Evidence-Based Reviews

Discuss this article at http://currentpsychiatry.blogspot.com/2010/08/depression-in-older-adults.html#comments

Depression in older adults (age ≥65) can devastate their quality of life and increase the likelihood of institutionalization because of behavioral problems.¹ Depression is a primary risk factor for suicide, and suicide rates are highest among those age ≥65, especially among white males.² The burden of geriatric depression can extend to caregivers.¹ Prompt recognition and treatment of depression could help minimize morbidity and reduce suffering in older adults and their caregivers.

Although geriatric depression varies in severity and presentation, common categories include:

• major depressive disorder (MDD)
• vascular depression
• dysthymia
• depression in the context of dementias, psychosis, bipolar disorder, and executive dysfunction.

Diagnoses in this population generally correspond with DSM-IV-TR criteria, but geriatric depression has distinct clinical manifestations.^1,2 Compared with younger depressed patients, older adults are less likely to endorse depressed mood and more likely to report a lack of emotions.^1,2 Older patients report feelings of irritability and fearfulness more often than sadness.^1,2 Mood symptoms tend to be transient, reoccur frequently, and display either a diurnal pattern or multiple fluctuations in a single day.^1,2 Other common presentations include loss of interest in usual activities, lack of motivation, social withdrawal, and decline in activities of daily living.^1,2

Summary of recommendations

Age-specific recommendations for assessing and treating geriatric depression can be generated in part from evidence-based reviews, meta-analyses,³ and geriatric expert consensus guidelines.⁴ Such guidelines and recommendations often do not take into account the marked heterogeneity of medical, cognitive, and overall functioning in patients age ≥65, however, because they are based on studies of younger populations and patients with complicated issues often are excluded from studies. The recommendations in this article are based largely on findings from a National Institutes of Health (NIH)-sponsored project by Alexopoulos et al to develop consensus guidelines for managing geriatric depression and expert opinion from clinicians who treat geriatric patients.⁴

During your initial clinical evaluation, confirm the diagnosis and type, duration, and severity of depression. Seek to understand the biopsychosocial context of each patient’s presentation. Carefully consider your patient’s suicide risk. Hospitalization may be required if he or she is at high risk for suicide or has complex medical and social circumstances that cannot be managed adequately in an outpatient setting.⁵

Unipolar major depression

For unipolar, nonpsychotic geriatric depression, the NIH-Alexopoulos et al guidelines emphasize a combination of antidepressants and psychotherapy (Algorithm 1).⁴ Selective serotonin reuptake inhibitors (SSRIs) and venlafaxine are first-line options.^4,6,7 Tricyclic antidepressants (TCAs), bupropion, and mirtazapine are alternatives.⁴ Among SSRIs, citalopram, escitalopram, and sertraline are preferred initial antidepressants. Fluoxetine is used less frequently.⁴ Paroxetine also is less commonly used because of its anticholinergic effects and because the drug inhibits cytochrome P4502D6,² which metabolizes several medications commonly prescribed for older adults. Among TCAs, nortriptyline is preferred.⁴ Studies have shown that duloxetine improves depression and is safe and well-tolerated in older adults with recurrent MDD.⁸ Electroconvulsive therapy (ECT) is an option for treating severe or treatment-resistant unipolar major depression.⁹

For unipolar depression with psychotic symptoms, guidelines recommend a combination of an antidepressant and an antipsychotic or ECT.⁴ Atypical antipsychotics are preferred over typical antipsychotics⁴; risperidone, olanzapine, and quetiapine are most frequently used.⁴ Clinical data on aripiprazole and ziprasidone in older adults are limited. Many geriatric experts recommend continuing an antipsychotic for 6 months after symptom remission, then gradually tapering the dose.⁴

During acute illness, administer an anti-depressant for 6 to 12 weeks at the individually determined dose required to achieve symptom remission.⁶ For an older adult experiencing a first lifetime episode of major depression, continue antidepressant treatment for 1 year after remission.⁴ If your patient has had 2 lifetime episodes of major depression, continue the antidepressant at the same dose used to achieve remission for at least 3 years. For patients who have had ≥3 episodes of depression or whose index episode was particularly severe or involved significant suicidal thoughts or behaviors, continue maintenance treatment indefinitely.

Algorithm 1: Treatment for unipolar depression in geriatric patients

ECT: electroconvulsive therapy

Bipolar depression

Mood stabilizers such as lithium or valproate—as monotherapy or in combination with an antidepressant—are recommended to treat bipolar depression without psychotic symptoms in older adults (Algorithm 2).¹⁰ For bipolar depression with psychotic symptoms, a combination of a mood stabilizer and an atypical antipsychotic or ECT is recommended.¹⁰

Older adults’ increased sensitivity to side effects and reduced ability to tolerate lithium may limit its use and may prompt you to consider atypical antipsychotics as alternatives to other mood stabilizers. Although quetiapine and fluoxetineolanzapine combination are well studied in younger patients,^11,12 there is a lack of data to support their clinical effectiveness and tolerability in older adults. Among antidepressants, SSRIs or bupropion are preferred over TCAs to prevent a switch to mania.¹⁰ Lamotrigine is an effective maintenance treatment for bipolar depressive episodes in older adults.¹³

Although optimal mood stabilizer and antidepressant dosing for this population has not been adequately assessed, pharmacotherapy that has been effective generally should be continued without modification for at least 6 to 12 months.¹⁰ After the patient achieves remission, gradually discontinue antidepressants while maintaining the mood stabilizer.¹⁰

Algorithm 2: Bipolar depression: Options for combination therapy

ECT: electroconvulsive therapy; SSRIs: selective serotonin reuptake inhibitors

Depression in dementia

Managing depression in dementia patients is similar to treatment in older adults without dementia,^5,14 although pharmacologic agents must be carefully selected because of increased risk of side effects (Algorithm 3). American Psychiatric Association practice guidelines recommend considering antidepressants for depressed patients with dementia even if their mood disturbances do not meet DSM-IV-TR criteria for MDD.⁵

SSRIs’ lower side effect profile make them the preferred treatment; the selective serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine is a second-line option.^4,14 Avoid TCAs and other agents with anticholinergic side effects because of potential cardiovascular complications and cognitive side effects, unless SSRIs or SNRIs are ineffective or contraindicated.¹⁴ Recently clinicians have been reluctant to use antipsychotics in patients with dementia, because of the FDA’s “black-box” warning regarding the increased mortality risk associated with their use in this population.

When using ECT to treat depression in patients with dementia, the treatment protocol often is modified to twice-a-week, unilateral stimulus because of these patients’ increased risk of delirium.¹⁴ The safety of ECT to treat depression in patients with dementia has not been adequately assessed.¹⁴

Algorithm 3: Treating comorbid depression and dementia

ECT: electroconvulsive therapy; SNRI: selective serotoninnorepinephrine reuptake inhibitor; SSRI: selective serotonin reuptake inhibitor

Vascular depression

The “vascular depression hypothesis” proposes that accumulation of subcortical white matter hyperintensities can disrupt frontostriatal pathways, resulting in depressive symptoms.¹⁵ This hypothesis is supported by the confluence of depression and vascular risk factors.¹⁵ Sertraline, citalopram, nortriptyline,¹⁶ and trazodone¹⁵ have been shown to reduce depressive symptoms after a stroke.

Minor depression and dysthymia

Although the efficacy of antidepressants in minor depression—depression that does not meet criteria for MDD—is not well established, expert consensus guidelines recommend SSRIs and psychotherapy, separately or in combination, for minor depression and dysthymia in older adults (Algorithm 4).⁴ Depression in executive dysfunction responds poorly to SSRI treatment²; however, behaviorally oriented psychotherapeutic interventions such as problem-solving therapy (PST) show promise.²

Algorithm 4: Minor depression: SSRIs plus psychotherapy

SSRIs: selective serotonin reuptake inhibitors

Comorbid medical conditions

When an older adult has a medical problem that likely contributes to depression—such as hypothyroidism—treat the condition and prescribe antidepressants simultaneously.² However, if the medical problem likely causes depression—such as substance withdrawal—treat the condition first and prescribe antidepressants only if mood symptoms persist.²

Refractory depression

If your patient does not respond to an antidepressant trial of adequate dosage and duration, first make sure he or she is taking it correctly (Algorithm 5). After ruling out poor adherence, screen for comorbid psychiatric or medical conditions or psychosocial stressors and reassess the principal diagnosis.⁵

If these steps don’t address your patient’s depressive symptoms, expert consensus guidelines suggest switching to a different antidepressant:⁴

• If you first prescribed an SSRI, consider venlafaxine XR or bupropion SR.^4,17
• If your patient initially received a TCA or bupropion, an SSRI or venlafaxine XR would be appropriate.⁴
• If venlafaxine XR was the first antidepressant, a SSRI is recommended.⁴

If your patient experienced a partial response but not full remission with the initial antidepressant, consider adding a second antidepressant or an augmenting agent:⁴

• If your patient first received an SSRI, adding bupropion, lithium, or nortriptyline is recommended.
• If the initial antidepressant was a TCA or bupropion, consider adding lithium or an SSRI.
• Augmenting venlafaxine XR with lithium is recommended.⁴

The National Institutes of Mental Health-sponsored Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study of treatment-resistant depression in mixed-age groups reported that patients who do not attain remission with an initial SSRI may respond to switching to bupropion SR or venlafaxine XR.¹⁷ Augmenting an SSRI with bupropion SR has been shown to be effective.¹⁸ In addition, consider mirtazapine augmentation,¹⁹ especially if your patient experiences insomnia or anorexia. A combination of mirtazapine and venlafaxine have better efficacy and tolerability compared with the monoamine oxidase inhibitor tranylcypromine.¹⁹ Some studies have shown augmenting SSRIs with buspirone in patients with severe depression is efficacious and safe in younger adults,²⁰ but this practice is not well studied in older patients.

Algorithm 5: Treatment-resistant geriatric depression: Partial vs no response

SNRI: selective serotonin-norepinephrine reuptake inhibitor; SSRI: selective serotonin reuptake inhibitor; TCA: tricyclic antidepressant

Nonpharmacologic treatments

ECT is an important therapeutic intervention because of its safety, efficacy, and faster clinical response.^6,7,9,21 Consider ECT for older adults with severe or psychotic major depression, acute suicidality, catatonia, or severe malnutrition caused by refusal to eat. Patients who remain significantly symptomatic after multiple medication trials, do not tolerate medications well, or have comorbid medical conditions that preclude antidepressant use also are potential candidates for ECT.^5,22

ECT can be administered to many older depressed adults with relatively low complication rates. Pretreatment clinical and laboratory evaluations and consultation with medical colleagues may minimize the risk of adverse effects, including cardiovascular instability, delirium, and falls.⁹ Anterograde memory loss—a common concern for clinicians and patients—usually is temporary and can be reduced by modifying the ECT administration parameters, such as switching from bilateral to unilateral stimulus and spacing treatments.⁹ Use caution when considering ECT for patients with cardiovascular or neurologic conditions—such as myocardial infarction or cerebrovascular accident within 6 months of treatment—that may increase the risk of adverse effects. Some pharmacologic agents, such as benzodiazepines and anticonvulsant mood stabilizers, may decrease ECT’s efficacy by inhibiting seizure.²²

Depressive relapse after ECT is a major clinical concern.²¹ Continuation ECT— within the first 6 months of remission— aims to prevent relapse of the same episode, whereas maintenance ECT—beyond the first 6 months—helps avert occurrence of new episodes.^4,21 Relapse and recurrence also can be prevented with continuation or maintenance pharmacotherapy,^4,21 which should be initiated immediately after the index course of ECT.²¹ Typically, ECT continuation/maintenance treatments are provided weekly, then gradually spaced out to once a month based on the minimum frequency that is effective for an individual patient.²¹

Psychotherapy for geriatric depression generally is effective.²³ One-half of older patients prefer psychotherapy over pharmacotherapy.²⁴ Efficacious psychotherapies include behavioral therapy, cognitive-behavioral therapy (CBT), PST, brief dynamic therapy, interpersonal therapy, supportive therapy, and reminiscence therapy.²³ CBT has the most empiric support for treating geriatric depression.^5,6

Psychotherapy alone is appropriate for mild-to-moderate depression, although severe depression requires adding medication.²⁵ The combination of pharmacotherapy and psychotherapy appears to be more effective than either intervention alone in preventing recurrent major depression, especially when a specific psychosocial stressor has been identified.^5,6 CBT, interpersonal therapy, and family-focused therapy enhance pharmacotherapy outcomes in bipolar disorder.¹³

The Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) study found that in mixed-age patients, pharmacotherapy plus psychotherapy is more beneficial than medication alone in stabilizing bipolar depression.²⁶ For older adults with executive dysfunction, research suggests that PST is more effective than other psychotherapies.²⁷ Psychosocial interventions—such as psychoeducation for the family and caregivers, family counseling, and participation in senior citizen centers and services—are strongly recommended for many patients.⁴

Related Resources

• Blazer DG, Steffens DC, Koenig HG. Mood disorders. In: Blazer DG, Steffens DC, eds. The American Psychiatric Publishing textbook of geriatric psychiatry. 4th ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2009:275-300.
• American Association for Geriatric Psychiatry. www.aagponline.org.

Drug Brand Names

• Aripiprazole • Abilify
• Bupropion • Wellbutrin, Zyban
• Buspirone • Buspar
• Citalopram • Celexa
• Duloxetine • Cymbalta
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Fluoxetine-olanzapine • Symbyax
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Mirtazapine • Remeron
• Nortriptyline • Aventyl, Pamelor
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft
• Tranylcypromine • Parnate
• Trazodone • Desyrel
• Valproate • Depakote
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosure

The authors report no financial relationship with the manufacturer of any product mentioned in this article or with manufacturers of competing products.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/08/depression-in-older-adults.html#comments

Depression in older adults (age ≥65) can devastate their quality of life and increase the likelihood of institutionalization because of behavioral problems.¹ Depression is a primary risk factor for suicide, and suicide rates are highest among those age ≥65, especially among white males.² The burden of geriatric depression can extend to caregivers.¹ Prompt recognition and treatment of depression could help minimize morbidity and reduce suffering in older adults and their caregivers.

Although geriatric depression varies in severity and presentation, common categories include:

• major depressive disorder (MDD)
• vascular depression
• dysthymia
• depression in the context of dementias, psychosis, bipolar disorder, and executive dysfunction.

Diagnoses in this population generally correspond with DSM-IV-TR criteria, but geriatric depression has distinct clinical manifestations.^1,2 Compared with younger depressed patients, older adults are less likely to endorse depressed mood and more likely to report a lack of emotions.^1,2 Older patients report feelings of irritability and fearfulness more often than sadness.^1,2 Mood symptoms tend to be transient, reoccur frequently, and display either a diurnal pattern or multiple fluctuations in a single day.^1,2 Other common presentations include loss of interest in usual activities, lack of motivation, social withdrawal, and decline in activities of daily living.^1,2

Summary of recommendations

Age-specific recommendations for assessing and treating geriatric depression can be generated in part from evidence-based reviews, meta-analyses,³ and geriatric expert consensus guidelines.⁴ Such guidelines and recommendations often do not take into account the marked heterogeneity of medical, cognitive, and overall functioning in patients age ≥65, however, because they are based on studies of younger populations and patients with complicated issues often are excluded from studies. The recommendations in this article are based largely on findings from a National Institutes of Health (NIH)-sponsored project by Alexopoulos et al to develop consensus guidelines for managing geriatric depression and expert opinion from clinicians who treat geriatric patients.⁴

During your initial clinical evaluation, confirm the diagnosis and type, duration, and severity of depression. Seek to understand the biopsychosocial context of each patient’s presentation. Carefully consider your patient’s suicide risk. Hospitalization may be required if he or she is at high risk for suicide or has complex medical and social circumstances that cannot be managed adequately in an outpatient setting.⁵

Unipolar major depression

For unipolar, nonpsychotic geriatric depression, the NIH-Alexopoulos et al guidelines emphasize a combination of antidepressants and psychotherapy (Algorithm 1).⁴ Selective serotonin reuptake inhibitors (SSRIs) and venlafaxine are first-line options.^4,6,7 Tricyclic antidepressants (TCAs), bupropion, and mirtazapine are alternatives.⁴ Among SSRIs, citalopram, escitalopram, and sertraline are preferred initial antidepressants. Fluoxetine is used less frequently.⁴ Paroxetine also is less commonly used because of its anticholinergic effects and because the drug inhibits cytochrome P4502D6,² which metabolizes several medications commonly prescribed for older adults. Among TCAs, nortriptyline is preferred.⁴ Studies have shown that duloxetine improves depression and is safe and well-tolerated in older adults with recurrent MDD.⁸ Electroconvulsive therapy (ECT) is an option for treating severe or treatment-resistant unipolar major depression.⁹

For unipolar depression with psychotic symptoms, guidelines recommend a combination of an antidepressant and an antipsychotic or ECT.⁴ Atypical antipsychotics are preferred over typical antipsychotics⁴; risperidone, olanzapine, and quetiapine are most frequently used.⁴ Clinical data on aripiprazole and ziprasidone in older adults are limited. Many geriatric experts recommend continuing an antipsychotic for 6 months after symptom remission, then gradually tapering the dose.⁴

During acute illness, administer an anti-depressant for 6 to 12 weeks at the individually determined dose required to achieve symptom remission.⁶ For an older adult experiencing a first lifetime episode of major depression, continue antidepressant treatment for 1 year after remission.⁴ If your patient has had 2 lifetime episodes of major depression, continue the antidepressant at the same dose used to achieve remission for at least 3 years. For patients who have had ≥3 episodes of depression or whose index episode was particularly severe or involved significant suicidal thoughts or behaviors, continue maintenance treatment indefinitely.

Algorithm 1: Treatment for unipolar depression in geriatric patients

ECT: electroconvulsive therapy

Bipolar depression

Mood stabilizers such as lithium or valproate—as monotherapy or in combination with an antidepressant—are recommended to treat bipolar depression without psychotic symptoms in older adults (Algorithm 2).¹⁰ For bipolar depression with psychotic symptoms, a combination of a mood stabilizer and an atypical antipsychotic or ECT is recommended.¹⁰

Older adults’ increased sensitivity to side effects and reduced ability to tolerate lithium may limit its use and may prompt you to consider atypical antipsychotics as alternatives to other mood stabilizers. Although quetiapine and fluoxetineolanzapine combination are well studied in younger patients,^11,12 there is a lack of data to support their clinical effectiveness and tolerability in older adults. Among antidepressants, SSRIs or bupropion are preferred over TCAs to prevent a switch to mania.¹⁰ Lamotrigine is an effective maintenance treatment for bipolar depressive episodes in older adults.¹³

Although optimal mood stabilizer and antidepressant dosing for this population has not been adequately assessed, pharmacotherapy that has been effective generally should be continued without modification for at least 6 to 12 months.¹⁰ After the patient achieves remission, gradually discontinue antidepressants while maintaining the mood stabilizer.¹⁰

Algorithm 2: Bipolar depression: Options for combination therapy

ECT: electroconvulsive therapy; SSRIs: selective serotonin reuptake inhibitors

Depression in dementia

Managing depression in dementia patients is similar to treatment in older adults without dementia,^5,14 although pharmacologic agents must be carefully selected because of increased risk of side effects (Algorithm 3). American Psychiatric Association practice guidelines recommend considering antidepressants for depressed patients with dementia even if their mood disturbances do not meet DSM-IV-TR criteria for MDD.⁵

SSRIs’ lower side effect profile make them the preferred treatment; the selective serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine is a second-line option.^4,14 Avoid TCAs and other agents with anticholinergic side effects because of potential cardiovascular complications and cognitive side effects, unless SSRIs or SNRIs are ineffective or contraindicated.¹⁴ Recently clinicians have been reluctant to use antipsychotics in patients with dementia, because of the FDA’s “black-box” warning regarding the increased mortality risk associated with their use in this population.

When using ECT to treat depression in patients with dementia, the treatment protocol often is modified to twice-a-week, unilateral stimulus because of these patients’ increased risk of delirium.¹⁴ The safety of ECT to treat depression in patients with dementia has not been adequately assessed.¹⁴

Algorithm 3: Treating comorbid depression and dementia

ECT: electroconvulsive therapy; SNRI: selective serotoninnorepinephrine reuptake inhibitor; SSRI: selective serotonin reuptake inhibitor

Vascular depression

The “vascular depression hypothesis” proposes that accumulation of subcortical white matter hyperintensities can disrupt frontostriatal pathways, resulting in depressive symptoms.¹⁵ This hypothesis is supported by the confluence of depression and vascular risk factors.¹⁵ Sertraline, citalopram, nortriptyline,¹⁶ and trazodone¹⁵ have been shown to reduce depressive symptoms after a stroke.

Minor depression and dysthymia

Although the efficacy of antidepressants in minor depression—depression that does not meet criteria for MDD—is not well established, expert consensus guidelines recommend SSRIs and psychotherapy, separately or in combination, for minor depression and dysthymia in older adults (Algorithm 4).⁴ Depression in executive dysfunction responds poorly to SSRI treatment²; however, behaviorally oriented psychotherapeutic interventions such as problem-solving therapy (PST) show promise.²

Algorithm 4: Minor depression: SSRIs plus psychotherapy

SSRIs: selective serotonin reuptake inhibitors

Comorbid medical conditions

When an older adult has a medical problem that likely contributes to depression—such as hypothyroidism—treat the condition and prescribe antidepressants simultaneously.² However, if the medical problem likely causes depression—such as substance withdrawal—treat the condition first and prescribe antidepressants only if mood symptoms persist.²

Refractory depression

If your patient does not respond to an antidepressant trial of adequate dosage and duration, first make sure he or she is taking it correctly (Algorithm 5). After ruling out poor adherence, screen for comorbid psychiatric or medical conditions or psychosocial stressors and reassess the principal diagnosis.⁵

If these steps don’t address your patient’s depressive symptoms, expert consensus guidelines suggest switching to a different antidepressant:⁴

• If you first prescribed an SSRI, consider venlafaxine XR or bupropion SR.^4,17
• If your patient initially received a TCA or bupropion, an SSRI or venlafaxine XR would be appropriate.⁴
• If venlafaxine XR was the first antidepressant, a SSRI is recommended.⁴

If your patient experienced a partial response but not full remission with the initial antidepressant, consider adding a second antidepressant or an augmenting agent:⁴

• If your patient first received an SSRI, adding bupropion, lithium, or nortriptyline is recommended.
• If the initial antidepressant was a TCA or bupropion, consider adding lithium or an SSRI.
• Augmenting venlafaxine XR with lithium is recommended.⁴

The National Institutes of Mental Health-sponsored Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study of treatment-resistant depression in mixed-age groups reported that patients who do not attain remission with an initial SSRI may respond to switching to bupropion SR or venlafaxine XR.¹⁷ Augmenting an SSRI with bupropion SR has been shown to be effective.¹⁸ In addition, consider mirtazapine augmentation,¹⁹ especially if your patient experiences insomnia or anorexia. A combination of mirtazapine and venlafaxine have better efficacy and tolerability compared with the monoamine oxidase inhibitor tranylcypromine.¹⁹ Some studies have shown augmenting SSRIs with buspirone in patients with severe depression is efficacious and safe in younger adults,²⁰ but this practice is not well studied in older patients.

Algorithm 5: Treatment-resistant geriatric depression: Partial vs no response

SNRI: selective serotonin-norepinephrine reuptake inhibitor; SSRI: selective serotonin reuptake inhibitor; TCA: tricyclic antidepressant

Nonpharmacologic treatments

ECT is an important therapeutic intervention because of its safety, efficacy, and faster clinical response.^6,7,9,21 Consider ECT for older adults with severe or psychotic major depression, acute suicidality, catatonia, or severe malnutrition caused by refusal to eat. Patients who remain significantly symptomatic after multiple medication trials, do not tolerate medications well, or have comorbid medical conditions that preclude antidepressant use also are potential candidates for ECT.^5,22

ECT can be administered to many older depressed adults with relatively low complication rates. Pretreatment clinical and laboratory evaluations and consultation with medical colleagues may minimize the risk of adverse effects, including cardiovascular instability, delirium, and falls.⁹ Anterograde memory loss—a common concern for clinicians and patients—usually is temporary and can be reduced by modifying the ECT administration parameters, such as switching from bilateral to unilateral stimulus and spacing treatments.⁹ Use caution when considering ECT for patients with cardiovascular or neurologic conditions—such as myocardial infarction or cerebrovascular accident within 6 months of treatment—that may increase the risk of adverse effects. Some pharmacologic agents, such as benzodiazepines and anticonvulsant mood stabilizers, may decrease ECT’s efficacy by inhibiting seizure.²²

Depressive relapse after ECT is a major clinical concern.²¹ Continuation ECT— within the first 6 months of remission— aims to prevent relapse of the same episode, whereas maintenance ECT—beyond the first 6 months—helps avert occurrence of new episodes.^4,21 Relapse and recurrence also can be prevented with continuation or maintenance pharmacotherapy,^4,21 which should be initiated immediately after the index course of ECT.²¹ Typically, ECT continuation/maintenance treatments are provided weekly, then gradually spaced out to once a month based on the minimum frequency that is effective for an individual patient.²¹

Psychotherapy for geriatric depression generally is effective.²³ One-half of older patients prefer psychotherapy over pharmacotherapy.²⁴ Efficacious psychotherapies include behavioral therapy, cognitive-behavioral therapy (CBT), PST, brief dynamic therapy, interpersonal therapy, supportive therapy, and reminiscence therapy.²³ CBT has the most empiric support for treating geriatric depression.^5,6

Psychotherapy alone is appropriate for mild-to-moderate depression, although severe depression requires adding medication.²⁵ The combination of pharmacotherapy and psychotherapy appears to be more effective than either intervention alone in preventing recurrent major depression, especially when a specific psychosocial stressor has been identified.^5,6 CBT, interpersonal therapy, and family-focused therapy enhance pharmacotherapy outcomes in bipolar disorder.¹³

The Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) study found that in mixed-age patients, pharmacotherapy plus psychotherapy is more beneficial than medication alone in stabilizing bipolar depression.²⁶ For older adults with executive dysfunction, research suggests that PST is more effective than other psychotherapies.²⁷ Psychosocial interventions—such as psychoeducation for the family and caregivers, family counseling, and participation in senior citizen centers and services—are strongly recommended for many patients.⁴

Related Resources

• Blazer DG, Steffens DC, Koenig HG. Mood disorders. In: Blazer DG, Steffens DC, eds. The American Psychiatric Publishing textbook of geriatric psychiatry. 4th ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2009:275-300.
• American Association for Geriatric Psychiatry. www.aagponline.org.

Drug Brand Names

• Aripiprazole • Abilify
• Bupropion • Wellbutrin, Zyban
• Buspirone • Buspar
• Citalopram • Celexa
• Duloxetine • Cymbalta
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Fluoxetine-olanzapine • Symbyax
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Mirtazapine • Remeron
• Nortriptyline • Aventyl, Pamelor
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft
• Tranylcypromine • Parnate
• Trazodone • Desyrel
• Valproate • Depakote
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosure

The authors report no financial relationship with the manufacturer of any product mentioned in this article or with manufacturers of competing products.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/08/depression-in-older-adults.html#comments

Depression in older adults (age ≥65) can devastate their quality of life and increase the likelihood of institutionalization because of behavioral problems.¹ Depression is a primary risk factor for suicide, and suicide rates are highest among those age ≥65, especially among white males.² The burden of geriatric depression can extend to caregivers.¹ Prompt recognition and treatment of depression could help minimize morbidity and reduce suffering in older adults and their caregivers.

Although geriatric depression varies in severity and presentation, common categories include:

• major depressive disorder (MDD)
• vascular depression
• dysthymia
• depression in the context of dementias, psychosis, bipolar disorder, and executive dysfunction.

Diagnoses in this population generally correspond with DSM-IV-TR criteria, but geriatric depression has distinct clinical manifestations.^1,2 Compared with younger depressed patients, older adults are less likely to endorse depressed mood and more likely to report a lack of emotions.^1,2 Older patients report feelings of irritability and fearfulness more often than sadness.^1,2 Mood symptoms tend to be transient, reoccur frequently, and display either a diurnal pattern or multiple fluctuations in a single day.^1,2 Other common presentations include loss of interest in usual activities, lack of motivation, social withdrawal, and decline in activities of daily living.^1,2

Summary of recommendations

Age-specific recommendations for assessing and treating geriatric depression can be generated in part from evidence-based reviews, meta-analyses,³ and geriatric expert consensus guidelines.⁴ Such guidelines and recommendations often do not take into account the marked heterogeneity of medical, cognitive, and overall functioning in patients age ≥65, however, because they are based on studies of younger populations and patients with complicated issues often are excluded from studies. The recommendations in this article are based largely on findings from a National Institutes of Health (NIH)-sponsored project by Alexopoulos et al to develop consensus guidelines for managing geriatric depression and expert opinion from clinicians who treat geriatric patients.⁴

During your initial clinical evaluation, confirm the diagnosis and type, duration, and severity of depression. Seek to understand the biopsychosocial context of each patient’s presentation. Carefully consider your patient’s suicide risk. Hospitalization may be required if he or she is at high risk for suicide or has complex medical and social circumstances that cannot be managed adequately in an outpatient setting.⁵

Unipolar major depression

For unipolar, nonpsychotic geriatric depression, the NIH-Alexopoulos et al guidelines emphasize a combination of antidepressants and psychotherapy (Algorithm 1).⁴ Selective serotonin reuptake inhibitors (SSRIs) and venlafaxine are first-line options.^4,6,7 Tricyclic antidepressants (TCAs), bupropion, and mirtazapine are alternatives.⁴ Among SSRIs, citalopram, escitalopram, and sertraline are preferred initial antidepressants. Fluoxetine is used less frequently.⁴ Paroxetine also is less commonly used because of its anticholinergic effects and because the drug inhibits cytochrome P4502D6,² which metabolizes several medications commonly prescribed for older adults. Among TCAs, nortriptyline is preferred.⁴ Studies have shown that duloxetine improves depression and is safe and well-tolerated in older adults with recurrent MDD.⁸ Electroconvulsive therapy (ECT) is an option for treating severe or treatment-resistant unipolar major depression.⁹

For unipolar depression with psychotic symptoms, guidelines recommend a combination of an antidepressant and an antipsychotic or ECT.⁴ Atypical antipsychotics are preferred over typical antipsychotics⁴; risperidone, olanzapine, and quetiapine are most frequently used.⁴ Clinical data on aripiprazole and ziprasidone in older adults are limited. Many geriatric experts recommend continuing an antipsychotic for 6 months after symptom remission, then gradually tapering the dose.⁴

During acute illness, administer an anti-depressant for 6 to 12 weeks at the individually determined dose required to achieve symptom remission.⁶ For an older adult experiencing a first lifetime episode of major depression, continue antidepressant treatment for 1 year after remission.⁴ If your patient has had 2 lifetime episodes of major depression, continue the antidepressant at the same dose used to achieve remission for at least 3 years. For patients who have had ≥3 episodes of depression or whose index episode was particularly severe or involved significant suicidal thoughts or behaviors, continue maintenance treatment indefinitely.

Algorithm 1: Treatment for unipolar depression in geriatric patients

ECT: electroconvulsive therapy

Bipolar depression

Mood stabilizers such as lithium or valproate—as monotherapy or in combination with an antidepressant—are recommended to treat bipolar depression without psychotic symptoms in older adults (Algorithm 2).¹⁰ For bipolar depression with psychotic symptoms, a combination of a mood stabilizer and an atypical antipsychotic or ECT is recommended.¹⁰

Older adults’ increased sensitivity to side effects and reduced ability to tolerate lithium may limit its use and may prompt you to consider atypical antipsychotics as alternatives to other mood stabilizers. Although quetiapine and fluoxetineolanzapine combination are well studied in younger patients,^11,12 there is a lack of data to support their clinical effectiveness and tolerability in older adults. Among antidepressants, SSRIs or bupropion are preferred over TCAs to prevent a switch to mania.¹⁰ Lamotrigine is an effective maintenance treatment for bipolar depressive episodes in older adults.¹³

Although optimal mood stabilizer and antidepressant dosing for this population has not been adequately assessed, pharmacotherapy that has been effective generally should be continued without modification for at least 6 to 12 months.¹⁰ After the patient achieves remission, gradually discontinue antidepressants while maintaining the mood stabilizer.¹⁰

Algorithm 2: Bipolar depression: Options for combination therapy

ECT: electroconvulsive therapy; SSRIs: selective serotonin reuptake inhibitors

Depression in dementia

Managing depression in dementia patients is similar to treatment in older adults without dementia,^5,14 although pharmacologic agents must be carefully selected because of increased risk of side effects (Algorithm 3). American Psychiatric Association practice guidelines recommend considering antidepressants for depressed patients with dementia even if their mood disturbances do not meet DSM-IV-TR criteria for MDD.⁵

SSRIs’ lower side effect profile make them the preferred treatment; the selective serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine is a second-line option.^4,14 Avoid TCAs and other agents with anticholinergic side effects because of potential cardiovascular complications and cognitive side effects, unless SSRIs or SNRIs are ineffective or contraindicated.¹⁴ Recently clinicians have been reluctant to use antipsychotics in patients with dementia, because of the FDA’s “black-box” warning regarding the increased mortality risk associated with their use in this population.

When using ECT to treat depression in patients with dementia, the treatment protocol often is modified to twice-a-week, unilateral stimulus because of these patients’ increased risk of delirium.¹⁴ The safety of ECT to treat depression in patients with dementia has not been adequately assessed.¹⁴

Algorithm 3: Treating comorbid depression and dementia

ECT: electroconvulsive therapy; SNRI: selective serotoninnorepinephrine reuptake inhibitor; SSRI: selective serotonin reuptake inhibitor

Vascular depression

The “vascular depression hypothesis” proposes that accumulation of subcortical white matter hyperintensities can disrupt frontostriatal pathways, resulting in depressive symptoms.¹⁵ This hypothesis is supported by the confluence of depression and vascular risk factors.¹⁵ Sertraline, citalopram, nortriptyline,¹⁶ and trazodone¹⁵ have been shown to reduce depressive symptoms after a stroke.

Minor depression and dysthymia

Although the efficacy of antidepressants in minor depression—depression that does not meet criteria for MDD—is not well established, expert consensus guidelines recommend SSRIs and psychotherapy, separately or in combination, for minor depression and dysthymia in older adults (Algorithm 4).⁴ Depression in executive dysfunction responds poorly to SSRI treatment²; however, behaviorally oriented psychotherapeutic interventions such as problem-solving therapy (PST) show promise.²

Algorithm 4: Minor depression: SSRIs plus psychotherapy

SSRIs: selective serotonin reuptake inhibitors

Comorbid medical conditions

When an older adult has a medical problem that likely contributes to depression—such as hypothyroidism—treat the condition and prescribe antidepressants simultaneously.² However, if the medical problem likely causes depression—such as substance withdrawal—treat the condition first and prescribe antidepressants only if mood symptoms persist.²

Refractory depression

If your patient does not respond to an antidepressant trial of adequate dosage and duration, first make sure he or she is taking it correctly (Algorithm 5). After ruling out poor adherence, screen for comorbid psychiatric or medical conditions or psychosocial stressors and reassess the principal diagnosis.⁵

If these steps don’t address your patient’s depressive symptoms, expert consensus guidelines suggest switching to a different antidepressant:⁴

• If you first prescribed an SSRI, consider venlafaxine XR or bupropion SR.^4,17
• If your patient initially received a TCA or bupropion, an SSRI or venlafaxine XR would be appropriate.⁴
• If venlafaxine XR was the first antidepressant, a SSRI is recommended.⁴

If your patient experienced a partial response but not full remission with the initial antidepressant, consider adding a second antidepressant or an augmenting agent:⁴

• If your patient first received an SSRI, adding bupropion, lithium, or nortriptyline is recommended.
• If the initial antidepressant was a TCA or bupropion, consider adding lithium or an SSRI.
• Augmenting venlafaxine XR with lithium is recommended.⁴

The National Institutes of Mental Health-sponsored Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study of treatment-resistant depression in mixed-age groups reported that patients who do not attain remission with an initial SSRI may respond to switching to bupropion SR or venlafaxine XR.¹⁷ Augmenting an SSRI with bupropion SR has been shown to be effective.¹⁸ In addition, consider mirtazapine augmentation,¹⁹ especially if your patient experiences insomnia or anorexia. A combination of mirtazapine and venlafaxine have better efficacy and tolerability compared with the monoamine oxidase inhibitor tranylcypromine.¹⁹ Some studies have shown augmenting SSRIs with buspirone in patients with severe depression is efficacious and safe in younger adults,²⁰ but this practice is not well studied in older patients.

Algorithm 5: Treatment-resistant geriatric depression: Partial vs no response

SNRI: selective serotonin-norepinephrine reuptake inhibitor; SSRI: selective serotonin reuptake inhibitor; TCA: tricyclic antidepressant

Nonpharmacologic treatments

ECT is an important therapeutic intervention because of its safety, efficacy, and faster clinical response.^6,7,9,21 Consider ECT for older adults with severe or psychotic major depression, acute suicidality, catatonia, or severe malnutrition caused by refusal to eat. Patients who remain significantly symptomatic after multiple medication trials, do not tolerate medications well, or have comorbid medical conditions that preclude antidepressant use also are potential candidates for ECT.^5,22

ECT can be administered to many older depressed adults with relatively low complication rates. Pretreatment clinical and laboratory evaluations and consultation with medical colleagues may minimize the risk of adverse effects, including cardiovascular instability, delirium, and falls.⁹ Anterograde memory loss—a common concern for clinicians and patients—usually is temporary and can be reduced by modifying the ECT administration parameters, such as switching from bilateral to unilateral stimulus and spacing treatments.⁹ Use caution when considering ECT for patients with cardiovascular or neurologic conditions—such as myocardial infarction or cerebrovascular accident within 6 months of treatment—that may increase the risk of adverse effects. Some pharmacologic agents, such as benzodiazepines and anticonvulsant mood stabilizers, may decrease ECT’s efficacy by inhibiting seizure.²²

Depressive relapse after ECT is a major clinical concern.²¹ Continuation ECT— within the first 6 months of remission— aims to prevent relapse of the same episode, whereas maintenance ECT—beyond the first 6 months—helps avert occurrence of new episodes.^4,21 Relapse and recurrence also can be prevented with continuation or maintenance pharmacotherapy,^4,21 which should be initiated immediately after the index course of ECT.²¹ Typically, ECT continuation/maintenance treatments are provided weekly, then gradually spaced out to once a month based on the minimum frequency that is effective for an individual patient.²¹

Psychotherapy for geriatric depression generally is effective.²³ One-half of older patients prefer psychotherapy over pharmacotherapy.²⁴ Efficacious psychotherapies include behavioral therapy, cognitive-behavioral therapy (CBT), PST, brief dynamic therapy, interpersonal therapy, supportive therapy, and reminiscence therapy.²³ CBT has the most empiric support for treating geriatric depression.^5,6

Psychotherapy alone is appropriate for mild-to-moderate depression, although severe depression requires adding medication.²⁵ The combination of pharmacotherapy and psychotherapy appears to be more effective than either intervention alone in preventing recurrent major depression, especially when a specific psychosocial stressor has been identified.^5,6 CBT, interpersonal therapy, and family-focused therapy enhance pharmacotherapy outcomes in bipolar disorder.¹³

The Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) study found that in mixed-age patients, pharmacotherapy plus psychotherapy is more beneficial than medication alone in stabilizing bipolar depression.²⁶ For older adults with executive dysfunction, research suggests that PST is more effective than other psychotherapies.²⁷ Psychosocial interventions—such as psychoeducation for the family and caregivers, family counseling, and participation in senior citizen centers and services—are strongly recommended for many patients.⁴

Related Resources

• Blazer DG, Steffens DC, Koenig HG. Mood disorders. In: Blazer DG, Steffens DC, eds. The American Psychiatric Publishing textbook of geriatric psychiatry. 4th ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2009:275-300.
• American Association for Geriatric Psychiatry. www.aagponline.org.

Drug Brand Names

• Aripiprazole • Abilify
• Bupropion • Wellbutrin, Zyban
• Buspirone • Buspar
• Citalopram • Celexa
• Duloxetine • Cymbalta
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Fluoxetine-olanzapine • Symbyax
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Mirtazapine • Remeron
• Nortriptyline • Aventyl, Pamelor
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft
• Tranylcypromine • Parnate
• Trazodone • Desyrel
• Valproate • Depakote
• Venlafaxine • Effexor
• Ziprasidone • Geodon

Disclosure

The authors report no financial relationship with the manufacturer of any product mentioned in this article or with manufacturers of competing products.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/07/cholesterol-mood-and-vascular-health.html#comments

A growing body of literature examining the putative links among cholesterol, mood disorders, and suicide has produced inconsistent findings and unclear clinical implications that may leave psychiatrists unsure of how to interpret the data. Understanding cholesterol’s role in mood disorders may be relevant to the 2 primary causes of excess deaths in patients with mood disorders: suicide and vascular disease.¹

Plausible links

In the early 1990s several studies suggested a link between low cholesterol (<160 mg/dL) and unnatural deaths, including suicide.^2-4 Follow-up studies confirmed associations between low cholesterol and suicide attempts, especially violent ones.⁵ These associations are compelling given the neurobiologic effects of cholesterol, such as a net reduction of serotonergic function (Box 1). Low cholesterol may predispose an individual to aggression, impulsivity, and violence (Table 1).⁶ Many studies have found that patients with mood disorders have lower cholesterol levels;⁷ however, other research suggests they are at increased risk of hyperlipidemia, typically hypertriglyceridemia rather than hypercholesterolemia.⁸

Depression. Several studies have shown an association between low cholesterol and depressive symptoms, although this finding has not been replicated in Asian subjects.^9,10 Patients with manic or mixed syndromes have been found to have lower serum cholesterol,¹¹ and individuals with major depression and bipolar disorder have lower cholesterol levels in the brain compared with healthy controls.¹² Some studies have observed higher total cholesterol levels after patients receive pharmacotherapy for major depressive symptoms.¹³ These findings have led to speculation that low serum cholesterol in patients with mood disorders is partially a state-dependent effect of depressive illness.

Suicide. Cohort, case-control, and cross-sectional studies have linked low cholesterol to an increased risk of suicide.^2,5 Individuals who attempt suicide by violent means have lower cholesterol compared with those who use less violent methods.^5,14 A meta-analysis found statistically significant correlations between low cholesterol and future or past suicidal behavior; however, low cholesterol explained <0.01% of suicidal behavior.¹⁵ Studies comparing cholesterol levels of individuals following violent vs nonviolent suicide attempts have demonstrated stronger associations.¹⁵

Assessing suicide risk. Current evidence does not support considering low serum cholesterol a risk factor for suicide. One study used cholesterol as a clinical predictor of suicide,¹⁶ but this model has not been prospectively validated. As a whole, the evidence does not suggest that cholesterol levels explain a substantial portion of suicidal behaviors.

Box 1

Table 1
Psychiatric features associated with low cholesterol*

Effects of lipid-lowering agents

If there is a causal relationship between low cholesterol and mood disorders, then it stands to reason that using cholesterol-lowering drugs would increase the risk of depression and suicide. However, the data do not support that conclusion.

Many case reports have documented adverse psychiatric reactions to statins, including depression, suicidality, emotional lability, agitation, irritability, anxiety, panic, and euphoria.¹⁷ In an early analysis of primary prevention trials, patients receiving cholesterol-lowering treatment—mainly non-statins—were estimated to have twice the risk of death by suicide or violence compared with controls.³ However, a more recent meta-analysis of larger clinical trials of lipid-lowering agents including statins and observational studies did not reveal an association between lipid-lowering medications and suicide.^15,18

In a large case-control study, statin users had a lower risk of depression (adjusted odds ratio [OR] 0.4, 95% confidence interval [CI], 0.2 to 0.9) than patients taking non-statin lipid-lowering drugs (adjusted OR 1.0, 95% CI, 0.5 to 2.1).¹⁹ However, statins reduced cholesterol more (30% to 50%) than non-statin drugs (10% to 20%). A clinical trial of >1,000 patients with stable coronary artery disease treated with pravastatin—an HMG-CoA reductase inhibitor with low lipophilicity that is less likely than other statins to cross the blood-brain barrier—revealed no changes in self-reported anger, impulsiveness, anxiety, or depression.²⁰

This study did not exclude patients with psychiatric illness—who are at greatest risk of suicide—but other trials of lipid-lowering drugs did.²¹ As a result, the effects of lipid-lowering medications on psychiatric patients are unclear. A clinical trial is underway to assess the effects of pravastatin (low lipophilicity), simvastatin (high lipophilicity), or placebo on mood, sleep, and aggression.²¹

Low cholesterol: State or trait?

Much of the research linking low cholesterol, mood disorders, and suicidality could be confounded by depressed mood leading to reduced serum cholesterol. There has been considerable debate about whether low cholesterol predisposes patients to suicide or if depression independently leads to poor nutrition and therefore low cholesterol and increased suicide risk.^6,22

Some researchers have suggested that depression lowers cholesterol and increases risk of suicide,²³ but study designs have limited the ability to discern the directionality of the relationship. Attempts to control for depression-related malnutrition and weight loss—which lowers total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C)²⁴—suggest the association may be independent of these variables.^25-27 These findings suggest that cholesterol may be considered a trait marker and is not entirely state-dependent. However, multiple, large, long-term randomized controlled trials have not shown increased depression and suicide with use of lipid-lowering agents in healthy populations.²⁰

The Figure illustrates known epidemiologic associations of low cholesterol, low serotoninergic function, and suicide and contrasts conceptual models of cholesterol as a state and a trait marker. A case can be made for cholesterol as both a state and a trait marker, and these models could overlap, with depression-induced decreases in cholesterol further mediating changes in serotonergic function and related behavioral sequelae.

Figure
Cholesterol, depression, and suicide: How are they linked?

Low cholesterol may be considered a trait marker, predisposing patients to lower serotonergic function and placing them at greater risk for impulsivity, depression, aggression, and suicide. Other models suggest that lower cholesterol is a state-dependent consequence of depression, and not part of a causal chain toward suicide

Improving cardiac health

Limited epidemiologic studies suggest that patients with mood disorders may have lower levels of total cholesterol and LDL-C, but higher rates of hypertriglyceridemia compared with the general population.⁸ Unfortunately, psychiatric patients—who may be at increased risk of developing cardiovascular disease—may be less likely to be screened and appropriately treated for lipid abnormalities.²⁸ To address this disparity, consider assuming an active role in assessing and managing hyperlipidemia in your patients with mood disorders. Be aware of your patients’ lipid profile and ensure that they follow monitoring recommendations.

The National Cholesterol Education Program recommends screening all adults age >20 for hyperlipidemia every 5 years using measures of total cholesterol, LDL-C, HDL-C, and triglycerides. If LDL-C or triglycerides exceed target values (Table 2), appropriate management includes recommending lifestyle changes and pharmacotherapy (Box 2).

Patients should receive a fasting lipid profile before and 12 weeks after starting any antipsychotic and semiannually thereafter.²⁹ Consider closely monitoring lipids when patients gain weight with psychotropics. Refer patients with hyperlipidemia to a primary care physician, but in the absence of such a provider, mental health clinicians who are familiar with treatment guidelines can manage these patients.³⁰

Closely monitor individuals with mood disorders for changes in behavior or mental status after starting a lipid-lowering agent. Consider discontinuing the drug if a patient develops an adverse reaction. If symptoms return after medication rechallenge, consider other management strategies such as an alternate lipid-lowering agent or re-emphasizing behavioral measures.

Table 2
National Cholesterol Education Program recommended LDL levels

Box 2

Related Resources

• Fiedorowicz JG, Coryell WH. Cholesterol and suicide attempts: a prospective study of depressed inpatients. Psychiatry Res. 2007;152(1):11-20.
• National Cholesterol Education Program, Adult Treatment Panel III (ATP III) Quick Desk Reference. www.nhlbi.nih.gov/guidelines/cholesterol/atglance.htm.
• Executive Summary of the third report of the national Cholesterol Education Program (nCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285(19):2486-2497.

Drug Brand Names

• Ezetimibe • Zetia
• Pravastatin • Pravachol
• Simvastatin • Zocor

Acknowledgements

Dr. Fiedorowicz thanks Lois Warren and Miriam Weiner for their editorial assistance.

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Fiedorowicz is supported by the national Institutes of Health (1K23MH083695-01A210), nARSAD, and the Institute for Clinical and Translational Science at the University of Iowa (3 UL1 RR024979-03S4). He has received support for participating in a colleague’s investigator-initiated project with Eli Lilly. Dr. Haynes’ research is supported by grants from the national Institutes of Health (nHLBI: HL58972 & HL14388; nCRR CTSA: 1UL1RR024979).

Discuss this article at http://currentpsychiatry.blogspot.com/2010/07/cholesterol-mood-and-vascular-health.html#comments

A growing body of literature examining the putative links among cholesterol, mood disorders, and suicide has produced inconsistent findings and unclear clinical implications that may leave psychiatrists unsure of how to interpret the data. Understanding cholesterol’s role in mood disorders may be relevant to the 2 primary causes of excess deaths in patients with mood disorders: suicide and vascular disease.¹

Plausible links

In the early 1990s several studies suggested a link between low cholesterol (<160 mg/dL) and unnatural deaths, including suicide.^2-4 Follow-up studies confirmed associations between low cholesterol and suicide attempts, especially violent ones.⁵ These associations are compelling given the neurobiologic effects of cholesterol, such as a net reduction of serotonergic function (Box 1). Low cholesterol may predispose an individual to aggression, impulsivity, and violence (Table 1).⁶ Many studies have found that patients with mood disorders have lower cholesterol levels;⁷ however, other research suggests they are at increased risk of hyperlipidemia, typically hypertriglyceridemia rather than hypercholesterolemia.⁸

Depression. Several studies have shown an association between low cholesterol and depressive symptoms, although this finding has not been replicated in Asian subjects.^9,10 Patients with manic or mixed syndromes have been found to have lower serum cholesterol,¹¹ and individuals with major depression and bipolar disorder have lower cholesterol levels in the brain compared with healthy controls.¹² Some studies have observed higher total cholesterol levels after patients receive pharmacotherapy for major depressive symptoms.¹³ These findings have led to speculation that low serum cholesterol in patients with mood disorders is partially a state-dependent effect of depressive illness.

Suicide. Cohort, case-control, and cross-sectional studies have linked low cholesterol to an increased risk of suicide.^2,5 Individuals who attempt suicide by violent means have lower cholesterol compared with those who use less violent methods.^5,14 A meta-analysis found statistically significant correlations between low cholesterol and future or past suicidal behavior; however, low cholesterol explained <0.01% of suicidal behavior.¹⁵ Studies comparing cholesterol levels of individuals following violent vs nonviolent suicide attempts have demonstrated stronger associations.¹⁵

Assessing suicide risk. Current evidence does not support considering low serum cholesterol a risk factor for suicide. One study used cholesterol as a clinical predictor of suicide,¹⁶ but this model has not been prospectively validated. As a whole, the evidence does not suggest that cholesterol levels explain a substantial portion of suicidal behaviors.

Box 1

Table 1
Psychiatric features associated with low cholesterol*

Effects of lipid-lowering agents

If there is a causal relationship between low cholesterol and mood disorders, then it stands to reason that using cholesterol-lowering drugs would increase the risk of depression and suicide. However, the data do not support that conclusion.

Many case reports have documented adverse psychiatric reactions to statins, including depression, suicidality, emotional lability, agitation, irritability, anxiety, panic, and euphoria.¹⁷ In an early analysis of primary prevention trials, patients receiving cholesterol-lowering treatment—mainly non-statins—were estimated to have twice the risk of death by suicide or violence compared with controls.³ However, a more recent meta-analysis of larger clinical trials of lipid-lowering agents including statins and observational studies did not reveal an association between lipid-lowering medications and suicide.^15,18

In a large case-control study, statin users had a lower risk of depression (adjusted odds ratio [OR] 0.4, 95% confidence interval [CI], 0.2 to 0.9) than patients taking non-statin lipid-lowering drugs (adjusted OR 1.0, 95% CI, 0.5 to 2.1).¹⁹ However, statins reduced cholesterol more (30% to 50%) than non-statin drugs (10% to 20%). A clinical trial of >1,000 patients with stable coronary artery disease treated with pravastatin—an HMG-CoA reductase inhibitor with low lipophilicity that is less likely than other statins to cross the blood-brain barrier—revealed no changes in self-reported anger, impulsiveness, anxiety, or depression.²⁰

This study did not exclude patients with psychiatric illness—who are at greatest risk of suicide—but other trials of lipid-lowering drugs did.²¹ As a result, the effects of lipid-lowering medications on psychiatric patients are unclear. A clinical trial is underway to assess the effects of pravastatin (low lipophilicity), simvastatin (high lipophilicity), or placebo on mood, sleep, and aggression.²¹

Low cholesterol: State or trait?

Much of the research linking low cholesterol, mood disorders, and suicidality could be confounded by depressed mood leading to reduced serum cholesterol. There has been considerable debate about whether low cholesterol predisposes patients to suicide or if depression independently leads to poor nutrition and therefore low cholesterol and increased suicide risk.^6,22

Some researchers have suggested that depression lowers cholesterol and increases risk of suicide,²³ but study designs have limited the ability to discern the directionality of the relationship. Attempts to control for depression-related malnutrition and weight loss—which lowers total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C)²⁴—suggest the association may be independent of these variables.^25-27 These findings suggest that cholesterol may be considered a trait marker and is not entirely state-dependent. However, multiple, large, long-term randomized controlled trials have not shown increased depression and suicide with use of lipid-lowering agents in healthy populations.²⁰

The Figure illustrates known epidemiologic associations of low cholesterol, low serotoninergic function, and suicide and contrasts conceptual models of cholesterol as a state and a trait marker. A case can be made for cholesterol as both a state and a trait marker, and these models could overlap, with depression-induced decreases in cholesterol further mediating changes in serotonergic function and related behavioral sequelae.

Figure
Cholesterol, depression, and suicide: How are they linked?

Low cholesterol may be considered a trait marker, predisposing patients to lower serotonergic function and placing them at greater risk for impulsivity, depression, aggression, and suicide. Other models suggest that lower cholesterol is a state-dependent consequence of depression, and not part of a causal chain toward suicide

Improving cardiac health

Limited epidemiologic studies suggest that patients with mood disorders may have lower levels of total cholesterol and LDL-C, but higher rates of hypertriglyceridemia compared with the general population.⁸ Unfortunately, psychiatric patients—who may be at increased risk of developing cardiovascular disease—may be less likely to be screened and appropriately treated for lipid abnormalities.²⁸ To address this disparity, consider assuming an active role in assessing and managing hyperlipidemia in your patients with mood disorders. Be aware of your patients’ lipid profile and ensure that they follow monitoring recommendations.

The National Cholesterol Education Program recommends screening all adults age >20 for hyperlipidemia every 5 years using measures of total cholesterol, LDL-C, HDL-C, and triglycerides. If LDL-C or triglycerides exceed target values (Table 2), appropriate management includes recommending lifestyle changes and pharmacotherapy (Box 2).

Patients should receive a fasting lipid profile before and 12 weeks after starting any antipsychotic and semiannually thereafter.²⁹ Consider closely monitoring lipids when patients gain weight with psychotropics. Refer patients with hyperlipidemia to a primary care physician, but in the absence of such a provider, mental health clinicians who are familiar with treatment guidelines can manage these patients.³⁰

Closely monitor individuals with mood disorders for changes in behavior or mental status after starting a lipid-lowering agent. Consider discontinuing the drug if a patient develops an adverse reaction. If symptoms return after medication rechallenge, consider other management strategies such as an alternate lipid-lowering agent or re-emphasizing behavioral measures.

Table 2
National Cholesterol Education Program recommended LDL levels

Box 2

Related Resources

• Fiedorowicz JG, Coryell WH. Cholesterol and suicide attempts: a prospective study of depressed inpatients. Psychiatry Res. 2007;152(1):11-20.
• National Cholesterol Education Program, Adult Treatment Panel III (ATP III) Quick Desk Reference. www.nhlbi.nih.gov/guidelines/cholesterol/atglance.htm.
• Executive Summary of the third report of the national Cholesterol Education Program (nCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285(19):2486-2497.

Drug Brand Names

• Ezetimibe • Zetia
• Pravastatin • Pravachol
• Simvastatin • Zocor

Acknowledgements

Dr. Fiedorowicz thanks Lois Warren and Miriam Weiner for their editorial assistance.

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Fiedorowicz is supported by the national Institutes of Health (1K23MH083695-01A210), nARSAD, and the Institute for Clinical and Translational Science at the University of Iowa (3 UL1 RR024979-03S4). He has received support for participating in a colleague’s investigator-initiated project with Eli Lilly. Dr. Haynes’ research is supported by grants from the national Institutes of Health (nHLBI: HL58972 & HL14388; nCRR CTSA: 1UL1RR024979).

Discuss this article at http://currentpsychiatry.blogspot.com/2010/07/cholesterol-mood-and-vascular-health.html#comments

A growing body of literature examining the putative links among cholesterol, mood disorders, and suicide has produced inconsistent findings and unclear clinical implications that may leave psychiatrists unsure of how to interpret the data. Understanding cholesterol’s role in mood disorders may be relevant to the 2 primary causes of excess deaths in patients with mood disorders: suicide and vascular disease.¹

Plausible links

In the early 1990s several studies suggested a link between low cholesterol (<160 mg/dL) and unnatural deaths, including suicide.^2-4 Follow-up studies confirmed associations between low cholesterol and suicide attempts, especially violent ones.⁵ These associations are compelling given the neurobiologic effects of cholesterol, such as a net reduction of serotonergic function (Box 1). Low cholesterol may predispose an individual to aggression, impulsivity, and violence (Table 1).⁶ Many studies have found that patients with mood disorders have lower cholesterol levels;⁷ however, other research suggests they are at increased risk of hyperlipidemia, typically hypertriglyceridemia rather than hypercholesterolemia.⁸

Depression. Several studies have shown an association between low cholesterol and depressive symptoms, although this finding has not been replicated in Asian subjects.^9,10 Patients with manic or mixed syndromes have been found to have lower serum cholesterol,¹¹ and individuals with major depression and bipolar disorder have lower cholesterol levels in the brain compared with healthy controls.¹² Some studies have observed higher total cholesterol levels after patients receive pharmacotherapy for major depressive symptoms.¹³ These findings have led to speculation that low serum cholesterol in patients with mood disorders is partially a state-dependent effect of depressive illness.

Suicide. Cohort, case-control, and cross-sectional studies have linked low cholesterol to an increased risk of suicide.^2,5 Individuals who attempt suicide by violent means have lower cholesterol compared with those who use less violent methods.^5,14 A meta-analysis found statistically significant correlations between low cholesterol and future or past suicidal behavior; however, low cholesterol explained <0.01% of suicidal behavior.¹⁵ Studies comparing cholesterol levels of individuals following violent vs nonviolent suicide attempts have demonstrated stronger associations.¹⁵

Assessing suicide risk. Current evidence does not support considering low serum cholesterol a risk factor for suicide. One study used cholesterol as a clinical predictor of suicide,¹⁶ but this model has not been prospectively validated. As a whole, the evidence does not suggest that cholesterol levels explain a substantial portion of suicidal behaviors.

Box 1

Table 1
Psychiatric features associated with low cholesterol*

Effects of lipid-lowering agents

If there is a causal relationship between low cholesterol and mood disorders, then it stands to reason that using cholesterol-lowering drugs would increase the risk of depression and suicide. However, the data do not support that conclusion.

Many case reports have documented adverse psychiatric reactions to statins, including depression, suicidality, emotional lability, agitation, irritability, anxiety, panic, and euphoria.¹⁷ In an early analysis of primary prevention trials, patients receiving cholesterol-lowering treatment—mainly non-statins—were estimated to have twice the risk of death by suicide or violence compared with controls.³ However, a more recent meta-analysis of larger clinical trials of lipid-lowering agents including statins and observational studies did not reveal an association between lipid-lowering medications and suicide.^15,18

In a large case-control study, statin users had a lower risk of depression (adjusted odds ratio [OR] 0.4, 95% confidence interval [CI], 0.2 to 0.9) than patients taking non-statin lipid-lowering drugs (adjusted OR 1.0, 95% CI, 0.5 to 2.1).¹⁹ However, statins reduced cholesterol more (30% to 50%) than non-statin drugs (10% to 20%). A clinical trial of >1,000 patients with stable coronary artery disease treated with pravastatin—an HMG-CoA reductase inhibitor with low lipophilicity that is less likely than other statins to cross the blood-brain barrier—revealed no changes in self-reported anger, impulsiveness, anxiety, or depression.²⁰

This study did not exclude patients with psychiatric illness—who are at greatest risk of suicide—but other trials of lipid-lowering drugs did.²¹ As a result, the effects of lipid-lowering medications on psychiatric patients are unclear. A clinical trial is underway to assess the effects of pravastatin (low lipophilicity), simvastatin (high lipophilicity), or placebo on mood, sleep, and aggression.²¹

Low cholesterol: State or trait?

Much of the research linking low cholesterol, mood disorders, and suicidality could be confounded by depressed mood leading to reduced serum cholesterol. There has been considerable debate about whether low cholesterol predisposes patients to suicide or if depression independently leads to poor nutrition and therefore low cholesterol and increased suicide risk.^6,22

Some researchers have suggested that depression lowers cholesterol and increases risk of suicide,²³ but study designs have limited the ability to discern the directionality of the relationship. Attempts to control for depression-related malnutrition and weight loss—which lowers total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C)²⁴—suggest the association may be independent of these variables.^25-27 These findings suggest that cholesterol may be considered a trait marker and is not entirely state-dependent. However, multiple, large, long-term randomized controlled trials have not shown increased depression and suicide with use of lipid-lowering agents in healthy populations.²⁰

The Figure illustrates known epidemiologic associations of low cholesterol, low serotoninergic function, and suicide and contrasts conceptual models of cholesterol as a state and a trait marker. A case can be made for cholesterol as both a state and a trait marker, and these models could overlap, with depression-induced decreases in cholesterol further mediating changes in serotonergic function and related behavioral sequelae.

Figure
Cholesterol, depression, and suicide: How are they linked?

Low cholesterol may be considered a trait marker, predisposing patients to lower serotonergic function and placing them at greater risk for impulsivity, depression, aggression, and suicide. Other models suggest that lower cholesterol is a state-dependent consequence of depression, and not part of a causal chain toward suicide

Improving cardiac health

Limited epidemiologic studies suggest that patients with mood disorders may have lower levels of total cholesterol and LDL-C, but higher rates of hypertriglyceridemia compared with the general population.⁸ Unfortunately, psychiatric patients—who may be at increased risk of developing cardiovascular disease—may be less likely to be screened and appropriately treated for lipid abnormalities.²⁸ To address this disparity, consider assuming an active role in assessing and managing hyperlipidemia in your patients with mood disorders. Be aware of your patients’ lipid profile and ensure that they follow monitoring recommendations.

The National Cholesterol Education Program recommends screening all adults age >20 for hyperlipidemia every 5 years using measures of total cholesterol, LDL-C, HDL-C, and triglycerides. If LDL-C or triglycerides exceed target values (Table 2), appropriate management includes recommending lifestyle changes and pharmacotherapy (Box 2).

Patients should receive a fasting lipid profile before and 12 weeks after starting any antipsychotic and semiannually thereafter.²⁹ Consider closely monitoring lipids when patients gain weight with psychotropics. Refer patients with hyperlipidemia to a primary care physician, but in the absence of such a provider, mental health clinicians who are familiar with treatment guidelines can manage these patients.³⁰

Closely monitor individuals with mood disorders for changes in behavior or mental status after starting a lipid-lowering agent. Consider discontinuing the drug if a patient develops an adverse reaction. If symptoms return after medication rechallenge, consider other management strategies such as an alternate lipid-lowering agent or re-emphasizing behavioral measures.

Table 2
National Cholesterol Education Program recommended LDL levels

Box 2

Related Resources

• Fiedorowicz JG, Coryell WH. Cholesterol and suicide attempts: a prospective study of depressed inpatients. Psychiatry Res. 2007;152(1):11-20.
• National Cholesterol Education Program, Adult Treatment Panel III (ATP III) Quick Desk Reference. www.nhlbi.nih.gov/guidelines/cholesterol/atglance.htm.
• Executive Summary of the third report of the national Cholesterol Education Program (nCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285(19):2486-2497.

Drug Brand Names

• Ezetimibe • Zetia
• Pravastatin • Pravachol
• Simvastatin • Zocor

Acknowledgements

Dr. Fiedorowicz thanks Lois Warren and Miriam Weiner for their editorial assistance.

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Fiedorowicz is supported by the national Institutes of Health (1K23MH083695-01A210), nARSAD, and the Institute for Clinical and Translational Science at the University of Iowa (3 UL1 RR024979-03S4). He has received support for participating in a colleague’s investigator-initiated project with Eli Lilly. Dr. Haynes’ research is supported by grants from the national Institutes of Health (nHLBI: HL58972 & HL14388; nCRR CTSA: 1UL1RR024979).

Discuss this article

From all outward appearances Dr. S, a part-time psychiatrist at an inpatient psychiatric facility and in private practice for 12 years, is living the “perfect life,” with a wife, children, and successful practice.

In retrospect, his drug addiction began insidiously. In college, Dr. S continued to use oxycodone/acetaminophen prescribed for a shoulder injury long after his pain had resolved. He began to use cocaine in residency to help him “get through” the 36-hour call days, and it “helped” him earn the chief resident position because of his heightened energy and concentration. Dr. S’ primary care physician initially prescribed him benzodiazepines for anxiety and to help him sleep. Opiates were prescribed for a musculoskeletal injury. Dr. S obtained prescriptions for these medications from multiple providers. This ultimately escalated to self-prescription using aliases. Dr. S also began to drink heavily each evening.

Dr. S disregards colleagues’ comment about his obvious mood swings, which he attributes to his stressful job and “nagging” wife, despite having a family history of bipolar disorder. He becomes enraged when his wife or friends suggest he seek help. His colleagues whisper behind his back, but for years, no one confronts him about his unpredictable and frequently inappropriate behavior. Eventually, a nurse files a sexual harassment suit against Dr. S, and a patient complains to the medical board that Dr. S exhibited sexually inappropriate behavior during a therapy session.

As physicians, recognizing impairment in our colleagues or ourselves can be difficult. The American Medical Association defines an impaired physician as one who is unable to fulfill personal or professional responsibilities because of psychiatric illness, alcoholism, or drug dependence.¹ Impairment is present when a physician is unable to perform in a manner that conforms to acceptable standards of practice, exhibits serious flaws in judgment, and provides incompetent care.^1-3

Recognizing when a physician is impaired, deciding whether to report him or her to the state medical board, and referring a colleague for treatment can be challenging. This article will:

• review substance abuse, cognitive decline, and other causes of impairment
• address legal and ethical issues involved in reporting a colleague to the state medical board
• provide resources for physician treatment and assistance.

Physicians and addiction

Chemical dependence is the most frequent disabling illness among physicians,⁴ and substance abuse is the most common form of impairment that results in discipline by a state medical board.⁵ An estimated 6% to 8% of physicians abuse drugs, and approximately 14% develop alcohol use disorders; these rates are comparable to those of the general population.⁵ Psychiatrists, emergency room physicians, and solo practitioners are 3 times more likely to abuse substances than other doctors.⁶ An obsessive-compulsive personality and other factors may predispose physicians to substance abuse (Table 1).^7,8

Alcohol is the most commonly abused substance, followed by opiates, cocaine, and other stimulants.⁹ Physicians are estimated to use opiates and benzodiazepines at a rate 5 times greater than that of the general public.^10,11

An often-hidden problem. Physicians frequently deny substance abuse and many are able to conceal the problem from coworkers, even as their personal lives disintegrate.^1,12 Marital and relationship problems may be the first indication of impairment, which gradually spreads to other aspects of their lives (Table 2).^1,2,5 A doctor’s professional performance often is the last area to be affected.^1,12

Substance abuse in physicians may long go unreported. The clinician’s family may want to protect the physician’s reputation, career, and income. Colleagues may be intimidated, uncertain of their concerns, or fearful for their jobs if they report the physician’s impairment. Patients may be reluctant to report their concerns because they depend on their provider for health care, respect the physician, or deny that a doctor could have a drug or alcohol problem.⁵

Table 1

Physicians and substance abuse: Predisposing factors

Table 2

Signs of substance abuse

Screening for cognitive decline

Many people with cognitive impairment lack insight into their problem and may minimize or deny the degree of their impairment.¹³ The prevalence of dementia in individuals age ≥65 is 3% to 11%,¹⁴ and 18% of physicians are in this age group.¹⁵

Ethical, legal, and practical issues arise in determining who, when, and how to screen physicians for cognitive problems. Standard screening exams may not be adequately sensitive for a well-educated physician, and neuropsychological testing may be necessary to detect mild cognitive impairment.¹³ In addition, the cognitive, visual-spacial, reactivity, reasoning, and calculation skills required for capable medical practice vary among specialties.¹⁶

One screening option is a “360-degree review” of information obtained from peers, patients, and non-physician colleagues that the College of Physicians and Surgeons in Alberta, Canada, has incorporated into its Physician’s Achievement Review (PAR) for physicians age ≥65.¹⁷ Compiled in a confidential manner and shared with the physician, the 360-degree survey assesses his or her:

• skill and knowledge
• psychosocial functioning
• management skills
• performance
• collegiality.

In Alberta, physicians who score in the lower one-third of the survey are assessed with an on-site evaluation by physicians from his or her specialty appointed by the PAR Director of Practice Improvement.

Alternately, physicians age ≥65 could be required to undergo annual or biannual neuropsychological testing to screen for mild cognitive impairment or other evidence of cognitive decline. In the United States, any screening requirement must be structured to comply with the Age Discrimination in Employment Act.¹⁸

If a physician shows evidence of cognitive impairment, the state medical board should initiate closer scrutiny and modify or revoke privileges if indicated. Remediation programs designed to assist impaired physicians may not be effective for those with cognitive impairment because the decline in cognitive functioning associated with illnesses such as Alzheimer’s disease often is progressive.¹³

‘Disruptive’ physicians

Mental illnesses such as personality or affective disorders, interpersonal problems within or outside the workplace, or other stressors could lead a physician to disrupt the workplace or patient care. Numerous programs have been established across the United States to help evaluate and treat disruptive physicians. Remediation programs can help identify and offer education for “dyscompetent” physicians (see Related Resources).¹³

To report, or not to report

In a national survey of physicians, only 45% of respondents indicated that they had notified the state licensing board of a colleague they felt was impaired or incompetent, yet almost all (96%) indicated that these individuals should be reported.¹⁹ Any duty to report requires, at minimum, that the physician be affected by an illness that impairs his or her cognition, concentration, rapid decision making, and ability to handle emergencies or perform work functions safely.²⁰

Shouten²⁰ cautions that someone who is considering filing a report because of fear of liability if they don’t should balance this concern against potential liability for breaching confidentiality. If there is evidence of an imminent risk or serious harm to the physician or patients, you may be legally required to breach confidentiality. Some states require licensed health practitioners to report acts of professional misconduct, unless the information is obtained solely from directly treating the physician. These requirements apply only within the state, and only to that state’s licensees.^20-22

An ethical requirement to report also must be balanced against the obligation to maintain confidentiality. Ethics are largely a matter of individual standards, and individuals’ perceived ethical duties vary.

If you are considering reporting an impaired colleague, learn the laws in your state. If the physician is from another jurisdiction, the law provides little definitive guidance. Shouten recommends focusing on clinical outcomes for the doctor and his or her patients rather than on legal liability.²⁰

Physician health programs

Nationwide directories of physician health programs are available from the Federation of State Physician Health Programs and the Federation of State Medical Boards (see Related Resources). Some programs are affiliated with state licensing boards, some are branches of state medical societies, and some are independent. These programs provide confidential treatment and assistance to practitioners experiencing substance or alcohol abuse, mental illness, or disruptive behavior. Some institutions may offer physicians an employee assistance program.

State medical societies may provide information about accessing a physician health program. Programs sponsored by medical societies almost always are independent of state licensing boards. This arrangement allows physicians to seek help without fear of punishment or censure or revocation of their license. Noncompliance with a physician health program, however, likely will result in being reported to the medical board.

Physician health programs typically employ a rehabilitative approach. Punitive measures such as reporting physicians to the medical board usually are not pursued unless the individual does not comply with treatment and monitoring guidelines. A physician who abuses substances, for example, may be required to complete a residential treatment program, attend support group meetings such as 12-step programs, participate in individual therapy, and undergo random screening for alcohol and illicit drug use.⁵

Abstinence is the goal of treating clinicians who abuse substances. Physicians have better outcomes than the general population, with reported abstinence rates of 70% to 90% for those who complete treatment;^23,24 75% to 85% of physicians who complete rehabilitation and comply with close monitoring and follow-up care are able to return to work.^24,25 Acceptance of recovery as a lifelong process, monitoring, and self-vigilance often are necessary to achieve and maintain abstinence.⁵

Risk factors for relapse include:

• denial of illness
• poor stress-coping and relationship skills
• social and professional isolation
• inability to accept feedback
• complacency and overconfidence
• failure to attend support group meetings
• dysfunctional family dynamics
• feelings of self-pity, blame, and guilt.⁵

Treating an impaired colleague. Reid²⁶ recommends that psychiatrists should not evaluate or treat a self-referred, potentially impaired physician unless the relationship is strictly clinical. A physician may withhold symptoms, behaviors, or problems because his or her license, malpractice case, or career are at stake.

Advise a physician who requests evaluation or treatment related to license concerns or any legal matter to seek legal counsel. Working with such physician/patients only upon referral by a lawyer, licensing board, or physicians’ health committee provides treating psychiatrists with a clear professional role, allowing them to focus solely on the physician/patient’s treatment needs.

CASE CONTINUED: Extensive help, then success

The medical director of the hospital where Dr. S works refers him to his state’s impaired physician program. After investigating the complaints by the nurse and patient, the medical board suspends Dr. S’ license and requires him to enter a substance abuse treatment program. He completes an intensive residential program for impaired physicians and achieves sobriety from drugs and alcohol. His mood disorder is successfully treated with medications and psychotherapy. The medical board requires Dr. S to have a chaperone present for all visits with patients and submit random urine drug screens once his license is provisionally restored. The medical board also requires Dr. S to undergo ongoing psychiatric care and medication monitoring. He remains abstinent from alcohol and drugs, complies with the medical board’s requirements, and enjoys a productive practice and improved relationship with his family.

Related Resources

Disruptive physicians

• Samenow C, Swiggart W, Spickard A Jr. Consequence of physician disruptive behavior. Tenn Med. 2007;100(11):38-40.
• Leape LL, Fromson JA. Problem doctors: is there a system-level solution? Ann Intern Med. 2006;144(2):107-115.
• Linney BJ. Confronting the disruptive physician. Physician Exec. 1997;23:55-59.

Physician evaluation

• Anfang SA, Faulkner LR, Fromson JA, et al. The American Psychiatric Association’s resource document on guidelines for psychiatric fitness-for-duty evaluations of physicians. J Am Acad Psychiatry Law. 2005;33:85-88.
• Harmon L, Pomm R. Evaluation, treatment, and monitoring of disruptive physicians’ behavior. Psychiatr Ann. 2004; 34:770-774.

Other resources

• Federation of State Physician Health Programs. www.fsphp.org.
• Federation of State Medical Boards: Directory of Physician Assessment and Remedial Education Programs. www.fsmb.org/pdf/RemEdProg.pdf.
• The Center for Professional Health, Vanderbilt University Medical Center. www.mc.vanderbilt.edu/cph.
• Vanderbilt Comprehensive Assessment Program. www.mc.vanderbilt.edu/root/vcap.
• Alcoholics Anonymous. www.aa.org.
• Narcotics Anonymous. www.na.org.

Drug Brand Name

• Oxycodone/acetaminophen • Percocet

Disclosure

The authors report no financial relationship with the manufacturer of any product mentioned in this article or with manufacturers of competing products.

Discuss this article

From all outward appearances Dr. S, a part-time psychiatrist at an inpatient psychiatric facility and in private practice for 12 years, is living the “perfect life,” with a wife, children, and successful practice.

In retrospect, his drug addiction began insidiously. In college, Dr. S continued to use oxycodone/acetaminophen prescribed for a shoulder injury long after his pain had resolved. He began to use cocaine in residency to help him “get through” the 36-hour call days, and it “helped” him earn the chief resident position because of his heightened energy and concentration. Dr. S’ primary care physician initially prescribed him benzodiazepines for anxiety and to help him sleep. Opiates were prescribed for a musculoskeletal injury. Dr. S obtained prescriptions for these medications from multiple providers. This ultimately escalated to self-prescription using aliases. Dr. S also began to drink heavily each evening.

Dr. S disregards colleagues’ comment about his obvious mood swings, which he attributes to his stressful job and “nagging” wife, despite having a family history of bipolar disorder. He becomes enraged when his wife or friends suggest he seek help. His colleagues whisper behind his back, but for years, no one confronts him about his unpredictable and frequently inappropriate behavior. Eventually, a nurse files a sexual harassment suit against Dr. S, and a patient complains to the medical board that Dr. S exhibited sexually inappropriate behavior during a therapy session.

As physicians, recognizing impairment in our colleagues or ourselves can be difficult. The American Medical Association defines an impaired physician as one who is unable to fulfill personal or professional responsibilities because of psychiatric illness, alcoholism, or drug dependence.¹ Impairment is present when a physician is unable to perform in a manner that conforms to acceptable standards of practice, exhibits serious flaws in judgment, and provides incompetent care.^1-3

Recognizing when a physician is impaired, deciding whether to report him or her to the state medical board, and referring a colleague for treatment can be challenging. This article will:

• review substance abuse, cognitive decline, and other causes of impairment
• address legal and ethical issues involved in reporting a colleague to the state medical board
• provide resources for physician treatment and assistance.

Physicians and addiction

Chemical dependence is the most frequent disabling illness among physicians,⁴ and substance abuse is the most common form of impairment that results in discipline by a state medical board.⁵ An estimated 6% to 8% of physicians abuse drugs, and approximately 14% develop alcohol use disorders; these rates are comparable to those of the general population.⁵ Psychiatrists, emergency room physicians, and solo practitioners are 3 times more likely to abuse substances than other doctors.⁶ An obsessive-compulsive personality and other factors may predispose physicians to substance abuse (Table 1).^7,8

Alcohol is the most commonly abused substance, followed by opiates, cocaine, and other stimulants.⁹ Physicians are estimated to use opiates and benzodiazepines at a rate 5 times greater than that of the general public.^10,11

An often-hidden problem. Physicians frequently deny substance abuse and many are able to conceal the problem from coworkers, even as their personal lives disintegrate.^1,12 Marital and relationship problems may be the first indication of impairment, which gradually spreads to other aspects of their lives (Table 2).^1,2,5 A doctor’s professional performance often is the last area to be affected.^1,12

Substance abuse in physicians may long go unreported. The clinician’s family may want to protect the physician’s reputation, career, and income. Colleagues may be intimidated, uncertain of their concerns, or fearful for their jobs if they report the physician’s impairment. Patients may be reluctant to report their concerns because they depend on their provider for health care, respect the physician, or deny that a doctor could have a drug or alcohol problem.⁵

Table 1

Physicians and substance abuse: Predisposing factors

Table 2

Signs of substance abuse

Screening for cognitive decline

Many people with cognitive impairment lack insight into their problem and may minimize or deny the degree of their impairment.¹³ The prevalence of dementia in individuals age ≥65 is 3% to 11%,¹⁴ and 18% of physicians are in this age group.¹⁵

Ethical, legal, and practical issues arise in determining who, when, and how to screen physicians for cognitive problems. Standard screening exams may not be adequately sensitive for a well-educated physician, and neuropsychological testing may be necessary to detect mild cognitive impairment.¹³ In addition, the cognitive, visual-spacial, reactivity, reasoning, and calculation skills required for capable medical practice vary among specialties.¹⁶

One screening option is a “360-degree review” of information obtained from peers, patients, and non-physician colleagues that the College of Physicians and Surgeons in Alberta, Canada, has incorporated into its Physician’s Achievement Review (PAR) for physicians age ≥65.¹⁷ Compiled in a confidential manner and shared with the physician, the 360-degree survey assesses his or her:

• skill and knowledge
• psychosocial functioning
• management skills
• performance
• collegiality.

In Alberta, physicians who score in the lower one-third of the survey are assessed with an on-site evaluation by physicians from his or her specialty appointed by the PAR Director of Practice Improvement.

Alternately, physicians age ≥65 could be required to undergo annual or biannual neuropsychological testing to screen for mild cognitive impairment or other evidence of cognitive decline. In the United States, any screening requirement must be structured to comply with the Age Discrimination in Employment Act.¹⁸

If a physician shows evidence of cognitive impairment, the state medical board should initiate closer scrutiny and modify or revoke privileges if indicated. Remediation programs designed to assist impaired physicians may not be effective for those with cognitive impairment because the decline in cognitive functioning associated with illnesses such as Alzheimer’s disease often is progressive.¹³

‘Disruptive’ physicians

Mental illnesses such as personality or affective disorders, interpersonal problems within or outside the workplace, or other stressors could lead a physician to disrupt the workplace or patient care. Numerous programs have been established across the United States to help evaluate and treat disruptive physicians. Remediation programs can help identify and offer education for “dyscompetent” physicians (see Related Resources).¹³

To report, or not to report

In a national survey of physicians, only 45% of respondents indicated that they had notified the state licensing board of a colleague they felt was impaired or incompetent, yet almost all (96%) indicated that these individuals should be reported.¹⁹ Any duty to report requires, at minimum, that the physician be affected by an illness that impairs his or her cognition, concentration, rapid decision making, and ability to handle emergencies or perform work functions safely.²⁰

Shouten²⁰ cautions that someone who is considering filing a report because of fear of liability if they don’t should balance this concern against potential liability for breaching confidentiality. If there is evidence of an imminent risk or serious harm to the physician or patients, you may be legally required to breach confidentiality. Some states require licensed health practitioners to report acts of professional misconduct, unless the information is obtained solely from directly treating the physician. These requirements apply only within the state, and only to that state’s licensees.^20-22

An ethical requirement to report also must be balanced against the obligation to maintain confidentiality. Ethics are largely a matter of individual standards, and individuals’ perceived ethical duties vary.

If you are considering reporting an impaired colleague, learn the laws in your state. If the physician is from another jurisdiction, the law provides little definitive guidance. Shouten recommends focusing on clinical outcomes for the doctor and his or her patients rather than on legal liability.²⁰

Physician health programs

Nationwide directories of physician health programs are available from the Federation of State Physician Health Programs and the Federation of State Medical Boards (see Related Resources). Some programs are affiliated with state licensing boards, some are branches of state medical societies, and some are independent. These programs provide confidential treatment and assistance to practitioners experiencing substance or alcohol abuse, mental illness, or disruptive behavior. Some institutions may offer physicians an employee assistance program.

State medical societies may provide information about accessing a physician health program. Programs sponsored by medical societies almost always are independent of state licensing boards. This arrangement allows physicians to seek help without fear of punishment or censure or revocation of their license. Noncompliance with a physician health program, however, likely will result in being reported to the medical board.

Physician health programs typically employ a rehabilitative approach. Punitive measures such as reporting physicians to the medical board usually are not pursued unless the individual does not comply with treatment and monitoring guidelines. A physician who abuses substances, for example, may be required to complete a residential treatment program, attend support group meetings such as 12-step programs, participate in individual therapy, and undergo random screening for alcohol and illicit drug use.⁵

Abstinence is the goal of treating clinicians who abuse substances. Physicians have better outcomes than the general population, with reported abstinence rates of 70% to 90% for those who complete treatment;^23,24 75% to 85% of physicians who complete rehabilitation and comply with close monitoring and follow-up care are able to return to work.^24,25 Acceptance of recovery as a lifelong process, monitoring, and self-vigilance often are necessary to achieve and maintain abstinence.⁵

Risk factors for relapse include:

• denial of illness
• poor stress-coping and relationship skills
• social and professional isolation
• inability to accept feedback
• complacency and overconfidence
• failure to attend support group meetings
• dysfunctional family dynamics
• feelings of self-pity, blame, and guilt.⁵

Treating an impaired colleague. Reid²⁶ recommends that psychiatrists should not evaluate or treat a self-referred, potentially impaired physician unless the relationship is strictly clinical. A physician may withhold symptoms, behaviors, or problems because his or her license, malpractice case, or career are at stake.

Advise a physician who requests evaluation or treatment related to license concerns or any legal matter to seek legal counsel. Working with such physician/patients only upon referral by a lawyer, licensing board, or physicians’ health committee provides treating psychiatrists with a clear professional role, allowing them to focus solely on the physician/patient’s treatment needs.

CASE CONTINUED: Extensive help, then success

The medical director of the hospital where Dr. S works refers him to his state’s impaired physician program. After investigating the complaints by the nurse and patient, the medical board suspends Dr. S’ license and requires him to enter a substance abuse treatment program. He completes an intensive residential program for impaired physicians and achieves sobriety from drugs and alcohol. His mood disorder is successfully treated with medications and psychotherapy. The medical board requires Dr. S to have a chaperone present for all visits with patients and submit random urine drug screens once his license is provisionally restored. The medical board also requires Dr. S to undergo ongoing psychiatric care and medication monitoring. He remains abstinent from alcohol and drugs, complies with the medical board’s requirements, and enjoys a productive practice and improved relationship with his family.

Related Resources

Disruptive physicians

• Samenow C, Swiggart W, Spickard A Jr. Consequence of physician disruptive behavior. Tenn Med. 2007;100(11):38-40.
• Leape LL, Fromson JA. Problem doctors: is there a system-level solution? Ann Intern Med. 2006;144(2):107-115.
• Linney BJ. Confronting the disruptive physician. Physician Exec. 1997;23:55-59.

Physician evaluation

• Anfang SA, Faulkner LR, Fromson JA, et al. The American Psychiatric Association’s resource document on guidelines for psychiatric fitness-for-duty evaluations of physicians. J Am Acad Psychiatry Law. 2005;33:85-88.
• Harmon L, Pomm R. Evaluation, treatment, and monitoring of disruptive physicians’ behavior. Psychiatr Ann. 2004; 34:770-774.

Other resources

• Federation of State Physician Health Programs. www.fsphp.org.
• Federation of State Medical Boards: Directory of Physician Assessment and Remedial Education Programs. www.fsmb.org/pdf/RemEdProg.pdf.
• The Center for Professional Health, Vanderbilt University Medical Center. www.mc.vanderbilt.edu/cph.
• Vanderbilt Comprehensive Assessment Program. www.mc.vanderbilt.edu/root/vcap.
• Alcoholics Anonymous. www.aa.org.
• Narcotics Anonymous. www.na.org.

Drug Brand Name

• Oxycodone/acetaminophen • Percocet

Disclosure

The authors report no financial relationship with the manufacturer of any product mentioned in this article or with manufacturers of competing products.

Discuss this article

From all outward appearances Dr. S, a part-time psychiatrist at an inpatient psychiatric facility and in private practice for 12 years, is living the “perfect life,” with a wife, children, and successful practice.

In retrospect, his drug addiction began insidiously. In college, Dr. S continued to use oxycodone/acetaminophen prescribed for a shoulder injury long after his pain had resolved. He began to use cocaine in residency to help him “get through” the 36-hour call days, and it “helped” him earn the chief resident position because of his heightened energy and concentration. Dr. S’ primary care physician initially prescribed him benzodiazepines for anxiety and to help him sleep. Opiates were prescribed for a musculoskeletal injury. Dr. S obtained prescriptions for these medications from multiple providers. This ultimately escalated to self-prescription using aliases. Dr. S also began to drink heavily each evening.

Dr. S disregards colleagues’ comment about his obvious mood swings, which he attributes to his stressful job and “nagging” wife, despite having a family history of bipolar disorder. He becomes enraged when his wife or friends suggest he seek help. His colleagues whisper behind his back, but for years, no one confronts him about his unpredictable and frequently inappropriate behavior. Eventually, a nurse files a sexual harassment suit against Dr. S, and a patient complains to the medical board that Dr. S exhibited sexually inappropriate behavior during a therapy session.

As physicians, recognizing impairment in our colleagues or ourselves can be difficult. The American Medical Association defines an impaired physician as one who is unable to fulfill personal or professional responsibilities because of psychiatric illness, alcoholism, or drug dependence.¹ Impairment is present when a physician is unable to perform in a manner that conforms to acceptable standards of practice, exhibits serious flaws in judgment, and provides incompetent care.^1-3

Recognizing when a physician is impaired, deciding whether to report him or her to the state medical board, and referring a colleague for treatment can be challenging. This article will:

• review substance abuse, cognitive decline, and other causes of impairment
• address legal and ethical issues involved in reporting a colleague to the state medical board
• provide resources for physician treatment and assistance.

Physicians and addiction

Chemical dependence is the most frequent disabling illness among physicians,⁴ and substance abuse is the most common form of impairment that results in discipline by a state medical board.⁵ An estimated 6% to 8% of physicians abuse drugs, and approximately 14% develop alcohol use disorders; these rates are comparable to those of the general population.⁵ Psychiatrists, emergency room physicians, and solo practitioners are 3 times more likely to abuse substances than other doctors.⁶ An obsessive-compulsive personality and other factors may predispose physicians to substance abuse (Table 1).^7,8

Alcohol is the most commonly abused substance, followed by opiates, cocaine, and other stimulants.⁹ Physicians are estimated to use opiates and benzodiazepines at a rate 5 times greater than that of the general public.^10,11

An often-hidden problem. Physicians frequently deny substance abuse and many are able to conceal the problem from coworkers, even as their personal lives disintegrate.^1,12 Marital and relationship problems may be the first indication of impairment, which gradually spreads to other aspects of their lives (Table 2).^1,2,5 A doctor’s professional performance often is the last area to be affected.^1,12

Substance abuse in physicians may long go unreported. The clinician’s family may want to protect the physician’s reputation, career, and income. Colleagues may be intimidated, uncertain of their concerns, or fearful for their jobs if they report the physician’s impairment. Patients may be reluctant to report their concerns because they depend on their provider for health care, respect the physician, or deny that a doctor could have a drug or alcohol problem.⁵

Table 1

Physicians and substance abuse: Predisposing factors

Table 2

Signs of substance abuse

Screening for cognitive decline

Many people with cognitive impairment lack insight into their problem and may minimize or deny the degree of their impairment.¹³ The prevalence of dementia in individuals age ≥65 is 3% to 11%,¹⁴ and 18% of physicians are in this age group.¹⁵

Ethical, legal, and practical issues arise in determining who, when, and how to screen physicians for cognitive problems. Standard screening exams may not be adequately sensitive for a well-educated physician, and neuropsychological testing may be necessary to detect mild cognitive impairment.¹³ In addition, the cognitive, visual-spacial, reactivity, reasoning, and calculation skills required for capable medical practice vary among specialties.¹⁶

One screening option is a “360-degree review” of information obtained from peers, patients, and non-physician colleagues that the College of Physicians and Surgeons in Alberta, Canada, has incorporated into its Physician’s Achievement Review (PAR) for physicians age ≥65.¹⁷ Compiled in a confidential manner and shared with the physician, the 360-degree survey assesses his or her:

• skill and knowledge
• psychosocial functioning
• management skills
• performance
• collegiality.

In Alberta, physicians who score in the lower one-third of the survey are assessed with an on-site evaluation by physicians from his or her specialty appointed by the PAR Director of Practice Improvement.

Alternately, physicians age ≥65 could be required to undergo annual or biannual neuropsychological testing to screen for mild cognitive impairment or other evidence of cognitive decline. In the United States, any screening requirement must be structured to comply with the Age Discrimination in Employment Act.¹⁸

If a physician shows evidence of cognitive impairment, the state medical board should initiate closer scrutiny and modify or revoke privileges if indicated. Remediation programs designed to assist impaired physicians may not be effective for those with cognitive impairment because the decline in cognitive functioning associated with illnesses such as Alzheimer’s disease often is progressive.¹³

‘Disruptive’ physicians

Mental illnesses such as personality or affective disorders, interpersonal problems within or outside the workplace, or other stressors could lead a physician to disrupt the workplace or patient care. Numerous programs have been established across the United States to help evaluate and treat disruptive physicians. Remediation programs can help identify and offer education for “dyscompetent” physicians (see Related Resources).¹³

To report, or not to report

In a national survey of physicians, only 45% of respondents indicated that they had notified the state licensing board of a colleague they felt was impaired or incompetent, yet almost all (96%) indicated that these individuals should be reported.¹⁹ Any duty to report requires, at minimum, that the physician be affected by an illness that impairs his or her cognition, concentration, rapid decision making, and ability to handle emergencies or perform work functions safely.²⁰

Shouten²⁰ cautions that someone who is considering filing a report because of fear of liability if they don’t should balance this concern against potential liability for breaching confidentiality. If there is evidence of an imminent risk or serious harm to the physician or patients, you may be legally required to breach confidentiality. Some states require licensed health practitioners to report acts of professional misconduct, unless the information is obtained solely from directly treating the physician. These requirements apply only within the state, and only to that state’s licensees.^20-22

An ethical requirement to report also must be balanced against the obligation to maintain confidentiality. Ethics are largely a matter of individual standards, and individuals’ perceived ethical duties vary.

If you are considering reporting an impaired colleague, learn the laws in your state. If the physician is from another jurisdiction, the law provides little definitive guidance. Shouten recommends focusing on clinical outcomes for the doctor and his or her patients rather than on legal liability.²⁰

Physician health programs

Nationwide directories of physician health programs are available from the Federation of State Physician Health Programs and the Federation of State Medical Boards (see Related Resources). Some programs are affiliated with state licensing boards, some are branches of state medical societies, and some are independent. These programs provide confidential treatment and assistance to practitioners experiencing substance or alcohol abuse, mental illness, or disruptive behavior. Some institutions may offer physicians an employee assistance program.

State medical societies may provide information about accessing a physician health program. Programs sponsored by medical societies almost always are independent of state licensing boards. This arrangement allows physicians to seek help without fear of punishment or censure or revocation of their license. Noncompliance with a physician health program, however, likely will result in being reported to the medical board.

Physician health programs typically employ a rehabilitative approach. Punitive measures such as reporting physicians to the medical board usually are not pursued unless the individual does not comply with treatment and monitoring guidelines. A physician who abuses substances, for example, may be required to complete a residential treatment program, attend support group meetings such as 12-step programs, participate in individual therapy, and undergo random screening for alcohol and illicit drug use.⁵

Abstinence is the goal of treating clinicians who abuse substances. Physicians have better outcomes than the general population, with reported abstinence rates of 70% to 90% for those who complete treatment;^23,24 75% to 85% of physicians who complete rehabilitation and comply with close monitoring and follow-up care are able to return to work.^24,25 Acceptance of recovery as a lifelong process, monitoring, and self-vigilance often are necessary to achieve and maintain abstinence.⁵

Risk factors for relapse include:

• denial of illness
• poor stress-coping and relationship skills
• social and professional isolation
• inability to accept feedback
• complacency and overconfidence
• failure to attend support group meetings
• dysfunctional family dynamics
• feelings of self-pity, blame, and guilt.⁵

Treating an impaired colleague. Reid²⁶ recommends that psychiatrists should not evaluate or treat a self-referred, potentially impaired physician unless the relationship is strictly clinical. A physician may withhold symptoms, behaviors, or problems because his or her license, malpractice case, or career are at stake.

Advise a physician who requests evaluation or treatment related to license concerns or any legal matter to seek legal counsel. Working with such physician/patients only upon referral by a lawyer, licensing board, or physicians’ health committee provides treating psychiatrists with a clear professional role, allowing them to focus solely on the physician/patient’s treatment needs.

CASE CONTINUED: Extensive help, then success

The medical director of the hospital where Dr. S works refers him to his state’s impaired physician program. After investigating the complaints by the nurse and patient, the medical board suspends Dr. S’ license and requires him to enter a substance abuse treatment program. He completes an intensive residential program for impaired physicians and achieves sobriety from drugs and alcohol. His mood disorder is successfully treated with medications and psychotherapy. The medical board requires Dr. S to have a chaperone present for all visits with patients and submit random urine drug screens once his license is provisionally restored. The medical board also requires Dr. S to undergo ongoing psychiatric care and medication monitoring. He remains abstinent from alcohol and drugs, complies with the medical board’s requirements, and enjoys a productive practice and improved relationship with his family.

Related Resources

Disruptive physicians

• Samenow C, Swiggart W, Spickard A Jr. Consequence of physician disruptive behavior. Tenn Med. 2007;100(11):38-40.
• Leape LL, Fromson JA. Problem doctors: is there a system-level solution? Ann Intern Med. 2006;144(2):107-115.
• Linney BJ. Confronting the disruptive physician. Physician Exec. 1997;23:55-59.

Physician evaluation

• Anfang SA, Faulkner LR, Fromson JA, et al. The American Psychiatric Association’s resource document on guidelines for psychiatric fitness-for-duty evaluations of physicians. J Am Acad Psychiatry Law. 2005;33:85-88.
• Harmon L, Pomm R. Evaluation, treatment, and monitoring of disruptive physicians’ behavior. Psychiatr Ann. 2004; 34:770-774.

Other resources

• Federation of State Physician Health Programs. www.fsphp.org.
• Federation of State Medical Boards: Directory of Physician Assessment and Remedial Education Programs. www.fsmb.org/pdf/RemEdProg.pdf.
• The Center for Professional Health, Vanderbilt University Medical Center. www.mc.vanderbilt.edu/cph.
• Vanderbilt Comprehensive Assessment Program. www.mc.vanderbilt.edu/root/vcap.
• Alcoholics Anonymous. www.aa.org.
• Narcotics Anonymous. www.na.org.

Drug Brand Name

• Oxycodone/acetaminophen • Percocet

Disclosure

The authors report no financial relationship with the manufacturer of any product mentioned in this article or with manufacturers of competing products.

Dr. Muzyk is a clinical pharmacist, Duke University Medical Center, and Dr. Galiardi is assistant professor of psychiatry and behavioral sciences and assistant clinical professor of medicine, Duke University School of Medicine, Durham, NC.

Beyond their well-known role for treating cardiovascular disease, beta adrenergic receptor antagonists—beta blockers—are used for a variety of medical conditions, including coronary artery disease, hypertension, migraines, and tremor. Their usefulness makes them 1 of the most commonly prescribed medication classes. Unfortunately, their increased use comes with increased reports of depression. Being able to sort fact from fiction will help guide your care for patients taking beta blockers who report new or worsening depressive symptoms.

Does research support a link?

First reported in the 1960s, beta blocker-induced depression was thought to result from the drugs’ antagonistic effect on norepinephrine at ß1 post-synaptic brain receptors. Prompted by case reports of a possible association between beta blockers and depression, 2 prescription database reviews found that patients taking beta blockers were more likely to receive a concurrent antidepressant prescription than patients prescribed other cardiovascular and diabetic medications.^1,2 However, these reviews had major limitations, such as inadequately defined methods for defining depression and lack of control for potential confounding factors.

Mechanistically, peripheral effects of beta blockers on the heart and kidneys lead to decreased chronotropy and inotropy as well as lower blood pressure. These cardiovascular and hemodynamic changes could cause fatigue, decreased energy, and sexual dysfunction that may be interpreted as symptoms of new-onset depression.

Researchers found that beta-blocker use was not associated with depression in a case-control study examining 4,302 New Jersey Medicaid records.³ Also, because most patients in this study received propranolol, the authors were unable to confirm a long-held belief that highly lipophilic beta blockers (such as propranolol, metoprolol, and timolol) are more likely than hydrophilic beta blockers such as atenolol to produce depression.

A retrospective cohort study analyzed 381 patients from 2 myocardial infarction (MI) trials who had been assessed for depressive symptoms and severity.⁴ Researchers matched 254 subjects taking beta blockers during hospitalization for MI with 127 subjects not taking beta blockers. Patients in the study were well balanced on multiple baseline characteristics, including demographics, history of depression, and left ventricular ejection fraction, although those who did not take beta blockers had a significantly higher incidence of chronic obstructive pulmonary disease, digoxin use, and pre-MI beta-blocker use. Researchers assessed depressive symptoms using the Beck Depression Inventory (BDI) at baseline and 3, 6, and 12 months post-MI and identified patients with depression using a Composite International Diagnostic Interview. They found no statistically significant difference in BDI scores between beta-blockers users and nonusers at discharge and at 3, 6, and 12 months post-MI after accounting for potential confounding factors, including:

• contraindications for beta-blocker use (other than history of depression)
• indicators and risk factors for cardiac disease
• baseline depressive symptoms
• benzodiazepine use.

In fact, after controlling for baseline depression, researchers found that beta-blocker users demonstrated significantly lower BDI scores 3 months post-MI than nonusers. Based on these results, the authors concluded that clinicians should not be deterred from prescribing beta blockers because the drugs’ benefit in reducing morbidity and mortality in cardiovascular disease greatly outweighs the risk—if any—of new-onset depression associated with beta-blocker use.

Two additional studies reported no significant difference in the incidence of depression between patients who received beta blockers and those who received other antihypertensives or placebo.^5,6 Future studies assessing depression among subjects randomized to beta blockers vs placebo would be helpful, though withholding beta blockers in some cardiac conditions is not justifiable, and such studies may not be feasible.

Treatment for psychiatric patients

Evidence supports beta-blocker use in coronary artery disease and congestive heart failure. Although patients with these conditions are at increased risk for developing depression,⁷ there is little evidence that their risk will be further increased by adding beta blockers (Table),^3-6 Although patients taking beta blockers report a higher incidence of fatigue and sexual side effects—which could be interpreted as related to depression—studies do not support an association between these medications and depression. As with any medication, initiate beta-blocker therapy with the lowest possible dose and titrate slowly to minimize side effects. Any patient who develops signs and symptoms of major depression should be thoroughly evaluated and treated with appropriate psychotherapy, psychotropics, and careful monitoring.

Table

Beta blockers and depression: Is there a link?

Related resources

• Rivelli S, Jiang W. Depression and ischemic heart disease: what have we learned from clinical trials? Curr Opin Cardiol. 2007;22(4):286-291.
• National guideline clearinghouse. Secondary prevention of coronary artery disease. www.guideline.gov/summary/summary.aspx?doc_id=14585.

Drug brand names

• Atenolol • Tenormin
• Digoxin • Lanoxin
• Metoprolol • Lopressor, Toprol-XL
• Propranolol • Inderal
• Timolol • Blocadren

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Muzyk is a clinical pharmacist, Duke University Medical Center, and Dr. Galiardi is assistant professor of psychiatry and behavioral sciences and assistant clinical professor of medicine, Duke University School of Medicine, Durham, NC.

Beyond their well-known role for treating cardiovascular disease, beta adrenergic receptor antagonists—beta blockers—are used for a variety of medical conditions, including coronary artery disease, hypertension, migraines, and tremor. Their usefulness makes them 1 of the most commonly prescribed medication classes. Unfortunately, their increased use comes with increased reports of depression. Being able to sort fact from fiction will help guide your care for patients taking beta blockers who report new or worsening depressive symptoms.

Does research support a link?

First reported in the 1960s, beta blocker-induced depression was thought to result from the drugs’ antagonistic effect on norepinephrine at ß1 post-synaptic brain receptors. Prompted by case reports of a possible association between beta blockers and depression, 2 prescription database reviews found that patients taking beta blockers were more likely to receive a concurrent antidepressant prescription than patients prescribed other cardiovascular and diabetic medications.^1,2 However, these reviews had major limitations, such as inadequately defined methods for defining depression and lack of control for potential confounding factors.

Mechanistically, peripheral effects of beta blockers on the heart and kidneys lead to decreased chronotropy and inotropy as well as lower blood pressure. These cardiovascular and hemodynamic changes could cause fatigue, decreased energy, and sexual dysfunction that may be interpreted as symptoms of new-onset depression.

Researchers found that beta-blocker use was not associated with depression in a case-control study examining 4,302 New Jersey Medicaid records.³ Also, because most patients in this study received propranolol, the authors were unable to confirm a long-held belief that highly lipophilic beta blockers (such as propranolol, metoprolol, and timolol) are more likely than hydrophilic beta blockers such as atenolol to produce depression.

A retrospective cohort study analyzed 381 patients from 2 myocardial infarction (MI) trials who had been assessed for depressive symptoms and severity.⁴ Researchers matched 254 subjects taking beta blockers during hospitalization for MI with 127 subjects not taking beta blockers. Patients in the study were well balanced on multiple baseline characteristics, including demographics, history of depression, and left ventricular ejection fraction, although those who did not take beta blockers had a significantly higher incidence of chronic obstructive pulmonary disease, digoxin use, and pre-MI beta-blocker use. Researchers assessed depressive symptoms using the Beck Depression Inventory (BDI) at baseline and 3, 6, and 12 months post-MI and identified patients with depression using a Composite International Diagnostic Interview. They found no statistically significant difference in BDI scores between beta-blockers users and nonusers at discharge and at 3, 6, and 12 months post-MI after accounting for potential confounding factors, including:

• contraindications for beta-blocker use (other than history of depression)
• indicators and risk factors for cardiac disease
• baseline depressive symptoms
• benzodiazepine use.

In fact, after controlling for baseline depression, researchers found that beta-blocker users demonstrated significantly lower BDI scores 3 months post-MI than nonusers. Based on these results, the authors concluded that clinicians should not be deterred from prescribing beta blockers because the drugs’ benefit in reducing morbidity and mortality in cardiovascular disease greatly outweighs the risk—if any—of new-onset depression associated with beta-blocker use.

Two additional studies reported no significant difference in the incidence of depression between patients who received beta blockers and those who received other antihypertensives or placebo.^5,6 Future studies assessing depression among subjects randomized to beta blockers vs placebo would be helpful, though withholding beta blockers in some cardiac conditions is not justifiable, and such studies may not be feasible.

Treatment for psychiatric patients

Evidence supports beta-blocker use in coronary artery disease and congestive heart failure. Although patients with these conditions are at increased risk for developing depression,⁷ there is little evidence that their risk will be further increased by adding beta blockers (Table),^3-6 Although patients taking beta blockers report a higher incidence of fatigue and sexual side effects—which could be interpreted as related to depression—studies do not support an association between these medications and depression. As with any medication, initiate beta-blocker therapy with the lowest possible dose and titrate slowly to minimize side effects. Any patient who develops signs and symptoms of major depression should be thoroughly evaluated and treated with appropriate psychotherapy, psychotropics, and careful monitoring.

Table

Beta blockers and depression: Is there a link?

Related resources

• Rivelli S, Jiang W. Depression and ischemic heart disease: what have we learned from clinical trials? Curr Opin Cardiol. 2007;22(4):286-291.
• National guideline clearinghouse. Secondary prevention of coronary artery disease. www.guideline.gov/summary/summary.aspx?doc_id=14585.

Drug brand names

• Atenolol • Tenormin
• Digoxin • Lanoxin
• Metoprolol • Lopressor, Toprol-XL
• Propranolol • Inderal
• Timolol • Blocadren

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Muzyk is a clinical pharmacist, Duke University Medical Center, and Dr. Galiardi is assistant professor of psychiatry and behavioral sciences and assistant clinical professor of medicine, Duke University School of Medicine, Durham, NC.

Beyond their well-known role for treating cardiovascular disease, beta adrenergic receptor antagonists—beta blockers—are used for a variety of medical conditions, including coronary artery disease, hypertension, migraines, and tremor. Their usefulness makes them 1 of the most commonly prescribed medication classes. Unfortunately, their increased use comes with increased reports of depression. Being able to sort fact from fiction will help guide your care for patients taking beta blockers who report new or worsening depressive symptoms.

Does research support a link?

First reported in the 1960s, beta blocker-induced depression was thought to result from the drugs’ antagonistic effect on norepinephrine at ß1 post-synaptic brain receptors. Prompted by case reports of a possible association between beta blockers and depression, 2 prescription database reviews found that patients taking beta blockers were more likely to receive a concurrent antidepressant prescription than patients prescribed other cardiovascular and diabetic medications.^1,2 However, these reviews had major limitations, such as inadequately defined methods for defining depression and lack of control for potential confounding factors.

Mechanistically, peripheral effects of beta blockers on the heart and kidneys lead to decreased chronotropy and inotropy as well as lower blood pressure. These cardiovascular and hemodynamic changes could cause fatigue, decreased energy, and sexual dysfunction that may be interpreted as symptoms of new-onset depression.

Researchers found that beta-blocker use was not associated with depression in a case-control study examining 4,302 New Jersey Medicaid records.³ Also, because most patients in this study received propranolol, the authors were unable to confirm a long-held belief that highly lipophilic beta blockers (such as propranolol, metoprolol, and timolol) are more likely than hydrophilic beta blockers such as atenolol to produce depression.

A retrospective cohort study analyzed 381 patients from 2 myocardial infarction (MI) trials who had been assessed for depressive symptoms and severity.⁴ Researchers matched 254 subjects taking beta blockers during hospitalization for MI with 127 subjects not taking beta blockers. Patients in the study were well balanced on multiple baseline characteristics, including demographics, history of depression, and left ventricular ejection fraction, although those who did not take beta blockers had a significantly higher incidence of chronic obstructive pulmonary disease, digoxin use, and pre-MI beta-blocker use. Researchers assessed depressive symptoms using the Beck Depression Inventory (BDI) at baseline and 3, 6, and 12 months post-MI and identified patients with depression using a Composite International Diagnostic Interview. They found no statistically significant difference in BDI scores between beta-blockers users and nonusers at discharge and at 3, 6, and 12 months post-MI after accounting for potential confounding factors, including:

• contraindications for beta-blocker use (other than history of depression)
• indicators and risk factors for cardiac disease
• baseline depressive symptoms
• benzodiazepine use.

In fact, after controlling for baseline depression, researchers found that beta-blocker users demonstrated significantly lower BDI scores 3 months post-MI than nonusers. Based on these results, the authors concluded that clinicians should not be deterred from prescribing beta blockers because the drugs’ benefit in reducing morbidity and mortality in cardiovascular disease greatly outweighs the risk—if any—of new-onset depression associated with beta-blocker use.

Two additional studies reported no significant difference in the incidence of depression between patients who received beta blockers and those who received other antihypertensives or placebo.^5,6 Future studies assessing depression among subjects randomized to beta blockers vs placebo would be helpful, though withholding beta blockers in some cardiac conditions is not justifiable, and such studies may not be feasible.

Treatment for psychiatric patients

Evidence supports beta-blocker use in coronary artery disease and congestive heart failure. Although patients with these conditions are at increased risk for developing depression,⁷ there is little evidence that their risk will be further increased by adding beta blockers (Table),^3-6 Although patients taking beta blockers report a higher incidence of fatigue and sexual side effects—which could be interpreted as related to depression—studies do not support an association between these medications and depression. As with any medication, initiate beta-blocker therapy with the lowest possible dose and titrate slowly to minimize side effects. Any patient who develops signs and symptoms of major depression should be thoroughly evaluated and treated with appropriate psychotherapy, psychotropics, and careful monitoring.

Table

Beta blockers and depression: Is there a link?

Related resources

• Rivelli S, Jiang W. Depression and ischemic heart disease: what have we learned from clinical trials? Curr Opin Cardiol. 2007;22(4):286-291.
• National guideline clearinghouse. Secondary prevention of coronary artery disease. www.guideline.gov/summary/summary.aspx?doc_id=14585.

Drug brand names

• Atenolol • Tenormin
• Digoxin • Lanoxin
• Metoprolol • Lopressor, Toprol-XL
• Propranolol • Inderal
• Timolol • Blocadren

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article

With a history of panic disorder, perfectionistic tendencies, and depression, Ms. C, age 32, presents 29 weeks into her first pregnancy with a chief complaint that “the Zoloft is not working; my sadness and anxiety are increased and I feel dizzy, like when I miss a dose.” For the past 7 years, she has done well on sertraline, 50 mg/d; she has had no depressive symptoms and experienced minimal to manageable anxiety. Ms. C has found psychotherapy helpful for the last 2 years, including during her pregnancy.

After discussion with her obstetrician, Ms. C remained on sertraline through her early pregnancy. She did well until several weeks ago, when she noticed a return of sadness and incessant worry. She resumed an old habit of excessively cleaning her home. Ms. C denies missing doses but states she has the physical feeling as if she were—a lightheadedness that she clearly distinguishes from pregnancy symptoms.

Both men and women respond well to antidepressants, yet there are notable differences between the 2. Understanding why men and women may differ in response to antidepressants helps clinicians better tailor their treatment choice and dosing.