Somatic Disorders

NEW ORLEANS – Younger women with acute MI are a particularly high-priority target population in terms of screening for and treatment of postinfarct depression, Susmita Mallik, M.D., said at the annual scientific sessions of the American Heart Association.

She reported on 2,501 patients admitted with acute MI to 19 U.S. medical centers participating in the Prospective Registry Evaluating Outcomes After Myocardial Infarction: Events and Recovery (PREMIER) study. Roughly half the patients were age 60 or younger, and 815 participants were women.

The prevalence of in-hospital depression–as defined by a score of at least 10 on the Primary Care Evaluation of Mental Disorders Brief Patient Health Questionnaire–was 40% in women and 22% in men age 60 or younger, and 21% among women and 16% in men above age 60, reported Dr. Mallik of Emory University, Atlanta.

After adjusting for several factors, the odds of in-hospital depression after n acute MI were nearly fourfold greater in women under age 60 than in men over age 60.

NEW ORLEANS – Younger women with acute MI are a particularly high-priority target population in terms of screening for and treatment of postinfarct depression, Susmita Mallik, M.D., said at the annual scientific sessions of the American Heart Association.

She reported on 2,501 patients admitted with acute MI to 19 U.S. medical centers participating in the Prospective Registry Evaluating Outcomes After Myocardial Infarction: Events and Recovery (PREMIER) study. Roughly half the patients were age 60 or younger, and 815 participants were women.

The prevalence of in-hospital depression–as defined by a score of at least 10 on the Primary Care Evaluation of Mental Disorders Brief Patient Health Questionnaire–was 40% in women and 22% in men age 60 or younger, and 21% among women and 16% in men above age 60, reported Dr. Mallik of Emory University, Atlanta.

After adjusting for several factors, the odds of in-hospital depression after n acute MI were nearly fourfold greater in women under age 60 than in men over age 60.

NEW ORLEANS – Younger women with acute MI are a particularly high-priority target population in terms of screening for and treatment of postinfarct depression, Susmita Mallik, M.D., said at the annual scientific sessions of the American Heart Association.

She reported on 2,501 patients admitted with acute MI to 19 U.S. medical centers participating in the Prospective Registry Evaluating Outcomes After Myocardial Infarction: Events and Recovery (PREMIER) study. Roughly half the patients were age 60 or younger, and 815 participants were women.

The prevalence of in-hospital depression–as defined by a score of at least 10 on the Primary Care Evaluation of Mental Disorders Brief Patient Health Questionnaire–was 40% in women and 22% in men age 60 or younger, and 21% among women and 16% in men above age 60, reported Dr. Mallik of Emory University, Atlanta.

After adjusting for several factors, the odds of in-hospital depression after n acute MI were nearly fourfold greater in women under age 60 than in men over age 60.

SAN DIEGO – Most patients with chronic obstructive pulmonary disease have at least moderate levels of anxiety or depression, results from a Veterans Affairs hospital study showed.

In fact, most such patients have anxiety as well as depressive symptoms, often at moderate to severe levels, Mark E. Kunik, M.D., reported at the annual meeting of the American Association for Geriatric Psychiatry.

“We need to develop interventions that are aimed at the level of diagnosis, acute treatment, and long-term management that targets both anxiety and depression,” Dr. Kunik said.

In a study that was part of a larger randomized, controlled trial of cognitive behavioral therapy for cognitively intact COPD patients who are anxious or depressed, Dr. Kunik and his associates at the Michael E. DeBakey VA Medical Center, Houston, screened 557 men with COPD or related diagnoses by telephone with five questions from the Primary Care Evaluation of Mental Disorders (PRIME-MD):

1. During the past month, have you been bothered often by “nerves” or feeling anxious or on edge?

2. During the past month, have you been bothered often by worrying about a lot of different things?

3. During the past month, have you had an anxiety attack (suddenly feeling fear or panic)?

4. During the past month, have you been bothered often by feeling down, depressed, or hopeless?

5. During the past month, have you been bothered often by having little interest or pleasure in doing things?

Patients who screened positive by phone were assessed at the medical center with the Beck Depression Inventory, the Beck Anxiety Inventory, spirometry, the Mini Mental State Examination, and the structured clinical interview for DSM-III-R (SCID). Of the 557 men, 204 met eligibility for the trial. The rest did not have COPD by spirometry, did not have anxiety or depression based on the Beck scales, or were excluded for other reasons.

Of the 204 eligible men, 24 (12%) met SCID criteria for depressive disorder only, 48 (23%) met SCID criteria for anxiety disorder only, and 53 (26%) met criteria for co-occurring depressive and anxiety disorder, whereas 79 (39%) did not meet SCID criteria for anxiety or depression, reported Dr. Kunik, a geropsychiatry health services researcher at the medical center.

“When we looked at the spectrum of diagnosis, the most common was major depressive disorder (23%), followed by generalized anxiety disorder (19%),” he said. “One of the surprises is that there wasn't more panic disorder.”

A limitation of the study, he noted, was that the sample consisted only of males in the VA system. “Anxiety and depression occur more frequently in females,” Dr. Kunik said. “That's a key limitation.”

SAN DIEGO – Most patients with chronic obstructive pulmonary disease have at least moderate levels of anxiety or depression, results from a Veterans Affairs hospital study showed.

In fact, most such patients have anxiety as well as depressive symptoms, often at moderate to severe levels, Mark E. Kunik, M.D., reported at the annual meeting of the American Association for Geriatric Psychiatry.

“We need to develop interventions that are aimed at the level of diagnosis, acute treatment, and long-term management that targets both anxiety and depression,” Dr. Kunik said.

In a study that was part of a larger randomized, controlled trial of cognitive behavioral therapy for cognitively intact COPD patients who are anxious or depressed, Dr. Kunik and his associates at the Michael E. DeBakey VA Medical Center, Houston, screened 557 men with COPD or related diagnoses by telephone with five questions from the Primary Care Evaluation of Mental Disorders (PRIME-MD):

1. During the past month, have you been bothered often by “nerves” or feeling anxious or on edge?

2. During the past month, have you been bothered often by worrying about a lot of different things?

3. During the past month, have you had an anxiety attack (suddenly feeling fear or panic)?

4. During the past month, have you been bothered often by feeling down, depressed, or hopeless?

5. During the past month, have you been bothered often by having little interest or pleasure in doing things?

Patients who screened positive by phone were assessed at the medical center with the Beck Depression Inventory, the Beck Anxiety Inventory, spirometry, the Mini Mental State Examination, and the structured clinical interview for DSM-III-R (SCID). Of the 557 men, 204 met eligibility for the trial. The rest did not have COPD by spirometry, did not have anxiety or depression based on the Beck scales, or were excluded for other reasons.

Of the 204 eligible men, 24 (12%) met SCID criteria for depressive disorder only, 48 (23%) met SCID criteria for anxiety disorder only, and 53 (26%) met criteria for co-occurring depressive and anxiety disorder, whereas 79 (39%) did not meet SCID criteria for anxiety or depression, reported Dr. Kunik, a geropsychiatry health services researcher at the medical center.

“When we looked at the spectrum of diagnosis, the most common was major depressive disorder (23%), followed by generalized anxiety disorder (19%),” he said. “One of the surprises is that there wasn't more panic disorder.”

A limitation of the study, he noted, was that the sample consisted only of males in the VA system. “Anxiety and depression occur more frequently in females,” Dr. Kunik said. “That's a key limitation.”

SAN DIEGO – Most patients with chronic obstructive pulmonary disease have at least moderate levels of anxiety or depression, results from a Veterans Affairs hospital study showed.

In fact, most such patients have anxiety as well as depressive symptoms, often at moderate to severe levels, Mark E. Kunik, M.D., reported at the annual meeting of the American Association for Geriatric Psychiatry.

“We need to develop interventions that are aimed at the level of diagnosis, acute treatment, and long-term management that targets both anxiety and depression,” Dr. Kunik said.

In a study that was part of a larger randomized, controlled trial of cognitive behavioral therapy for cognitively intact COPD patients who are anxious or depressed, Dr. Kunik and his associates at the Michael E. DeBakey VA Medical Center, Houston, screened 557 men with COPD or related diagnoses by telephone with five questions from the Primary Care Evaluation of Mental Disorders (PRIME-MD):

1. During the past month, have you been bothered often by “nerves” or feeling anxious or on edge?

2. During the past month, have you been bothered often by worrying about a lot of different things?

3. During the past month, have you had an anxiety attack (suddenly feeling fear or panic)?

4. During the past month, have you been bothered often by feeling down, depressed, or hopeless?

5. During the past month, have you been bothered often by having little interest or pleasure in doing things?

Patients who screened positive by phone were assessed at the medical center with the Beck Depression Inventory, the Beck Anxiety Inventory, spirometry, the Mini Mental State Examination, and the structured clinical interview for DSM-III-R (SCID). Of the 557 men, 204 met eligibility for the trial. The rest did not have COPD by spirometry, did not have anxiety or depression based on the Beck scales, or were excluded for other reasons.

Of the 204 eligible men, 24 (12%) met SCID criteria for depressive disorder only, 48 (23%) met SCID criteria for anxiety disorder only, and 53 (26%) met criteria for co-occurring depressive and anxiety disorder, whereas 79 (39%) did not meet SCID criteria for anxiety or depression, reported Dr. Kunik, a geropsychiatry health services researcher at the medical center.

“When we looked at the spectrum of diagnosis, the most common was major depressive disorder (23%), followed by generalized anxiety disorder (19%),” he said. “One of the surprises is that there wasn't more panic disorder.”

A limitation of the study, he noted, was that the sample consisted only of males in the VA system. “Anxiety and depression occur more frequently in females,” Dr. Kunik said. “That's a key limitation.”

Women who feel chronic anxiety or suppress anxiety in daily life are more likely to be traumatized by a diagnosis of breast cancer, compared with those who are generally less anxious, said Yumi Iwamitsu, Ph.D., of Kitasato University, Kanagawa, Japan, and colleagues.

The investigators examined the differences in emotional responses among 21 women who had received a diagnosis of breast cancer and 72 women who had benign tumors. Their mean age was 46 years.

Each woman completed the Profile of Mood States (POMS), the Courtauld Emotional Control Scale, and the Manifest Anxiety Scale during a first visit to an outpatient clinic for a breast biopsy (Psychosomatics 2005;46:19-24). They completed the POMS again after a second visit at which they learned the biopsy results.

Both the breast cancer patients and benign tumor patients were assigned to either low anxiety or high anxiety subgroups based on the Manifest Anxiety Scale scores, and either negative emotion suppression or negative emotion expression groups based on the Courtauld Emotional Control Scale scores. The researchers compared POMS scores before and after biopsy results among the eight subgroups.

In women with breast cancer, the total mood disturbance scores were significantly higher among those in the high anxiety subgroup than in the low anxiety subgroup. Those scores were higher in the negative emotion suppression group than in the negative emotion expression group.

Among women with benign tumors, those in the high anxiety subgroup showed higher overall total mood disturbance scores at the first visit. The total mood disturbance scores in the negative emotion expression group were not significantly different between the first and second clinic visits, regardless of the diagnosis.

Women who feel chronic anxiety or suppress anxiety in daily life are more likely to be traumatized by a diagnosis of breast cancer, compared with those who are generally less anxious, said Yumi Iwamitsu, Ph.D., of Kitasato University, Kanagawa, Japan, and colleagues.

The investigators examined the differences in emotional responses among 21 women who had received a diagnosis of breast cancer and 72 women who had benign tumors. Their mean age was 46 years.

Each woman completed the Profile of Mood States (POMS), the Courtauld Emotional Control Scale, and the Manifest Anxiety Scale during a first visit to an outpatient clinic for a breast biopsy (Psychosomatics 2005;46:19-24). They completed the POMS again after a second visit at which they learned the biopsy results.

Both the breast cancer patients and benign tumor patients were assigned to either low anxiety or high anxiety subgroups based on the Manifest Anxiety Scale scores, and either negative emotion suppression or negative emotion expression groups based on the Courtauld Emotional Control Scale scores. The researchers compared POMS scores before and after biopsy results among the eight subgroups.

In women with breast cancer, the total mood disturbance scores were significantly higher among those in the high anxiety subgroup than in the low anxiety subgroup. Those scores were higher in the negative emotion suppression group than in the negative emotion expression group.

Among women with benign tumors, those in the high anxiety subgroup showed higher overall total mood disturbance scores at the first visit. The total mood disturbance scores in the negative emotion expression group were not significantly different between the first and second clinic visits, regardless of the diagnosis.

Women who feel chronic anxiety or suppress anxiety in daily life are more likely to be traumatized by a diagnosis of breast cancer, compared with those who are generally less anxious, said Yumi Iwamitsu, Ph.D., of Kitasato University, Kanagawa, Japan, and colleagues.

The investigators examined the differences in emotional responses among 21 women who had received a diagnosis of breast cancer and 72 women who had benign tumors. Their mean age was 46 years.

Each woman completed the Profile of Mood States (POMS), the Courtauld Emotional Control Scale, and the Manifest Anxiety Scale during a first visit to an outpatient clinic for a breast biopsy (Psychosomatics 2005;46:19-24). They completed the POMS again after a second visit at which they learned the biopsy results.

Both the breast cancer patients and benign tumor patients were assigned to either low anxiety or high anxiety subgroups based on the Manifest Anxiety Scale scores, and either negative emotion suppression or negative emotion expression groups based on the Courtauld Emotional Control Scale scores. The researchers compared POMS scores before and after biopsy results among the eight subgroups.

In women with breast cancer, the total mood disturbance scores were significantly higher among those in the high anxiety subgroup than in the low anxiety subgroup. Those scores were higher in the negative emotion suppression group than in the negative emotion expression group.

Among women with benign tumors, those in the high anxiety subgroup showed higher overall total mood disturbance scores at the first visit. The total mood disturbance scores in the negative emotion expression group were not significantly different between the first and second clinic visits, regardless of the diagnosis.

At what point do the five risk factors that predict type 2 diabetes and cardiovascular disease (CVD) signal metabolic syndrome? When and how often should psychiatrists check for metabolic abnormalities? How can you manage metabolic problems caused by a psychotropic that controls the patient’s psychiatric symptoms?

This article answers those questions by addressing:

• clinical guidelines for diagnosing metabolic syndrome
• suggested intervals for monitoring at-risk patients
• strategies for managing metabolic abnormalities with lifestyle changes or medication.

CASE REPORT: 'FAT' AND FRUSTRATED

Ms. S, age 37, has had bipolar disorder for 10 years. She has tried numerous medications including mood stabilizers, antidepressants, and atypical antipsychotics. The combination of quetiapine, 200 mg bid, and lithium, 300 mg bid, has controlled her symptoms for the past 6 months.

Her weight has increased 40 lbs over the past decade; much of her weight gain has occurred since the birth of her two children, ages 4 and 6. At 5 feet, 3 inches and 170 lbs, she is frustrated over her weight gain, especially on the eve of her 20-year high school reunion. She is convinced that her medications have prevented weight loss.

Her waist, measured at the umbilicus, is 37 inches. Her body mass index (BMI) is 30—indicating clinical obesity—and her blood pressure is in the high normal range (134/80 mm Hg). She has not had gestational diabetes and has not seen a medical doctor since her last pregnancy, but her father has type 2 diabetes and hypertension. She drinks wine occasionally at social events and does not smoke.

The psychiatrist orders a fasting lipid panel and fasting glucose test to further assess her risk of heart disease. Total cholesterol and low-density lipoprotein (LDL) cholesterol are normal. Triglycerides are 125 mg/dL (normal) and her high-density lipoprotein (HDL) is 45 mg/dL—5 mg/dL below normal for a woman her age. Fasting glucose is 86 mg/dL (normal).

The psychiatrist schedules a visit the following month to assess her cardiac and diabetic risk and to discuss weight-loss interventions.

Discussion. In a busy clinical setting, the psychiatrist must accurately gauge Ms. S’ metabolic risk and devise a management strategy. Do her weight and low HDL suggest metabolic syndrome? Is she overeating or making unhealthy dietary choices, or are her psychotropics causing weight gain? Would switching psychotropics lead to bipolar relapse?

IMPLICATIONS OF METABOLIC SYNDROME

Patients with metabolic syndrome are at increased risk for:

• type 2 diabetes¹
• CVD²
• increased mortality from CVD and all causes.³

In a prospective study that followed 1,209 Finnish men over an average 11.4 years,⁴ men with metabolic syndrome were more likely than those with no metabolic problems to die from coronary heart disease, CVD, and any cause after adjustment for conventional cardiovascular risk factors. No one in either group had a baseline illness, suggesting that metabolic syndrome increases the risk of CVD or death regardless of whether underlying illness is present.

DEFINING METABOLIC SYNDROME

Metabolic syndrome is not a disease but a constellation of risk factors that provides a definable point of intervention before onset of type 2 diabetes or CVD.

According to the National Cholesterol Education Program—Adult Treatment Panel III (NCEP-ATP III), presence of three of these five criteria suggest metabolic syndrome:

• abdominal obesity
• insulin resistance
• high blood pressure
• elevated triglycerides
• below-normal HDL.

This definition offers a starting point for measuring risk factors in clinical practice and provides a definable target and parameters to avoid (Table 1).⁵ The guideline is also easy to follow: Waist circumference and blood pressure can be measured within seconds; blood glucose, HDL, and triglycerides can easily be measured before breakfast, after the patient has fasted for at least 6 hours.

Table 1

5 defined risk factors* for metabolic syndrome

MONITORING FREQUENCY

Although no empirical studies have addressed monitoring frequency for metabolic risk factors, several guidelines provide preliminary recommendations. Table 2 summarizes suggested intervals for monitoring weight, lipids, glucose, and waist circumference for patients taking atypical antipsychotics, based on recommendations from the 2004 American Diabetes Association (ADA) and American Psychiatric Association (APA) consensus development conference.⁶

Because atypicals are associated with serious metabolic risks, screen patients taking these agents for metabolic abnormalities at baseline and at regular intervals. Most guidelines recommend measuring blood pressure, BMI, waist circumference, fasting serum lipids (total, LDL, HDL, and triglycerides) and fasting glucose before starting or switching to an atypical and again 12 weeks later. Established risk for metabolic disturbances or dramatic metabolic changes (such as weight gain ≥7%, waist circumference ≥35 inches in women and ≥40 inches in men, or fasting blood sugars >110 mg/dL) demand more-frequent monitoring (ie, monitor high-risk patients quarterly).

Table 2

Suggested monitoring intervals for patients taking atypical antipsychotics*

MANAGING METABOLIC PROBLEMS

Managing metabolic abnormalities or metabolic syndrome is aimed at preventing type 2 diabetes and CVD. Levels of intervention include:

• weight management, weight control education, and promoting regular exercise and a healthy diet
• switching to a psychotropic that is less likely to cause weight gain, if clinically appropriate
• working with the patient’s primary care physician to manage dyslipidemia, hypertension, obesity, or hyperglycemia.

Weight management. Start by controlling weight and promoting regular exercise and healthy eating. Switching medications—often the first response—may not be the best option, particularly if the offending agent is relieving the patient’s psychiatric symptoms.

Losing weight, increasing exercise, and reducing fat and carbohydrate intake can reverse metabolic syndrome and delay onset of type 2 diabetes and CVD.⁷ Even a small weight loss, such as 10% of baseline body weight in persons who are overweight (BMI >25) or obese (BMI >30) can significantly reduce the risk of hypertension, hyperlipidemia, hyperglycemia, and death.⁷

Rather than promoting a single diet, tailor dietary advice to each patient’s metabolic abnormalities (Table 3). Although researchers disagree over whether a low-fat or low-carbohydrate diet produces better results, either diet will work as long as the patient consumes fewer calories than he or she expends. This is because weight loss alone reverses metabolic syndrome.

Likewise, exercise can reverse metabolic syndrome independent of diet change. Regular exercise at modest levels improves HDL,² triglycerides,¹⁷ blood pressure,¹⁸ and hyperglycemia.¹⁹

In one prospective study,²⁰ 621 subjects without chronic disease or injury underwent supervised aerobic training three times weekly for 20 weeks. Participants were told not to otherwise change their health and lifestyle habits.

Of the 105 persons in the cohort who had metabolic syndrome at baseline, 32 (30%) no longer had it after the aerobics program. Among these participants:

• 43% had lower triglycerides than at baseline
• 16% had higher HDL cholesterol
• 38% had lower blood pressure
• 9% had improved fasting glucose
• 28% reduced their waist circumference.

Table 3

Interventions for specific metabolic complications

Selling the benefits of exercise and weight loss to a mentally ill patient can be difficult. Attention, memory, and motivation deficits as well as smoking and substance abuse often get in the way.

By teaming up with clinicians with expertise in dieting such as nurses, dietitians, and recreational therapists, psychiatrists can more effectively promote long-term diet, exercise, and lifestyle changes.²¹

In a prospective 12-month trial,²² 20 patients who were taking atypical antipsychotics for schizophrenia or schizoaffective disorder completed a 52-week program that incorporated nutrition, exercise, and behavioral interventions. Twenty similar patients received treatment as usual. Patients in the program saw significant improvements in weight, blood pressure, exercise habits, nutrition, and hemoglobin A1c compared with the treatment-as-usual group.²²

Psychiatrists who treat privately insured patients should collaborate with the patient’s primary care physician. Many insurance plans will pay for 1 or 2 personal or group sessions with a dietitian, especially if the patient is diagnosed as being obese (BMI >30). Some large plans, such as Kaiser Permanente, will cover intensive multimodal treatment, especially for patients with a BMI >35. Calculating the patient’s BMI can help you document the need for antiobesity treatment (see Related resources).

Medication. If weight control and exercise do not reduce metabolic risk factors after 3 to 6 months, consider switching to an atypical antipsychotic with a lower propensity for causing metabolic effects.

Which agents most decrease metabolic risk has been debated. Preliminary evidence indicates that switching from other antipsychotics to aripiprazole or ziprasidone may reduce weight and improve cholesterol ratios.^23,24 These findings are consistent with the ADA/APA consensus guidelines, which indicate that metabolic risk varies among atypical antipsychotics (Table 4).⁶

Table 4

Atypical antipsychotics and their propensity for causing metabolic abnormalities

Targeted pharmacotherapy. Wait another 3 to 6 months to see if the medication change and weight loss/exercise interventions reduce metabolic risk factors. If they don’t, work with the patient’s primary care physician to manage hypertension, dyslipidemia, and obesity (Table 3).

Although no agents are approved for treating metabolic syndrome per se, medications targeted at individual symptoms are becoming the standard of care. Controlling blood pressure, HDL, and LDL in patients with metabolic syndrome can reduce risk for coronary heart disease by >50%.²⁵ Insulin-sensitizing agents and metformin in combination with lifestyle changes or used alone have been shown to delay onset of type 2 diabetes (Table 3).

CASE CONTINUED: 10 LBS IN 10 WEEKS

At her follow-up visit, Ms. S and her psychiatrist discuss her increased risk for diabetes and cardiovascular disease. She meets criteria for metabolic syndrome (low HDL, elevated blood pressure, and increased waist circumference).

Ms. S agrees to try a formal diet program with set menus, along with group support at her local community center. She also commits to walking 30 minutes three to four times a week with a target heart rate of 100 beats per minute. Although both quetiapine and lithium carry considerable risk of weight gain, she and her psychiatrist decide to wait at least 3 months before considering a medication change, as she is stable on this combination.

Ms. S schedules a follow-up visit with her primary care physician to ensure that she sticks to her weight loss and exercise programs. In the interim, the primary care physician and psychiatrist agree that her goal will be to lose 10 lbs over 10 weeks.

Related resources

• National Alliance for the Mentally Ill. Hearts and Minds Program, a booklet and program geared toward raising awareness regarding diabetes, diet, exercise, and smoking. Download at www.nami.org.
• Centers for Disease Control and Prevention: Body mass index formula for adults. http://www.cdc.gov/nccdphp/dnpa/bmi/bmi-adult-formula.htm.
• National Heart, Lung and Blood Institute body mass index calculator. http://www.nhlbisupport.com/bmi/bmicalc.htm.
• Keck PE Jr, Buse JB, Dagago-Jack S, et al. Managing metabolic concerns in patients with severe mental illness. A special report. Postgraduate Med 2003;1-92.

Drug brand names

• Aripiprazole • Abilify
• Clozapine • Clozaril
• Metformin • Glucophage
• Olanzapine • Zyprexa
• Orlistat • Xenical
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sibutramine • Meridia
• Ziprasidone • Geodon

Disclosure

Dr. Bermudes is a speaker for Bristol-Myers Squibb Co. and Pfizer Inc.

At what point do the five risk factors that predict type 2 diabetes and cardiovascular disease (CVD) signal metabolic syndrome? When and how often should psychiatrists check for metabolic abnormalities? How can you manage metabolic problems caused by a psychotropic that controls the patient’s psychiatric symptoms?

This article answers those questions by addressing:

• clinical guidelines for diagnosing metabolic syndrome
• suggested intervals for monitoring at-risk patients
• strategies for managing metabolic abnormalities with lifestyle changes or medication.

CASE REPORT: 'FAT' AND FRUSTRATED

Ms. S, age 37, has had bipolar disorder for 10 years. She has tried numerous medications including mood stabilizers, antidepressants, and atypical antipsychotics. The combination of quetiapine, 200 mg bid, and lithium, 300 mg bid, has controlled her symptoms for the past 6 months.

Her weight has increased 40 lbs over the past decade; much of her weight gain has occurred since the birth of her two children, ages 4 and 6. At 5 feet, 3 inches and 170 lbs, she is frustrated over her weight gain, especially on the eve of her 20-year high school reunion. She is convinced that her medications have prevented weight loss.

Her waist, measured at the umbilicus, is 37 inches. Her body mass index (BMI) is 30—indicating clinical obesity—and her blood pressure is in the high normal range (134/80 mm Hg). She has not had gestational diabetes and has not seen a medical doctor since her last pregnancy, but her father has type 2 diabetes and hypertension. She drinks wine occasionally at social events and does not smoke.

The psychiatrist orders a fasting lipid panel and fasting glucose test to further assess her risk of heart disease. Total cholesterol and low-density lipoprotein (LDL) cholesterol are normal. Triglycerides are 125 mg/dL (normal) and her high-density lipoprotein (HDL) is 45 mg/dL—5 mg/dL below normal for a woman her age. Fasting glucose is 86 mg/dL (normal).

The psychiatrist schedules a visit the following month to assess her cardiac and diabetic risk and to discuss weight-loss interventions.

Discussion. In a busy clinical setting, the psychiatrist must accurately gauge Ms. S’ metabolic risk and devise a management strategy. Do her weight and low HDL suggest metabolic syndrome? Is she overeating or making unhealthy dietary choices, or are her psychotropics causing weight gain? Would switching psychotropics lead to bipolar relapse?

IMPLICATIONS OF METABOLIC SYNDROME

Patients with metabolic syndrome are at increased risk for:

• type 2 diabetes¹
• CVD²
• increased mortality from CVD and all causes.³

In a prospective study that followed 1,209 Finnish men over an average 11.4 years,⁴ men with metabolic syndrome were more likely than those with no metabolic problems to die from coronary heart disease, CVD, and any cause after adjustment for conventional cardiovascular risk factors. No one in either group had a baseline illness, suggesting that metabolic syndrome increases the risk of CVD or death regardless of whether underlying illness is present.

DEFINING METABOLIC SYNDROME

Metabolic syndrome is not a disease but a constellation of risk factors that provides a definable point of intervention before onset of type 2 diabetes or CVD.

According to the National Cholesterol Education Program—Adult Treatment Panel III (NCEP-ATP III), presence of three of these five criteria suggest metabolic syndrome:

• abdominal obesity
• insulin resistance
• high blood pressure
• elevated triglycerides
• below-normal HDL.

This definition offers a starting point for measuring risk factors in clinical practice and provides a definable target and parameters to avoid (Table 1).⁵ The guideline is also easy to follow: Waist circumference and blood pressure can be measured within seconds; blood glucose, HDL, and triglycerides can easily be measured before breakfast, after the patient has fasted for at least 6 hours.

Table 1

5 defined risk factors* for metabolic syndrome

MONITORING FREQUENCY

Although no empirical studies have addressed monitoring frequency for metabolic risk factors, several guidelines provide preliminary recommendations. Table 2 summarizes suggested intervals for monitoring weight, lipids, glucose, and waist circumference for patients taking atypical antipsychotics, based on recommendations from the 2004 American Diabetes Association (ADA) and American Psychiatric Association (APA) consensus development conference.⁶

Because atypicals are associated with serious metabolic risks, screen patients taking these agents for metabolic abnormalities at baseline and at regular intervals. Most guidelines recommend measuring blood pressure, BMI, waist circumference, fasting serum lipids (total, LDL, HDL, and triglycerides) and fasting glucose before starting or switching to an atypical and again 12 weeks later. Established risk for metabolic disturbances or dramatic metabolic changes (such as weight gain ≥7%, waist circumference ≥35 inches in women and ≥40 inches in men, or fasting blood sugars >110 mg/dL) demand more-frequent monitoring (ie, monitor high-risk patients quarterly).

Table 2

Suggested monitoring intervals for patients taking atypical antipsychotics*

MANAGING METABOLIC PROBLEMS

Managing metabolic abnormalities or metabolic syndrome is aimed at preventing type 2 diabetes and CVD. Levels of intervention include:

• weight management, weight control education, and promoting regular exercise and a healthy diet
• switching to a psychotropic that is less likely to cause weight gain, if clinically appropriate
• working with the patient’s primary care physician to manage dyslipidemia, hypertension, obesity, or hyperglycemia.

Weight management. Start by controlling weight and promoting regular exercise and healthy eating. Switching medications—often the first response—may not be the best option, particularly if the offending agent is relieving the patient’s psychiatric symptoms.

Losing weight, increasing exercise, and reducing fat and carbohydrate intake can reverse metabolic syndrome and delay onset of type 2 diabetes and CVD.⁷ Even a small weight loss, such as 10% of baseline body weight in persons who are overweight (BMI >25) or obese (BMI >30) can significantly reduce the risk of hypertension, hyperlipidemia, hyperglycemia, and death.⁷

Rather than promoting a single diet, tailor dietary advice to each patient’s metabolic abnormalities (Table 3). Although researchers disagree over whether a low-fat or low-carbohydrate diet produces better results, either diet will work as long as the patient consumes fewer calories than he or she expends. This is because weight loss alone reverses metabolic syndrome.

Likewise, exercise can reverse metabolic syndrome independent of diet change. Regular exercise at modest levels improves HDL,² triglycerides,¹⁷ blood pressure,¹⁸ and hyperglycemia.¹⁹

In one prospective study,²⁰ 621 subjects without chronic disease or injury underwent supervised aerobic training three times weekly for 20 weeks. Participants were told not to otherwise change their health and lifestyle habits.

Of the 105 persons in the cohort who had metabolic syndrome at baseline, 32 (30%) no longer had it after the aerobics program. Among these participants:

• 43% had lower triglycerides than at baseline
• 16% had higher HDL cholesterol
• 38% had lower blood pressure
• 9% had improved fasting glucose
• 28% reduced their waist circumference.

Table 3

Interventions for specific metabolic complications

Selling the benefits of exercise and weight loss to a mentally ill patient can be difficult. Attention, memory, and motivation deficits as well as smoking and substance abuse often get in the way.

By teaming up with clinicians with expertise in dieting such as nurses, dietitians, and recreational therapists, psychiatrists can more effectively promote long-term diet, exercise, and lifestyle changes.²¹

In a prospective 12-month trial,²² 20 patients who were taking atypical antipsychotics for schizophrenia or schizoaffective disorder completed a 52-week program that incorporated nutrition, exercise, and behavioral interventions. Twenty similar patients received treatment as usual. Patients in the program saw significant improvements in weight, blood pressure, exercise habits, nutrition, and hemoglobin A1c compared with the treatment-as-usual group.²²

Psychiatrists who treat privately insured patients should collaborate with the patient’s primary care physician. Many insurance plans will pay for 1 or 2 personal or group sessions with a dietitian, especially if the patient is diagnosed as being obese (BMI >30). Some large plans, such as Kaiser Permanente, will cover intensive multimodal treatment, especially for patients with a BMI >35. Calculating the patient’s BMI can help you document the need for antiobesity treatment (see Related resources).

Medication. If weight control and exercise do not reduce metabolic risk factors after 3 to 6 months, consider switching to an atypical antipsychotic with a lower propensity for causing metabolic effects.

Which agents most decrease metabolic risk has been debated. Preliminary evidence indicates that switching from other antipsychotics to aripiprazole or ziprasidone may reduce weight and improve cholesterol ratios.^23,24 These findings are consistent with the ADA/APA consensus guidelines, which indicate that metabolic risk varies among atypical antipsychotics (Table 4).⁶

Table 4

Atypical antipsychotics and their propensity for causing metabolic abnormalities

Targeted pharmacotherapy. Wait another 3 to 6 months to see if the medication change and weight loss/exercise interventions reduce metabolic risk factors. If they don’t, work with the patient’s primary care physician to manage hypertension, dyslipidemia, and obesity (Table 3).

Although no agents are approved for treating metabolic syndrome per se, medications targeted at individual symptoms are becoming the standard of care. Controlling blood pressure, HDL, and LDL in patients with metabolic syndrome can reduce risk for coronary heart disease by >50%.²⁵ Insulin-sensitizing agents and metformin in combination with lifestyle changes or used alone have been shown to delay onset of type 2 diabetes (Table 3).

CASE CONTINUED: 10 LBS IN 10 WEEKS

At her follow-up visit, Ms. S and her psychiatrist discuss her increased risk for diabetes and cardiovascular disease. She meets criteria for metabolic syndrome (low HDL, elevated blood pressure, and increased waist circumference).

Ms. S agrees to try a formal diet program with set menus, along with group support at her local community center. She also commits to walking 30 minutes three to four times a week with a target heart rate of 100 beats per minute. Although both quetiapine and lithium carry considerable risk of weight gain, she and her psychiatrist decide to wait at least 3 months before considering a medication change, as she is stable on this combination.

Ms. S schedules a follow-up visit with her primary care physician to ensure that she sticks to her weight loss and exercise programs. In the interim, the primary care physician and psychiatrist agree that her goal will be to lose 10 lbs over 10 weeks.

Related resources

• National Alliance for the Mentally Ill. Hearts and Minds Program, a booklet and program geared toward raising awareness regarding diabetes, diet, exercise, and smoking. Download at www.nami.org.
• Centers for Disease Control and Prevention: Body mass index formula for adults. http://www.cdc.gov/nccdphp/dnpa/bmi/bmi-adult-formula.htm.
• National Heart, Lung and Blood Institute body mass index calculator. http://www.nhlbisupport.com/bmi/bmicalc.htm.
• Keck PE Jr, Buse JB, Dagago-Jack S, et al. Managing metabolic concerns in patients with severe mental illness. A special report. Postgraduate Med 2003;1-92.

Drug brand names

• Aripiprazole • Abilify
• Clozapine • Clozaril
• Metformin • Glucophage
• Olanzapine • Zyprexa
• Orlistat • Xenical
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sibutramine • Meridia
• Ziprasidone • Geodon

Disclosure

Dr. Bermudes is a speaker for Bristol-Myers Squibb Co. and Pfizer Inc.

At what point do the five risk factors that predict type 2 diabetes and cardiovascular disease (CVD) signal metabolic syndrome? When and how often should psychiatrists check for metabolic abnormalities? How can you manage metabolic problems caused by a psychotropic that controls the patient’s psychiatric symptoms?

This article answers those questions by addressing:

• clinical guidelines for diagnosing metabolic syndrome
• suggested intervals for monitoring at-risk patients
• strategies for managing metabolic abnormalities with lifestyle changes or medication.

CASE REPORT: 'FAT' AND FRUSTRATED

Ms. S, age 37, has had bipolar disorder for 10 years. She has tried numerous medications including mood stabilizers, antidepressants, and atypical antipsychotics. The combination of quetiapine, 200 mg bid, and lithium, 300 mg bid, has controlled her symptoms for the past 6 months.

Her weight has increased 40 lbs over the past decade; much of her weight gain has occurred since the birth of her two children, ages 4 and 6. At 5 feet, 3 inches and 170 lbs, she is frustrated over her weight gain, especially on the eve of her 20-year high school reunion. She is convinced that her medications have prevented weight loss.

Her waist, measured at the umbilicus, is 37 inches. Her body mass index (BMI) is 30—indicating clinical obesity—and her blood pressure is in the high normal range (134/80 mm Hg). She has not had gestational diabetes and has not seen a medical doctor since her last pregnancy, but her father has type 2 diabetes and hypertension. She drinks wine occasionally at social events and does not smoke.

The psychiatrist orders a fasting lipid panel and fasting glucose test to further assess her risk of heart disease. Total cholesterol and low-density lipoprotein (LDL) cholesterol are normal. Triglycerides are 125 mg/dL (normal) and her high-density lipoprotein (HDL) is 45 mg/dL—5 mg/dL below normal for a woman her age. Fasting glucose is 86 mg/dL (normal).

The psychiatrist schedules a visit the following month to assess her cardiac and diabetic risk and to discuss weight-loss interventions.

Discussion. In a busy clinical setting, the psychiatrist must accurately gauge Ms. S’ metabolic risk and devise a management strategy. Do her weight and low HDL suggest metabolic syndrome? Is she overeating or making unhealthy dietary choices, or are her psychotropics causing weight gain? Would switching psychotropics lead to bipolar relapse?

IMPLICATIONS OF METABOLIC SYNDROME

Patients with metabolic syndrome are at increased risk for:

• type 2 diabetes¹
• CVD²
• increased mortality from CVD and all causes.³

In a prospective study that followed 1,209 Finnish men over an average 11.4 years,⁴ men with metabolic syndrome were more likely than those with no metabolic problems to die from coronary heart disease, CVD, and any cause after adjustment for conventional cardiovascular risk factors. No one in either group had a baseline illness, suggesting that metabolic syndrome increases the risk of CVD or death regardless of whether underlying illness is present.

DEFINING METABOLIC SYNDROME

Metabolic syndrome is not a disease but a constellation of risk factors that provides a definable point of intervention before onset of type 2 diabetes or CVD.

According to the National Cholesterol Education Program—Adult Treatment Panel III (NCEP-ATP III), presence of three of these five criteria suggest metabolic syndrome:

• abdominal obesity
• insulin resistance
• high blood pressure
• elevated triglycerides
• below-normal HDL.

This definition offers a starting point for measuring risk factors in clinical practice and provides a definable target and parameters to avoid (Table 1).⁵ The guideline is also easy to follow: Waist circumference and blood pressure can be measured within seconds; blood glucose, HDL, and triglycerides can easily be measured before breakfast, after the patient has fasted for at least 6 hours.

Table 1

5 defined risk factors* for metabolic syndrome

MONITORING FREQUENCY

Although no empirical studies have addressed monitoring frequency for metabolic risk factors, several guidelines provide preliminary recommendations. Table 2 summarizes suggested intervals for monitoring weight, lipids, glucose, and waist circumference for patients taking atypical antipsychotics, based on recommendations from the 2004 American Diabetes Association (ADA) and American Psychiatric Association (APA) consensus development conference.⁶

Because atypicals are associated with serious metabolic risks, screen patients taking these agents for metabolic abnormalities at baseline and at regular intervals. Most guidelines recommend measuring blood pressure, BMI, waist circumference, fasting serum lipids (total, LDL, HDL, and triglycerides) and fasting glucose before starting or switching to an atypical and again 12 weeks later. Established risk for metabolic disturbances or dramatic metabolic changes (such as weight gain ≥7%, waist circumference ≥35 inches in women and ≥40 inches in men, or fasting blood sugars >110 mg/dL) demand more-frequent monitoring (ie, monitor high-risk patients quarterly).

Table 2

Suggested monitoring intervals for patients taking atypical antipsychotics*

MANAGING METABOLIC PROBLEMS

Managing metabolic abnormalities or metabolic syndrome is aimed at preventing type 2 diabetes and CVD. Levels of intervention include:

• weight management, weight control education, and promoting regular exercise and a healthy diet
• switching to a psychotropic that is less likely to cause weight gain, if clinically appropriate
• working with the patient’s primary care physician to manage dyslipidemia, hypertension, obesity, or hyperglycemia.

Weight management. Start by controlling weight and promoting regular exercise and healthy eating. Switching medications—often the first response—may not be the best option, particularly if the offending agent is relieving the patient’s psychiatric symptoms.

Losing weight, increasing exercise, and reducing fat and carbohydrate intake can reverse metabolic syndrome and delay onset of type 2 diabetes and CVD.⁷ Even a small weight loss, such as 10% of baseline body weight in persons who are overweight (BMI >25) or obese (BMI >30) can significantly reduce the risk of hypertension, hyperlipidemia, hyperglycemia, and death.⁷

Rather than promoting a single diet, tailor dietary advice to each patient’s metabolic abnormalities (Table 3). Although researchers disagree over whether a low-fat or low-carbohydrate diet produces better results, either diet will work as long as the patient consumes fewer calories than he or she expends. This is because weight loss alone reverses metabolic syndrome.

Likewise, exercise can reverse metabolic syndrome independent of diet change. Regular exercise at modest levels improves HDL,² triglycerides,¹⁷ blood pressure,¹⁸ and hyperglycemia.¹⁹

In one prospective study,²⁰ 621 subjects without chronic disease or injury underwent supervised aerobic training three times weekly for 20 weeks. Participants were told not to otherwise change their health and lifestyle habits.

Of the 105 persons in the cohort who had metabolic syndrome at baseline, 32 (30%) no longer had it after the aerobics program. Among these participants:

• 43% had lower triglycerides than at baseline
• 16% had higher HDL cholesterol
• 38% had lower blood pressure
• 9% had improved fasting glucose
• 28% reduced their waist circumference.

Table 3

Interventions for specific metabolic complications

Selling the benefits of exercise and weight loss to a mentally ill patient can be difficult. Attention, memory, and motivation deficits as well as smoking and substance abuse often get in the way.

By teaming up with clinicians with expertise in dieting such as nurses, dietitians, and recreational therapists, psychiatrists can more effectively promote long-term diet, exercise, and lifestyle changes.²¹

In a prospective 12-month trial,²² 20 patients who were taking atypical antipsychotics for schizophrenia or schizoaffective disorder completed a 52-week program that incorporated nutrition, exercise, and behavioral interventions. Twenty similar patients received treatment as usual. Patients in the program saw significant improvements in weight, blood pressure, exercise habits, nutrition, and hemoglobin A1c compared with the treatment-as-usual group.²²

Psychiatrists who treat privately insured patients should collaborate with the patient’s primary care physician. Many insurance plans will pay for 1 or 2 personal or group sessions with a dietitian, especially if the patient is diagnosed as being obese (BMI >30). Some large plans, such as Kaiser Permanente, will cover intensive multimodal treatment, especially for patients with a BMI >35. Calculating the patient’s BMI can help you document the need for antiobesity treatment (see Related resources).

Medication. If weight control and exercise do not reduce metabolic risk factors after 3 to 6 months, consider switching to an atypical antipsychotic with a lower propensity for causing metabolic effects.

Which agents most decrease metabolic risk has been debated. Preliminary evidence indicates that switching from other antipsychotics to aripiprazole or ziprasidone may reduce weight and improve cholesterol ratios.^23,24 These findings are consistent with the ADA/APA consensus guidelines, which indicate that metabolic risk varies among atypical antipsychotics (Table 4).⁶

Table 4

Atypical antipsychotics and their propensity for causing metabolic abnormalities

Targeted pharmacotherapy. Wait another 3 to 6 months to see if the medication change and weight loss/exercise interventions reduce metabolic risk factors. If they don’t, work with the patient’s primary care physician to manage hypertension, dyslipidemia, and obesity (Table 3).

Although no agents are approved for treating metabolic syndrome per se, medications targeted at individual symptoms are becoming the standard of care. Controlling blood pressure, HDL, and LDL in patients with metabolic syndrome can reduce risk for coronary heart disease by >50%.²⁵ Insulin-sensitizing agents and metformin in combination with lifestyle changes or used alone have been shown to delay onset of type 2 diabetes (Table 3).

CASE CONTINUED: 10 LBS IN 10 WEEKS

At her follow-up visit, Ms. S and her psychiatrist discuss her increased risk for diabetes and cardiovascular disease. She meets criteria for metabolic syndrome (low HDL, elevated blood pressure, and increased waist circumference).

Ms. S agrees to try a formal diet program with set menus, along with group support at her local community center. She also commits to walking 30 minutes three to four times a week with a target heart rate of 100 beats per minute. Although both quetiapine and lithium carry considerable risk of weight gain, she and her psychiatrist decide to wait at least 3 months before considering a medication change, as she is stable on this combination.

Ms. S schedules a follow-up visit with her primary care physician to ensure that she sticks to her weight loss and exercise programs. In the interim, the primary care physician and psychiatrist agree that her goal will be to lose 10 lbs over 10 weeks.

Related resources

• National Alliance for the Mentally Ill. Hearts and Minds Program, a booklet and program geared toward raising awareness regarding diabetes, diet, exercise, and smoking. Download at www.nami.org.
• Centers for Disease Control and Prevention: Body mass index formula for adults. http://www.cdc.gov/nccdphp/dnpa/bmi/bmi-adult-formula.htm.
• National Heart, Lung and Blood Institute body mass index calculator. http://www.nhlbisupport.com/bmi/bmicalc.htm.
• Keck PE Jr, Buse JB, Dagago-Jack S, et al. Managing metabolic concerns in patients with severe mental illness. A special report. Postgraduate Med 2003;1-92.

Drug brand names

• Aripiprazole • Abilify
• Clozapine • Clozaril
• Metformin • Glucophage
• Olanzapine • Zyprexa
• Orlistat • Xenical
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sibutramine • Meridia
• Ziprasidone • Geodon

Disclosure

Dr. Bermudes is a speaker for Bristol-Myers Squibb Co. and Pfizer Inc.

Given those findings, routine screening of high-risk patients with heart failure followed by psychosocial interventions aimed at reducing the incidence of depression deserves study, said Dr. Havranek of Denver Health Medical Center.

“This would be consistent with the Institute of Medicine position that one of the changes necessary for American health care is for the system to anticipate patient needs rather than simply to react to events,” he said.

The four-item checklist consists of living alone, alcohol abuse, poor health status as measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), and the patient's perception that his or her medical care poses a substantial economic burden. A heart failure patient's risk of developing depression within 1 year rises in stepwise fashion as the number of applicable risk factors increases (see chart), Dr. Havranek said.

The checklist was developed as part of a multicenter prospective cohort study involving 245 outpatients with heart failure (HF) and a left ventricular ejection fraction less than 40% who were free of depression at baseline. During 1 year of follow-up, 21.5% of patients developed clinically significant symptoms of depression as defined by a score above 0.06 on the widely used Medical Outcomes Study Depression Scale.

Multivariate analysis identified four independent predictors of onset of depression in this HF population. Alcohol abuse was associated with a 3-fold elevated risk, living alone conferred a 2.8-fold risk, and medical care being seen by the patient as a substantial economic burden carried a 2.9-fold increased risk.

In addition, the risk of patients developing depression rose by 22% for each 10-point decrement on the KCCQ. The study results were published in December (J. Am. Coll. Cardiol. 2004;44:2333-8).

The KCCQ is a self-administered 23-item multiple-choice instrument that inquires about the impact of HF upon a patient's life. For example, the KCCQ asks patients how much swelling in their feet, ankles, or legs has bothered them in the last 2 weeks, how many times during that period they have been forced by shortness of breath to sleep sitting in a chair propped up by at least three pillows, and how much HF has limited their enjoyment of life during the last 2 weeks.

The range of possible scores on the KCCQ is 0-100. Higher scores indicate less disease impact. Study participants with a baseline score greater than 75 had a 13% incidence of depression onset within 1 year.

The incidence of depression among the patients rose to 20% among those with a baseline score of 51-75, 42% in those who scored 26-50, and 44% with a score of 25 or less, Dr. Havranek said.

Given those findings, routine screening of high-risk patients with heart failure followed by psychosocial interventions aimed at reducing the incidence of depression deserves study, said Dr. Havranek of Denver Health Medical Center.

“This would be consistent with the Institute of Medicine position that one of the changes necessary for American health care is for the system to anticipate patient needs rather than simply to react to events,” he said.

The four-item checklist consists of living alone, alcohol abuse, poor health status as measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), and the patient's perception that his or her medical care poses a substantial economic burden. A heart failure patient's risk of developing depression within 1 year rises in stepwise fashion as the number of applicable risk factors increases (see chart), Dr. Havranek said.

The checklist was developed as part of a multicenter prospective cohort study involving 245 outpatients with heart failure (HF) and a left ventricular ejection fraction less than 40% who were free of depression at baseline. During 1 year of follow-up, 21.5% of patients developed clinically significant symptoms of depression as defined by a score above 0.06 on the widely used Medical Outcomes Study Depression Scale.

Multivariate analysis identified four independent predictors of onset of depression in this HF population. Alcohol abuse was associated with a 3-fold elevated risk, living alone conferred a 2.8-fold risk, and medical care being seen by the patient as a substantial economic burden carried a 2.9-fold increased risk.

In addition, the risk of patients developing depression rose by 22% for each 10-point decrement on the KCCQ. The study results were published in December (J. Am. Coll. Cardiol. 2004;44:2333-8).

The KCCQ is a self-administered 23-item multiple-choice instrument that inquires about the impact of HF upon a patient's life. For example, the KCCQ asks patients how much swelling in their feet, ankles, or legs has bothered them in the last 2 weeks, how many times during that period they have been forced by shortness of breath to sleep sitting in a chair propped up by at least three pillows, and how much HF has limited their enjoyment of life during the last 2 weeks.

The range of possible scores on the KCCQ is 0-100. Higher scores indicate less disease impact. Study participants with a baseline score greater than 75 had a 13% incidence of depression onset within 1 year.

The incidence of depression among the patients rose to 20% among those with a baseline score of 51-75, 42% in those who scored 26-50, and 44% with a score of 25 or less, Dr. Havranek said.

Given those findings, routine screening of high-risk patients with heart failure followed by psychosocial interventions aimed at reducing the incidence of depression deserves study, said Dr. Havranek of Denver Health Medical Center.

“This would be consistent with the Institute of Medicine position that one of the changes necessary for American health care is for the system to anticipate patient needs rather than simply to react to events,” he said.

The four-item checklist consists of living alone, alcohol abuse, poor health status as measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), and the patient's perception that his or her medical care poses a substantial economic burden. A heart failure patient's risk of developing depression within 1 year rises in stepwise fashion as the number of applicable risk factors increases (see chart), Dr. Havranek said.

The checklist was developed as part of a multicenter prospective cohort study involving 245 outpatients with heart failure (HF) and a left ventricular ejection fraction less than 40% who were free of depression at baseline. During 1 year of follow-up, 21.5% of patients developed clinically significant symptoms of depression as defined by a score above 0.06 on the widely used Medical Outcomes Study Depression Scale.

Multivariate analysis identified four independent predictors of onset of depression in this HF population. Alcohol abuse was associated with a 3-fold elevated risk, living alone conferred a 2.8-fold risk, and medical care being seen by the patient as a substantial economic burden carried a 2.9-fold increased risk.

In addition, the risk of patients developing depression rose by 22% for each 10-point decrement on the KCCQ. The study results were published in December (J. Am. Coll. Cardiol. 2004;44:2333-8).

The KCCQ is a self-administered 23-item multiple-choice instrument that inquires about the impact of HF upon a patient's life. For example, the KCCQ asks patients how much swelling in their feet, ankles, or legs has bothered them in the last 2 weeks, how many times during that period they have been forced by shortness of breath to sleep sitting in a chair propped up by at least three pillows, and how much HF has limited their enjoyment of life during the last 2 weeks.

The range of possible scores on the KCCQ is 0-100. Higher scores indicate less disease impact. Study participants with a baseline score greater than 75 had a 13% incidence of depression onset within 1 year.

The incidence of depression among the patients rose to 20% among those with a baseline score of 51-75, 42% in those who scored 26-50, and 44% with a score of 25 or less, Dr. Havranek said.

PARIS – Depressed children with persistent abdominal pain were significantly more likely than their nondepressed peers to report additional problems such as dizziness, weakness, and heart palpitations, Cheryl Little, M.D., said in a poster presentation at the Second World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition.

In a study of 243 consecutive cases of children aged 8-15 years who were referred to gastroenterologists for persistent abdominal pain, 52 met the criteria for depression based on the Children's Depression Inventory. The presence of nebulous GI symptoms, such as an upset stomach, in addition to persistent abdominal pain should be a flag to primary care providers to screen for depression, Dr. Little noted.

Depressed children were significantly more likely than nondepressed children to report nonspecific nongastrointestinal symptoms including dizziness (57% vs. 28%, respectively), chest pain (43% vs. 22%), weakness (73% vs. 37%), back pain (47% vs. 26%), fatigue (75% vs. 53%), and heart palpitations (42% vs. 19%), said Dr. Little of Vanderbilt University in Nashville, Tenn.

In addition, the depressed children were significantly more likely than nondepressed children to report GI symptoms, including stomach upset (92% vs. 72%, respectively) and an urge to vomit (82% vs. 58%), in addition to their persistent abdominal pain. Complaints of feeling full were not significantly different between the two groups.

Headaches were common among both depressed (63%) and nondepressed (52%) children in addition to persistent abdominal pain, regardless of their other accompanying symptoms. No gender differences relating to specific symptoms appeared in this study.

PARIS – Depressed children with persistent abdominal pain were significantly more likely than their nondepressed peers to report additional problems such as dizziness, weakness, and heart palpitations, Cheryl Little, M.D., said in a poster presentation at the Second World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition.

In a study of 243 consecutive cases of children aged 8-15 years who were referred to gastroenterologists for persistent abdominal pain, 52 met the criteria for depression based on the Children's Depression Inventory. The presence of nebulous GI symptoms, such as an upset stomach, in addition to persistent abdominal pain should be a flag to primary care providers to screen for depression, Dr. Little noted.

Depressed children were significantly more likely than nondepressed children to report nonspecific nongastrointestinal symptoms including dizziness (57% vs. 28%, respectively), chest pain (43% vs. 22%), weakness (73% vs. 37%), back pain (47% vs. 26%), fatigue (75% vs. 53%), and heart palpitations (42% vs. 19%), said Dr. Little of Vanderbilt University in Nashville, Tenn.

In addition, the depressed children were significantly more likely than nondepressed children to report GI symptoms, including stomach upset (92% vs. 72%, respectively) and an urge to vomit (82% vs. 58%), in addition to their persistent abdominal pain. Complaints of feeling full were not significantly different between the two groups.

Headaches were common among both depressed (63%) and nondepressed (52%) children in addition to persistent abdominal pain, regardless of their other accompanying symptoms. No gender differences relating to specific symptoms appeared in this study.

PARIS – Depressed children with persistent abdominal pain were significantly more likely than their nondepressed peers to report additional problems such as dizziness, weakness, and heart palpitations, Cheryl Little, M.D., said in a poster presentation at the Second World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition.

In a study of 243 consecutive cases of children aged 8-15 years who were referred to gastroenterologists for persistent abdominal pain, 52 met the criteria for depression based on the Children's Depression Inventory. The presence of nebulous GI symptoms, such as an upset stomach, in addition to persistent abdominal pain should be a flag to primary care providers to screen for depression, Dr. Little noted.

Depressed children were significantly more likely than nondepressed children to report nonspecific nongastrointestinal symptoms including dizziness (57% vs. 28%, respectively), chest pain (43% vs. 22%), weakness (73% vs. 37%), back pain (47% vs. 26%), fatigue (75% vs. 53%), and heart palpitations (42% vs. 19%), said Dr. Little of Vanderbilt University in Nashville, Tenn.

In addition, the depressed children were significantly more likely than nondepressed children to report GI symptoms, including stomach upset (92% vs. 72%, respectively) and an urge to vomit (82% vs. 58%), in addition to their persistent abdominal pain. Complaints of feeling full were not significantly different between the two groups.

Headaches were common among both depressed (63%) and nondepressed (52%) children in addition to persistent abdominal pain, regardless of their other accompanying symptoms. No gender differences relating to specific symptoms appeared in this study.

NEW ORLEANS – Underrecognition and undertreatment of clinically significant depression among patients with acute coronary syndrome is common–and strikingly more so among black patients, Alpesh A. Amin, M.D., reported at the annual scientific sessions of the American Heart Association.

Among 1,181 patients who were hospitalized with acute coronary syndrome (ACS) at two major Kansas City-area medical centers, the prevalence of moderate to severe depressive symptoms as assessed by trained evaluators using the Primary Care Evaluation of Mental Disorders Brief Patient Health Questionnaire was 14.9% among the 80.3% of ACS patients who were white–and fully twice as great in the 16.4% of patients who were black.

Yet these significant depressive symptoms were three times as likely to go unrecognized by clinicians in black than in white patients, said Dr. Amin, a research fellow at the Saint Luke's Hospital Center for Innovation and Research and the University of Missouri, Kansas City.

Moreover, the racial disparity in treatment of depression was even more pronounced than the disparity in recognition. Only 3.6% of black patients with moderate to severe depressive symptoms were discharged on antidepressant medication, compared with 28.5% of depressed white patients.

Depressive symptoms were recognized by clinicians in just 10.3% of black patients with moderate to severe depressive symptom scores, compared with 31.2% of affected white patients.

Recognizing depression should be an important goal for any physician who provides care for patients with ACS, Dr. Amin stressed. Depressed ACS patients have been shown to have a greater risk of future cardiac events and death than nondepressed ones. Plus, the psychologic, social, and functional impairment inflicted by depression make depressive symptoms in patients with ACS worthy of treatment, regardless of whether antidepressant therapy improves cardiovascular outcomes, an issue currently under study.

NEW ORLEANS – Underrecognition and undertreatment of clinically significant depression among patients with acute coronary syndrome is common–and strikingly more so among black patients, Alpesh A. Amin, M.D., reported at the annual scientific sessions of the American Heart Association.

Among 1,181 patients who were hospitalized with acute coronary syndrome (ACS) at two major Kansas City-area medical centers, the prevalence of moderate to severe depressive symptoms as assessed by trained evaluators using the Primary Care Evaluation of Mental Disorders Brief Patient Health Questionnaire was 14.9% among the 80.3% of ACS patients who were white–and fully twice as great in the 16.4% of patients who were black.

Yet these significant depressive symptoms were three times as likely to go unrecognized by clinicians in black than in white patients, said Dr. Amin, a research fellow at the Saint Luke's Hospital Center for Innovation and Research and the University of Missouri, Kansas City.

Moreover, the racial disparity in treatment of depression was even more pronounced than the disparity in recognition. Only 3.6% of black patients with moderate to severe depressive symptoms were discharged on antidepressant medication, compared with 28.5% of depressed white patients.

Depressive symptoms were recognized by clinicians in just 10.3% of black patients with moderate to severe depressive symptom scores, compared with 31.2% of affected white patients.

Recognizing depression should be an important goal for any physician who provides care for patients with ACS, Dr. Amin stressed. Depressed ACS patients have been shown to have a greater risk of future cardiac events and death than nondepressed ones. Plus, the psychologic, social, and functional impairment inflicted by depression make depressive symptoms in patients with ACS worthy of treatment, regardless of whether antidepressant therapy improves cardiovascular outcomes, an issue currently under study.

NEW ORLEANS – Underrecognition and undertreatment of clinically significant depression among patients with acute coronary syndrome is common–and strikingly more so among black patients, Alpesh A. Amin, M.D., reported at the annual scientific sessions of the American Heart Association.

Among 1,181 patients who were hospitalized with acute coronary syndrome (ACS) at two major Kansas City-area medical centers, the prevalence of moderate to severe depressive symptoms as assessed by trained evaluators using the Primary Care Evaluation of Mental Disorders Brief Patient Health Questionnaire was 14.9% among the 80.3% of ACS patients who were white–and fully twice as great in the 16.4% of patients who were black.

Yet these significant depressive symptoms were three times as likely to go unrecognized by clinicians in black than in white patients, said Dr. Amin, a research fellow at the Saint Luke's Hospital Center for Innovation and Research and the University of Missouri, Kansas City.

Moreover, the racial disparity in treatment of depression was even more pronounced than the disparity in recognition. Only 3.6% of black patients with moderate to severe depressive symptoms were discharged on antidepressant medication, compared with 28.5% of depressed white patients.

Depressive symptoms were recognized by clinicians in just 10.3% of black patients with moderate to severe depressive symptom scores, compared with 31.2% of affected white patients.

Recognizing depression should be an important goal for any physician who provides care for patients with ACS, Dr. Amin stressed. Depressed ACS patients have been shown to have a greater risk of future cardiac events and death than nondepressed ones. Plus, the psychologic, social, and functional impairment inflicted by depression make depressive symptoms in patients with ACS worthy of treatment, regardless of whether antidepressant therapy improves cardiovascular outcomes, an issue currently under study.

NEW ORLEANS – Anxiety and other forms of psychological distress constitute a potent independent risk factor for development of new-onset atrial fibrillation in patients with chronic stable coronary artery disease, Charles M. Blatt, M.D., reported at the annual scientific sessions of the American Heart Association.

The relationship is dose dependent. The higher a CAD patient's level of anxiety, depression, somatization, or hostility, the greater the long-term risk of developing atrial fibrillation, explained Dr. Blatt of Harvard Medical School, Boston, and director of research at the Lown Cardiovascular Research Foundation, Brookline, Mass.

He reported on 354 men and 95 women with chronic stable CAD who were prospectively followed for an average of 5 years. Participants in the ongoing observational study are being assessed annually for various forms of psychological distress using the 92-item Kellner's Symptom Questionnaire.

The incidence of atrial fibrillation in patients in the lowest Kellner quartile for total psychological distress was 2 cases per 1,000 person-years, compared with 16 cases per 1,000 person-years in those in the fourth quartile. Similarly, the incidence of atrial fibrillation among patients in the lowest quartile for anxiety was 3 cases per 1,000 person-years, versus 16 in those in the highest quartile.

After adjustment for the standard risk factors for atrial fibrillation, including gender and age, patients in the second through fourth quartiles in terms of anxiety level had a 2.1-fold greater risk of developing atrial fibrillation for each quartile increase.

Each quartile of depression level was associated with a 1.7-fold greater risk of developing atrial fibrillation compared with that of patients in the bottom quartile in terms of depression. The risk of atrial fibrillation increased by an additional 50% with each of the second through fourth quartiles of somatization, and by 60% with each quartile of scoring on hostility.

Patients in the second quartile for total psychological distress had an adjusted 2.3-fold increased risk of developing atrial fibrillation compared with those in the lowest quartile. Those in the third quartile had an adjusted 4.6-fold increased risk, while patients in the fourth quartile had a 6.9-fold greater risk than those in the first quartile, according to Dr. Blatt.

NEW ORLEANS – Anxiety and other forms of psychological distress constitute a potent independent risk factor for development of new-onset atrial fibrillation in patients with chronic stable coronary artery disease, Charles M. Blatt, M.D., reported at the annual scientific sessions of the American Heart Association.

The relationship is dose dependent. The higher a CAD patient's level of anxiety, depression, somatization, or hostility, the greater the long-term risk of developing atrial fibrillation, explained Dr. Blatt of Harvard Medical School, Boston, and director of research at the Lown Cardiovascular Research Foundation, Brookline, Mass.

He reported on 354 men and 95 women with chronic stable CAD who were prospectively followed for an average of 5 years. Participants in the ongoing observational study are being assessed annually for various forms of psychological distress using the 92-item Kellner's Symptom Questionnaire.

The incidence of atrial fibrillation in patients in the lowest Kellner quartile for total psychological distress was 2 cases per 1,000 person-years, compared with 16 cases per 1,000 person-years in those in the fourth quartile. Similarly, the incidence of atrial fibrillation among patients in the lowest quartile for anxiety was 3 cases per 1,000 person-years, versus 16 in those in the highest quartile.

After adjustment for the standard risk factors for atrial fibrillation, including gender and age, patients in the second through fourth quartiles in terms of anxiety level had a 2.1-fold greater risk of developing atrial fibrillation for each quartile increase.

Each quartile of depression level was associated with a 1.7-fold greater risk of developing atrial fibrillation compared with that of patients in the bottom quartile in terms of depression. The risk of atrial fibrillation increased by an additional 50% with each of the second through fourth quartiles of somatization, and by 60% with each quartile of scoring on hostility.

Patients in the second quartile for total psychological distress had an adjusted 2.3-fold increased risk of developing atrial fibrillation compared with those in the lowest quartile. Those in the third quartile had an adjusted 4.6-fold increased risk, while patients in the fourth quartile had a 6.9-fold greater risk than those in the first quartile, according to Dr. Blatt.

NEW ORLEANS – Anxiety and other forms of psychological distress constitute a potent independent risk factor for development of new-onset atrial fibrillation in patients with chronic stable coronary artery disease, Charles M. Blatt, M.D., reported at the annual scientific sessions of the American Heart Association.

The relationship is dose dependent. The higher a CAD patient's level of anxiety, depression, somatization, or hostility, the greater the long-term risk of developing atrial fibrillation, explained Dr. Blatt of Harvard Medical School, Boston, and director of research at the Lown Cardiovascular Research Foundation, Brookline, Mass.

He reported on 354 men and 95 women with chronic stable CAD who were prospectively followed for an average of 5 years. Participants in the ongoing observational study are being assessed annually for various forms of psychological distress using the 92-item Kellner's Symptom Questionnaire.

The incidence of atrial fibrillation in patients in the lowest Kellner quartile for total psychological distress was 2 cases per 1,000 person-years, compared with 16 cases per 1,000 person-years in those in the fourth quartile. Similarly, the incidence of atrial fibrillation among patients in the lowest quartile for anxiety was 3 cases per 1,000 person-years, versus 16 in those in the highest quartile.

After adjustment for the standard risk factors for atrial fibrillation, including gender and age, patients in the second through fourth quartiles in terms of anxiety level had a 2.1-fold greater risk of developing atrial fibrillation for each quartile increase.

Each quartile of depression level was associated with a 1.7-fold greater risk of developing atrial fibrillation compared with that of patients in the bottom quartile in terms of depression. The risk of atrial fibrillation increased by an additional 50% with each of the second through fourth quartiles of somatization, and by 60% with each quartile of scoring on hostility.

Patients in the second quartile for total psychological distress had an adjusted 2.3-fold increased risk of developing atrial fibrillation compared with those in the lowest quartile. Those in the third quartile had an adjusted 4.6-fold increased risk, while patients in the fourth quartile had a 6.9-fold greater risk than those in the first quartile, according to Dr. Blatt.

▸ Gut-directed hypnotherapy results in significant, long-term improvements in symptoms of irritable bowel syndrome.

▸ A group of clinicians in North Carolina has developed a standardized hypnotherapy protocol that physicians can obtain at no cost.

Rationale for Use

Irritable bowel syndrome (IBS) is estimated to afflict about 10%-20% of the U.S. population. In its most severe form, IBS has an impact on quality of life that rivals that of congestive heart failure or recent stroke. Treatment consists largely of advice, reassurance, and symptomatic management with antidiarrheals, antispasmodics, and laxatives–and is notoriously ineffective.

Although the precise cause of IBS remains uncertain, research has shown that a fundamental physiologic component is dysregulation of the bidirectional communication between the enteric nervous system and the brain. This brain-gut axis involves the activity of numerous neurotransmitters and related receptors, including serotonin and the 5-HT3 and 5-HT4 receptors (Med. Sci. Monit. 2004;10:RA125–31).

Moreover, many patients with the disorder also experience anxiety and other psychological symptoms along with their diarrhea, constipation, and pain, and their digestive symptoms sometimes correlate with mental and emotional states. Because of this link with psychological symptoms, researchers for the past 20 years have been investigating ways of harnessing the brain-gut axis to alleviate the condition. One of the most successful approaches has been hypnosis.

The U.K. Experience

For more than 20 years, patients with IBS referred to University Hospitals of South Manchester, England, have been treated with hypnotherapy in a program devised by gastroenterologist Peter J. Whorwell, M.D. His protocol, known as gut-directed hypnotherapy, involves hypnotic deep progressive relaxation and suggestion directed toward control of gut function. Patients are encouraged to use imagery to gain control over their gut activity. For example, a patient with diarrhea might visualize the digestive tract as a rushing river that can be slowed to a calm stream. Pain can be alleviated by applying warmth generated when the patient places a hand on his or her belly.

The Manchester protocol includes 12 sessions over a 3-month period. Patients also are given audiotapes to use at home on a daily basis.

The first small study evaluating the technique randomized 30 patients with severe, refractory IBS to hypnotherapy or psychotherapy. Both groups showed improvements in abdominal pain and distension and well-being. However, the psychotherapy group had no improvement in bowel habits, while the hypnotherapy group experienced “dramatic improvements” in all outcome measures, and no relapses were seen during 3 months of follow-up (Lancet 1984;2:1232–4). In a subsequent report, clinical improvement was maintained in all of the hypnotherapy patients for 2 years (Gut 1987;28:423–5).

The Manchester center later became the first hypnotherapy unit in the British National Health Service dedicated to IBS treatment. Investigators there have continued to follow their patients, and now have reported on long-term outcomes. Among the first 204 patients who completed a course of gut-directed hypnotherapy and responded to a subjective assessment questionnaire, 106 (52%) reported that their symptoms were “very much better” in the immediate posttreatment period, while 39 (19%) were “moderately better” and 32 (16%) were “slightly better” (Gut 2003;52:1623–9).

And the benefits persisted. Among responders who replied to the questionnaire, 81.3% reported that the initial symptomatic improvements were maintained–or even increased further–for periods up to 5 years. Extracolonic symptoms such as anxiety and depression also continued to improve.

The hypnotherapy must be gut specific, according to Dr. Whorwell. “Over the years we have found that the therapy has to be focused on the gut rather than just directed in a more general way,” he said in an interview.

The U.S. Experience

A group of therapists at the University of North Carolina at Chapel Hill has instituted a similar program with equivalent success. They also have investigated the mechanisms by which hypnosis might affect IBS symptoms. In a series of tests, they found that hypnotherapy did not alter rectal pain thresholds or smooth muscle tone, autonomic nervous system activity, or frontalis muscle EMG activity (Dig. Dis. Sci. 2002;47:2605–14). Rather, they suggested that the effects of hypnosis are mediated through reduction in somatization, “primarily by altering the patient's focus of attention and/or by changing his or her beliefs about the meaning of sensations arising from the gastrointestinal tract.”

The North Carolina clinicians also have spearheaded efforts to make hypnotherapy more widely available to patients in the United States, noting that psychological treatments are currently offered to fewer than 10% of patients with functional GI disorders seen in primary care or gastroenterology clinics. They have established a Web site with links listing hypnotherapists and other resources for patients. Clinicians can request by e-mail their protocol package, free of charge, containing verbatim scripts and other materials, at

www.ibshypnosis.com

Unanswered Questions

Aside from uncertainty about the mechanisms of effect of gut-directed hypnotherapy, questions also remain concerning whether hypnotherapy is superior to other forms of psychological therapy. Benefits have been reported with cognitive-behavioral, interpersonal, and psychodynamic therapies, but no side-by-side comparisons have been done, according to Olafur S. Palsson, Psy.D., of the North Carolina group (Gastroenterology 2002;123:2132–5). Furthermore, data are lacking on using hypnotherapy as adjunctive therapy with medications such as antidepressants and the 5-HT modulators.

▸ Gut-directed hypnotherapy results in significant, long-term improvements in symptoms of irritable bowel syndrome.

▸ A group of clinicians in North Carolina has developed a standardized hypnotherapy protocol that physicians can obtain at no cost.

Rationale for Use

Irritable bowel syndrome (IBS) is estimated to afflict about 10%-20% of the U.S. population. In its most severe form, IBS has an impact on quality of life that rivals that of congestive heart failure or recent stroke. Treatment consists largely of advice, reassurance, and symptomatic management with antidiarrheals, antispasmodics, and laxatives–and is notoriously ineffective.

Although the precise cause of IBS remains uncertain, research has shown that a fundamental physiologic component is dysregulation of the bidirectional communication between the enteric nervous system and the brain. This brain-gut axis involves the activity of numerous neurotransmitters and related receptors, including serotonin and the 5-HT3 and 5-HT4 receptors (Med. Sci. Monit. 2004;10:RA125–31).

Moreover, many patients with the disorder also experience anxiety and other psychological symptoms along with their diarrhea, constipation, and pain, and their digestive symptoms sometimes correlate with mental and emotional states. Because of this link with psychological symptoms, researchers for the past 20 years have been investigating ways of harnessing the brain-gut axis to alleviate the condition. One of the most successful approaches has been hypnosis.

The U.K. Experience

For more than 20 years, patients with IBS referred to University Hospitals of South Manchester, England, have been treated with hypnotherapy in a program devised by gastroenterologist Peter J. Whorwell, M.D. His protocol, known as gut-directed hypnotherapy, involves hypnotic deep progressive relaxation and suggestion directed toward control of gut function. Patients are encouraged to use imagery to gain control over their gut activity. For example, a patient with diarrhea might visualize the digestive tract as a rushing river that can be slowed to a calm stream. Pain can be alleviated by applying warmth generated when the patient places a hand on his or her belly.

The Manchester protocol includes 12 sessions over a 3-month period. Patients also are given audiotapes to use at home on a daily basis.

The first small study evaluating the technique randomized 30 patients with severe, refractory IBS to hypnotherapy or psychotherapy. Both groups showed improvements in abdominal pain and distension and well-being. However, the psychotherapy group had no improvement in bowel habits, while the hypnotherapy group experienced “dramatic improvements” in all outcome measures, and no relapses were seen during 3 months of follow-up (Lancet 1984;2:1232–4). In a subsequent report, clinical improvement was maintained in all of the hypnotherapy patients for 2 years (Gut 1987;28:423–5).

The Manchester center later became the first hypnotherapy unit in the British National Health Service dedicated to IBS treatment. Investigators there have continued to follow their patients, and now have reported on long-term outcomes. Among the first 204 patients who completed a course of gut-directed hypnotherapy and responded to a subjective assessment questionnaire, 106 (52%) reported that their symptoms were “very much better” in the immediate posttreatment period, while 39 (19%) were “moderately better” and 32 (16%) were “slightly better” (Gut 2003;52:1623–9).

And the benefits persisted. Among responders who replied to the questionnaire, 81.3% reported that the initial symptomatic improvements were maintained–or even increased further–for periods up to 5 years. Extracolonic symptoms such as anxiety and depression also continued to improve.

The hypnotherapy must be gut specific, according to Dr. Whorwell. “Over the years we have found that the therapy has to be focused on the gut rather than just directed in a more general way,” he said in an interview.

The U.S. Experience

A group of therapists at the University of North Carolina at Chapel Hill has instituted a similar program with equivalent success. They also have investigated the mechanisms by which hypnosis might affect IBS symptoms. In a series of tests, they found that hypnotherapy did not alter rectal pain thresholds or smooth muscle tone, autonomic nervous system activity, or frontalis muscle EMG activity (Dig. Dis. Sci. 2002;47:2605–14). Rather, they suggested that the effects of hypnosis are mediated through reduction in somatization, “primarily by altering the patient's focus of attention and/or by changing his or her beliefs about the meaning of sensations arising from the gastrointestinal tract.”

The North Carolina clinicians also have spearheaded efforts to make hypnotherapy more widely available to patients in the United States, noting that psychological treatments are currently offered to fewer than 10% of patients with functional GI disorders seen in primary care or gastroenterology clinics. They have established a Web site with links listing hypnotherapists and other resources for patients. Clinicians can request by e-mail their protocol package, free of charge, containing verbatim scripts and other materials, at

www.ibshypnosis.com

Unanswered Questions

Aside from uncertainty about the mechanisms of effect of gut-directed hypnotherapy, questions also remain concerning whether hypnotherapy is superior to other forms of psychological therapy. Benefits have been reported with cognitive-behavioral, interpersonal, and psychodynamic therapies, but no side-by-side comparisons have been done, according to Olafur S. Palsson, Psy.D., of the North Carolina group (Gastroenterology 2002;123:2132–5). Furthermore, data are lacking on using hypnotherapy as adjunctive therapy with medications such as antidepressants and the 5-HT modulators.

▸ Gut-directed hypnotherapy results in significant, long-term improvements in symptoms of irritable bowel syndrome.

▸ A group of clinicians in North Carolina has developed a standardized hypnotherapy protocol that physicians can obtain at no cost.

Rationale for Use

Irritable bowel syndrome (IBS) is estimated to afflict about 10%-20% of the U.S. population. In its most severe form, IBS has an impact on quality of life that rivals that of congestive heart failure or recent stroke. Treatment consists largely of advice, reassurance, and symptomatic management with antidiarrheals, antispasmodics, and laxatives–and is notoriously ineffective.

Although the precise cause of IBS remains uncertain, research has shown that a fundamental physiologic component is dysregulation of the bidirectional communication between the enteric nervous system and the brain. This brain-gut axis involves the activity of numerous neurotransmitters and related receptors, including serotonin and the 5-HT3 and 5-HT4 receptors (Med. Sci. Monit. 2004;10:RA125–31).

Moreover, many patients with the disorder also experience anxiety and other psychological symptoms along with their diarrhea, constipation, and pain, and their digestive symptoms sometimes correlate with mental and emotional states. Because of this link with psychological symptoms, researchers for the past 20 years have been investigating ways of harnessing the brain-gut axis to alleviate the condition. One of the most successful approaches has been hypnosis.

The U.K. Experience

For more than 20 years, patients with IBS referred to University Hospitals of South Manchester, England, have been treated with hypnotherapy in a program devised by gastroenterologist Peter J. Whorwell, M.D. His protocol, known as gut-directed hypnotherapy, involves hypnotic deep progressive relaxation and suggestion directed toward control of gut function. Patients are encouraged to use imagery to gain control over their gut activity. For example, a patient with diarrhea might visualize the digestive tract as a rushing river that can be slowed to a calm stream. Pain can be alleviated by applying warmth generated when the patient places a hand on his or her belly.

The Manchester protocol includes 12 sessions over a 3-month period. Patients also are given audiotapes to use at home on a daily basis.

The first small study evaluating the technique randomized 30 patients with severe, refractory IBS to hypnotherapy or psychotherapy. Both groups showed improvements in abdominal pain and distension and well-being. However, the psychotherapy group had no improvement in bowel habits, while the hypnotherapy group experienced “dramatic improvements” in all outcome measures, and no relapses were seen during 3 months of follow-up (Lancet 1984;2:1232–4). In a subsequent report, clinical improvement was maintained in all of the hypnotherapy patients for 2 years (Gut 1987;28:423–5).

The Manchester center later became the first hypnotherapy unit in the British National Health Service dedicated to IBS treatment. Investigators there have continued to follow their patients, and now have reported on long-term outcomes. Among the first 204 patients who completed a course of gut-directed hypnotherapy and responded to a subjective assessment questionnaire, 106 (52%) reported that their symptoms were “very much better” in the immediate posttreatment period, while 39 (19%) were “moderately better” and 32 (16%) were “slightly better” (Gut 2003;52:1623–9).

And the benefits persisted. Among responders who replied to the questionnaire, 81.3% reported that the initial symptomatic improvements were maintained–or even increased further–for periods up to 5 years. Extracolonic symptoms such as anxiety and depression also continued to improve.

The hypnotherapy must be gut specific, according to Dr. Whorwell. “Over the years we have found that the therapy has to be focused on the gut rather than just directed in a more general way,” he said in an interview.

The U.S. Experience

A group of therapists at the University of North Carolina at Chapel Hill has instituted a similar program with equivalent success. They also have investigated the mechanisms by which hypnosis might affect IBS symptoms. In a series of tests, they found that hypnotherapy did not alter rectal pain thresholds or smooth muscle tone, autonomic nervous system activity, or frontalis muscle EMG activity (Dig. Dis. Sci. 2002;47:2605–14). Rather, they suggested that the effects of hypnosis are mediated through reduction in somatization, “primarily by altering the patient's focus of attention and/or by changing his or her beliefs about the meaning of sensations arising from the gastrointestinal tract.”

The North Carolina clinicians also have spearheaded efforts to make hypnotherapy more widely available to patients in the United States, noting that psychological treatments are currently offered to fewer than 10% of patients with functional GI disorders seen in primary care or gastroenterology clinics. They have established a Web site with links listing hypnotherapists and other resources for patients. Clinicians can request by e-mail their protocol package, free of charge, containing verbatim scripts and other materials, at

www.ibshypnosis.com

Unanswered Questions

Aside from uncertainty about the mechanisms of effect of gut-directed hypnotherapy, questions also remain concerning whether hypnotherapy is superior to other forms of psychological therapy. Benefits have been reported with cognitive-behavioral, interpersonal, and psychodynamic therapies, but no side-by-side comparisons have been done, according to Olafur S. Palsson, Psy.D., of the North Carolina group (Gastroenterology 2002;123:2132–5). Furthermore, data are lacking on using hypnotherapy as adjunctive therapy with medications such as antidepressants and the 5-HT modulators.

Obese patients with binge-eating disorder treated with topiramate in an open-label study binged significantly less often and lost weight, according to a study by Susan L. McElroy, M.D., and her colleagues.

A previous, randomized, placebo-controlled trial of 61 patients conducted by Dr. McElroy and her coinvestigators reported that topiramate (Topamax) reduced both binge-eating behavior and body weight in obese patients suffering from binge-eating disorder (BED). That study lasted 14 weeks (Am. J. Psychiatry 2003;160:255–61).

To assess topiramate's effectiveness and tolerability over a longer period, the investigators extended the study for an additional 42 weeks in subjects who completed the first study and wanted to pursue treatment with the drug. The 42-week extension was open-label, nonrandomized, and uncontrolled (J. Clin. Psychiatry 2004;65:1463–9).

Fifteen patients who received topiramate during the controlled study and participated in the extension study showed an average drop of 4.0 binges per week, compared with their binge frequency before they started taking the drug (P < .001), and lost 14.1 kg in weight (P = .023), compared with their baseline weight. Sixteen patients who received placebo during the controlled study and participated in the extension study showed a drop of 2.5 binges per week (P < .044), compared with their baseline rate, and lost 14.5 kg (P < .002), the researchers reported. Topiramate's mechanism of action in BED is unknown, but the investigators speculated that the antiseizure medication curbs appetite and enhances satiety through glutamate receptor antagonism.

Dr. McElroy consults for Ortho-McNeil Pharmaceutical Inc., the maker of topiramate.

Obese patients with binge-eating disorder treated with topiramate in an open-label study binged significantly less often and lost weight, according to a study by Susan L. McElroy, M.D., and her colleagues.

A previous, randomized, placebo-controlled trial of 61 patients conducted by Dr. McElroy and her coinvestigators reported that topiramate (Topamax) reduced both binge-eating behavior and body weight in obese patients suffering from binge-eating disorder (BED). That study lasted 14 weeks (Am. J. Psychiatry 2003;160:255–61).

To assess topiramate's effectiveness and tolerability over a longer period, the investigators extended the study for an additional 42 weeks in subjects who completed the first study and wanted to pursue treatment with the drug. The 42-week extension was open-label, nonrandomized, and uncontrolled (J. Clin. Psychiatry 2004;65:1463–9).

Fifteen patients who received topiramate during the controlled study and participated in the extension study showed an average drop of 4.0 binges per week, compared with their binge frequency before they started taking the drug (P < .001), and lost 14.1 kg in weight (P = .023), compared with their baseline weight. Sixteen patients who received placebo during the controlled study and participated in the extension study showed a drop of 2.5 binges per week (P < .044), compared with their baseline rate, and lost 14.5 kg (P < .002), the researchers reported. Topiramate's mechanism of action in BED is unknown, but the investigators speculated that the antiseizure medication curbs appetite and enhances satiety through glutamate receptor antagonism.

Dr. McElroy consults for Ortho-McNeil Pharmaceutical Inc., the maker of topiramate.

Obese patients with binge-eating disorder treated with topiramate in an open-label study binged significantly less often and lost weight, according to a study by Susan L. McElroy, M.D., and her colleagues.

A previous, randomized, placebo-controlled trial of 61 patients conducted by Dr. McElroy and her coinvestigators reported that topiramate (Topamax) reduced both binge-eating behavior and body weight in obese patients suffering from binge-eating disorder (BED). That study lasted 14 weeks (Am. J. Psychiatry 2003;160:255–61).

To assess topiramate's effectiveness and tolerability over a longer period, the investigators extended the study for an additional 42 weeks in subjects who completed the first study and wanted to pursue treatment with the drug. The 42-week extension was open-label, nonrandomized, and uncontrolled (J. Clin. Psychiatry 2004;65:1463–9).

Fifteen patients who received topiramate during the controlled study and participated in the extension study showed an average drop of 4.0 binges per week, compared with their binge frequency before they started taking the drug (P < .001), and lost 14.1 kg in weight (P = .023), compared with their baseline weight. Sixteen patients who received placebo during the controlled study and participated in the extension study showed a drop of 2.5 binges per week (P < .044), compared with their baseline rate, and lost 14.5 kg (P < .002), the researchers reported. Topiramate's mechanism of action in BED is unknown, but the investigators speculated that the antiseizure medication curbs appetite and enhances satiety through glutamate receptor antagonism.

Dr. McElroy consults for Ortho-McNeil Pharmaceutical Inc., the maker of topiramate.