cognitive dysfunction suggest other diagnoses.

Some years back I took a phone call from a university administrator in his late 60s. He had driven up to the keypad in his gated home and had forgotten the numeric combination. He assumed it was the stress he was under and that he should talk to me, a psychiatrist. Anxiety, depression, stress—none of these sounded right to me as an explanation of forgetting an over-learned four-digit code he used daily. I asked him to see his primary-care doctor immediately, and to be safe, I talked to his physician with the same sense of urgency. It turned out his blood pressure was extremely high (that’s where the stress factored in). He had experienced an encephalopathy. When his blood pressure returned to normal, his
cognition and memory also normalized.

The other day I got a call from an internist at my medical college. An 80-year-old patient who was also a long-time friend was upset about his son’s choice of a partner. The man’s wife believed he was depressed and phoned my colleague requesting that he prescribe an antidepressant for her husband. He preferred that his patient talk to a psychiatrist first. I phoned the man and was troubled when he described symptoms he attributed to family tensions. Having been married for over 40 years, he had recently called his wife by a wrong name several times. And when she drove to pick him up a day earlier, at first he didn’t recognize her. As in the case above, these sounded more “organic” to me. Differential
diagnoses that came to my mind included primary and secondary brain tumors (possibly setting off seizures), hypertension, other encephalopathies. Sometimes Alzheimer’s or other dementias begin in a stuttering fashion. In any case, the mental lapses he was experiencing didn’t sound to me like depression.

But when I met him in person, the picture changed. Showing a full and appropriate range of affect in the interview, and able to describe pleasurable activities with passion and relish, he was not depressed. Moreover, his short- and long-term memory and executive functions were impressive. Perhaps he would develop dementia over the coming years, as many people over 80 years do—but he wasn’t demonstrating it today. Instead, he described mounting marital tensions. At the end of my consultation, we discussed how he and his wife might address these. (His internist saw him and ordered additional tests. All were negative.)

Someday psychiatric diagnoses will entail biological tests. Today we rely on clinical knowledge.

- Alan J. Gelenberg, M.D.
Editor,
Biological Therapies in Psychiatry
Professor and Chair, Psychiatry, Penn State University
Editor-in-Chief,
Journal of Clinical Psychiatry

One More Question

December 20th, 2010

More than one senior colleague has advised me to include a family member as often as possible when interviewing a depressed patient. Often I’ve heard patients complain of sleeplessness or anhedonia, only to have a relative or friend present a very different picture. Such disparities should profoundly affect our diagnostic impressions and treatment decisions.

Yesterday there was only the resident and me in a room with a patient referred from a primary-care doctor for evaluation of depressive symptoms. The resident asked about low mood and anhedonia, both of which the man endorsed. But as I listened quietly, I thought I caught a spark of animation when the patient described some of his extracurricular interests. When it was my turn to ask a few questions, I inquired about what had given him pleasure over the past few days. Nothing, came the reply. There was no loved one to give collateral information, so I pursued an alternate tack. I asked the man about a few of his hobbies. As he described a team he played on and favorite spectator sports, he came alive, was engaged, passionate, and animated. His face lit up, and he smiled.  Our diagnosis and treatment recommendations shifted.

I enjoy the challenges of solving diagnostic puzzles. It’s one of the joys of medicine and psychiatry—and a reason ultra-brief visits can be costly in more ways than one.

- Alan J. Gelenberg, M.D.
Editor,
Biological Therapies in Psychiatry
Professor and Chair, Psychiatry, Penn State University
Editor-in-Chief,
Journal of Clinical Psychiatry

Bad, bad Benzos?

September 27th, 2010

Six or seven years ago, a patient of mine was moving to a nearby state. Through the local university’s psychiatry department, I arranged for her care to be delivered by a recent graduate from their residency. We spoke by phone about the transfer. She sounded competent and nice.

My patient was taking an SSRI daily and a prn benzodiazepine—diazepam, I seem to recall. My younger colleague was appalled. She repeatedly questioned me with an anxious tone about the need and justification for this dangerous drug. I sought to clarify and reassure her.

Used appropriately and cautiously, benzodiazepines can do good. They can offer immediate relief of anxiety and insomnia, and they certainly feel different than an antidepressant. They work fast. They are good during the first few weeks of antidepressant treatment of depression or many anxiety syndromes. Benzodiazepines are also good for prn use during a “rough patch.”

Downsides? They have many. They should be prescribed with great caution, if at all, to patients with a history of dependency. Sudden withdrawal (even an abrupt reduction in dose) can be lethal. And they cause the full range of sedative-hypnotic side effects—like sedation, amnesia, confusion, and ataxia. Add alcohol or another sedative-hypnotic, and these effects can mushroom.

I caution patients strongly to be careful about driving or anything that can be hazardous—like climbing a ladder. If a patient takes a benzo at bedtime, I advise the patient to look for hazards between bed and bathroom. It’s so easy to trip in the dark if one is unsteady. With older patients, this problem is magnified.

Which benzo to choose? It depends. Know the pharmacokinetics. Duration of action is terminated by distribution with single use, so a lipophilic agent like diazepam is quick in/quick out. With repeated use, half-life determines how long the drug works. The one benzo I really dislike is alprazolam. Alprazolam’s kinetics and dynamics make it troublingly addictive and hard to stop.

Are benzodiazepines good? Or bad? They are drugs—double-edged swords. We can prescribe them wisely.

Mood Disorders: Intervention works

July 29th, 2010

Bob Post just gave our weekly grand rounds at Penn State. Speaking from his long, productive (over 900 publications!), and illustrious career in studying mood disorders, Bob addressed the long-term course of unipolar and bipolar disorders. He speaks with the passion he feels for the topic and compassion for those who suffer from the ravages of these brain diseases.

Most probably people inherit a genetic vulnerability to mood disorders. It will be a long, long time before doctors can correct DNA anomalies. But stresses and abuse, especially in childhood but even long after, also contribute to the risk of episodes of depression. Current science suggests these environmental variables adversely affect brain structure and function, perhaps via epigenetic effects, which control how genes express coded proteins. More mood episodes are bad. They hurt, carry mortality and morbidity risks, and adversely affect function. Beyond that, they make future episodes even more likely, compromise long-term function and disease course, add medical and substance-abuse co-morbidity, and worsen treatment response.

The good news is that intervention works—decreasing the risk of future episodes, improving outcome, and saving lives. The broad array of treatments for bipolar disorder and recurrent depression—including medicines, stimulation techniques, psychotherapy, rehabilitation approaches, and perhaps even diet and exercise—protect the brain. Many increase levels of brain-derived neurotrophic factor (BDNF), which appears to attenuate the effects of bad life events.

Dr. Post emphasized the importance of early intervention in patients with mood disorders. (The typical lag from onset of bipolar disorder to first clinical attention is typically on the order of 10 to 15 years!) He also stressed the benefits of life-long treatment. In addition to warning patients about side effects, Bob suggests we tell patients about the positive benefits of psychiatric treatments for their brains.