Somatic Disorders

KEYSTONE, COLO. – A high index of suspicion for eating disorders is warranted in adolescents and young adults with type 1 diabetes, Stephanie H. Gerken said at a conference on the management of diabetes in youth.

The largest studies suggest the prevalence of eating disorders (EDs) meeting Diagnostic and Statistical Manual, Fourth Edition, criteria is about 10% in adolescent girls with type 1 diabetes. Another 14% have subthreshold variants. Both rates are roughly twice those found in nondiabetic adolescent girls.

The most common unhealthy weight-control practice among diabetic teens is intentional omission of insulin to lose weight. Many diabetic patients with weight concerns quickly figure out that skipping insulin injections is an easier way to drop pounds than restricting food intake or bingeing and purging, explained Ms. Gerken, a diabetes educator and registered dietician at the International Diabetes Center, Park Nicollet Clinics, Minneapolis.

The elevated risk of eating disorders in association with type 1 diabetes is not limited to adolescents.

“We've been surprised at how many adults we see in their 30s and 40s who've been struggling for over 10 years with this and are finally wanting and accepting help,” Ms. Gerken said at the conference sponsored by the University of Colorado and the Children's Diabetes Foundation, Denver.

She is part of a joint team composed of staff at the diabetes center and at the Park Nicollet Eating Disorders Institute–Minnesota's sole inpatient ED treatment facility. The unusual multidisciplinary program was created in recognition that this is a particularly challenging group of patients adept at exploiting the often conflicting management goals for the two diseases.

Patients with combined ED and type 1 diabetes experience poor metabolic control, with serious long-term consequences. British investigators who followed 87 type 1 diabetic females aged 11–25 years for 8–12 years found 26% had a clinical ED or evidence of bingeing and purging at baseline and/or follow-up. Thirty-six percent admitted to misusing insulin for weight control. The group with disordered eating had a high rate of microvascular complications at follow-up in addition to two deaths because of renal disease, one from cardiovascular disease, and one suicide (Diabetes Care 2005; 28:84–8).

Personality characteristics that have been associated with eating disorders in adolescent girls with type 1 diabetes include perfectionism, negative and avoidant coping skills such as self-blame and wishful thinking, and borderline personality characteristics.

Family factors also figure prominently in girls with type 1 diabetes and an ED. These patients tend to come from families who seldom eat together. The parents have a high level of weight-related concerns, are often dieting, and make negative comments about eating or weight.

“Every patient I work with has some kind of issues with the family,” Ms. Gerken observed.

Eating disorders are notoriously tough to diagnose. Affected individuals will hide the evidence because of shame, denial, and a powerful desire to keep losing weight.

Red flags that a diabetic patient may have an ED include frequent low blood sugar levels, anxiety about getting on the scale, an increase in glycosylated hemoglobin together with weight loss, repeated hospitalizations for diabetic ketoacidosis, a drop in self-monitoring of blood glucose, and frequent “forgetting” to bring the blood glucose monitor or records to office visits.

Other warning signs include withdrawal from friends and family, irritability, bodily dissatisfaction, delayed puberty, unexplained menstrual or fertility problems, deteriorating school performance, compulsive exercise, and food stealing.

Diabetic patients with weight concerns will intentionally skip insulin injections to drop pounds. DR. GERKEN

KEYSTONE, COLO. – A high index of suspicion for eating disorders is warranted in adolescents and young adults with type 1 diabetes, Stephanie H. Gerken said at a conference on the management of diabetes in youth.

The largest studies suggest the prevalence of eating disorders (EDs) meeting Diagnostic and Statistical Manual, Fourth Edition, criteria is about 10% in adolescent girls with type 1 diabetes. Another 14% have subthreshold variants. Both rates are roughly twice those found in nondiabetic adolescent girls.

The most common unhealthy weight-control practice among diabetic teens is intentional omission of insulin to lose weight. Many diabetic patients with weight concerns quickly figure out that skipping insulin injections is an easier way to drop pounds than restricting food intake or bingeing and purging, explained Ms. Gerken, a diabetes educator and registered dietician at the International Diabetes Center, Park Nicollet Clinics, Minneapolis.

The elevated risk of eating disorders in association with type 1 diabetes is not limited to adolescents.

“We've been surprised at how many adults we see in their 30s and 40s who've been struggling for over 10 years with this and are finally wanting and accepting help,” Ms. Gerken said at the conference sponsored by the University of Colorado and the Children's Diabetes Foundation, Denver.

She is part of a joint team composed of staff at the diabetes center and at the Park Nicollet Eating Disorders Institute–Minnesota's sole inpatient ED treatment facility. The unusual multidisciplinary program was created in recognition that this is a particularly challenging group of patients adept at exploiting the often conflicting management goals for the two diseases.

Patients with combined ED and type 1 diabetes experience poor metabolic control, with serious long-term consequences. British investigators who followed 87 type 1 diabetic females aged 11–25 years for 8–12 years found 26% had a clinical ED or evidence of bingeing and purging at baseline and/or follow-up. Thirty-six percent admitted to misusing insulin for weight control. The group with disordered eating had a high rate of microvascular complications at follow-up in addition to two deaths because of renal disease, one from cardiovascular disease, and one suicide (Diabetes Care 2005; 28:84–8).

Personality characteristics that have been associated with eating disorders in adolescent girls with type 1 diabetes include perfectionism, negative and avoidant coping skills such as self-blame and wishful thinking, and borderline personality characteristics.

Family factors also figure prominently in girls with type 1 diabetes and an ED. These patients tend to come from families who seldom eat together. The parents have a high level of weight-related concerns, are often dieting, and make negative comments about eating or weight.

“Every patient I work with has some kind of issues with the family,” Ms. Gerken observed.

Eating disorders are notoriously tough to diagnose. Affected individuals will hide the evidence because of shame, denial, and a powerful desire to keep losing weight.

Red flags that a diabetic patient may have an ED include frequent low blood sugar levels, anxiety about getting on the scale, an increase in glycosylated hemoglobin together with weight loss, repeated hospitalizations for diabetic ketoacidosis, a drop in self-monitoring of blood glucose, and frequent “forgetting” to bring the blood glucose monitor or records to office visits.

Other warning signs include withdrawal from friends and family, irritability, bodily dissatisfaction, delayed puberty, unexplained menstrual or fertility problems, deteriorating school performance, compulsive exercise, and food stealing.

Diabetic patients with weight concerns will intentionally skip insulin injections to drop pounds. DR. GERKEN

KEYSTONE, COLO. – A high index of suspicion for eating disorders is warranted in adolescents and young adults with type 1 diabetes, Stephanie H. Gerken said at a conference on the management of diabetes in youth.

The largest studies suggest the prevalence of eating disorders (EDs) meeting Diagnostic and Statistical Manual, Fourth Edition, criteria is about 10% in adolescent girls with type 1 diabetes. Another 14% have subthreshold variants. Both rates are roughly twice those found in nondiabetic adolescent girls.

The most common unhealthy weight-control practice among diabetic teens is intentional omission of insulin to lose weight. Many diabetic patients with weight concerns quickly figure out that skipping insulin injections is an easier way to drop pounds than restricting food intake or bingeing and purging, explained Ms. Gerken, a diabetes educator and registered dietician at the International Diabetes Center, Park Nicollet Clinics, Minneapolis.

The elevated risk of eating disorders in association with type 1 diabetes is not limited to adolescents.

“We've been surprised at how many adults we see in their 30s and 40s who've been struggling for over 10 years with this and are finally wanting and accepting help,” Ms. Gerken said at the conference sponsored by the University of Colorado and the Children's Diabetes Foundation, Denver.

She is part of a joint team composed of staff at the diabetes center and at the Park Nicollet Eating Disorders Institute–Minnesota's sole inpatient ED treatment facility. The unusual multidisciplinary program was created in recognition that this is a particularly challenging group of patients adept at exploiting the often conflicting management goals for the two diseases.

Patients with combined ED and type 1 diabetes experience poor metabolic control, with serious long-term consequences. British investigators who followed 87 type 1 diabetic females aged 11–25 years for 8–12 years found 26% had a clinical ED or evidence of bingeing and purging at baseline and/or follow-up. Thirty-six percent admitted to misusing insulin for weight control. The group with disordered eating had a high rate of microvascular complications at follow-up in addition to two deaths because of renal disease, one from cardiovascular disease, and one suicide (Diabetes Care 2005; 28:84–8).

Personality characteristics that have been associated with eating disorders in adolescent girls with type 1 diabetes include perfectionism, negative and avoidant coping skills such as self-blame and wishful thinking, and borderline personality characteristics.

Family factors also figure prominently in girls with type 1 diabetes and an ED. These patients tend to come from families who seldom eat together. The parents have a high level of weight-related concerns, are often dieting, and make negative comments about eating or weight.

“Every patient I work with has some kind of issues with the family,” Ms. Gerken observed.

Eating disorders are notoriously tough to diagnose. Affected individuals will hide the evidence because of shame, denial, and a powerful desire to keep losing weight.

Red flags that a diabetic patient may have an ED include frequent low blood sugar levels, anxiety about getting on the scale, an increase in glycosylated hemoglobin together with weight loss, repeated hospitalizations for diabetic ketoacidosis, a drop in self-monitoring of blood glucose, and frequent “forgetting” to bring the blood glucose monitor or records to office visits.

Other warning signs include withdrawal from friends and family, irritability, bodily dissatisfaction, delayed puberty, unexplained menstrual or fertility problems, deteriorating school performance, compulsive exercise, and food stealing.

Diabetic patients with weight concerns will intentionally skip insulin injections to drop pounds. DR. GERKEN

TORONTO – Comorbid obsessive and compulsive behaviors persist in women with bulimia nervosa, even after the abnormal eating patterns associated with the condition have been successfully treated, Dr. Jessica C. Morgan said at the annual meeting of the American Psychiatric Association.

This finding suggests that elevated obsessive and compulsive ratings may reflect a persistent trait characteristic in individuals who develop the eating disorder–a discovery that “could lead to new treatment strategies for managing anxiety symptoms in at-risk individuals, particularly those in the recovery stages of bulimia,” said Dr. Morgan of the department of psychiatry at Dartmouth Medical School in Hanover, N.H.

Because previous studies have linked obsessive and compulsive behaviors to the primary symptoms of bulimia, Dr. Morgan and her colleagues sought to determine whether remission from bulimia had an impact on co-occurring obsessive-compulsive symptoms.

Using subject self-ratings on the Maudsley Obsessive-Compulsive Inventory (MOCI), the investigators compared the obsessive-compulsive characteristics of 25 women with active bulimia, 21 of whom were in recovery from bulimia, and 28 healthy controls–all of whom were medication free at the time of the assessment. The investigators also looked at participants' mean scores on the Eating Attitudes Test (EAT), which assesses disordered eating attitudes, and the Spielberger Trait Anxiety Inventory (STAI), which tests for anxiety disorders.

“As we had expected, the MOCI scores for the bulimia group were significantly elevated, compared to those of the controls,” said Dr. Morgan, noting that the respective scores were 5.4 vs. 2.5 on the 30-item true-false questionnaire designed to assess overt rituals and their related obsessions. “The recovery group had similarly elevated MOCI scores [5.5],” she said, which suggests that those aspects of the disease associated with obsessive-compulsive behaviors were not affected by treatment.

In contrast, the EAT and STAI scores for the women in recovery were significantly reduced, compared with those of the women with active bulimia, “although they were still significantly higher than what we observed in the control group,” Dr. Morgan said.

The persistence of obsessive-compulsive symptoms after recovery from bulimia not only suggests that such behaviors may be trait related in affected individuals, but also raises the possibility that the behaviors contribute somehow to the pathogenesis of the eating disorder, she noted.

Although more research is needed to clarify the relationship between the cooccurring conditions, the demonstrated link between the two may help clinicians more readily identify bulimia patients at risk for lingering obsessive-compulsive symptoms, Dr. Morgan said.

TORONTO – Comorbid obsessive and compulsive behaviors persist in women with bulimia nervosa, even after the abnormal eating patterns associated with the condition have been successfully treated, Dr. Jessica C. Morgan said at the annual meeting of the American Psychiatric Association.

This finding suggests that elevated obsessive and compulsive ratings may reflect a persistent trait characteristic in individuals who develop the eating disorder–a discovery that “could lead to new treatment strategies for managing anxiety symptoms in at-risk individuals, particularly those in the recovery stages of bulimia,” said Dr. Morgan of the department of psychiatry at Dartmouth Medical School in Hanover, N.H.

Because previous studies have linked obsessive and compulsive behaviors to the primary symptoms of bulimia, Dr. Morgan and her colleagues sought to determine whether remission from bulimia had an impact on co-occurring obsessive-compulsive symptoms.

Using subject self-ratings on the Maudsley Obsessive-Compulsive Inventory (MOCI), the investigators compared the obsessive-compulsive characteristics of 25 women with active bulimia, 21 of whom were in recovery from bulimia, and 28 healthy controls–all of whom were medication free at the time of the assessment. The investigators also looked at participants' mean scores on the Eating Attitudes Test (EAT), which assesses disordered eating attitudes, and the Spielberger Trait Anxiety Inventory (STAI), which tests for anxiety disorders.

“As we had expected, the MOCI scores for the bulimia group were significantly elevated, compared to those of the controls,” said Dr. Morgan, noting that the respective scores were 5.4 vs. 2.5 on the 30-item true-false questionnaire designed to assess overt rituals and their related obsessions. “The recovery group had similarly elevated MOCI scores [5.5],” she said, which suggests that those aspects of the disease associated with obsessive-compulsive behaviors were not affected by treatment.

In contrast, the EAT and STAI scores for the women in recovery were significantly reduced, compared with those of the women with active bulimia, “although they were still significantly higher than what we observed in the control group,” Dr. Morgan said.

The persistence of obsessive-compulsive symptoms after recovery from bulimia not only suggests that such behaviors may be trait related in affected individuals, but also raises the possibility that the behaviors contribute somehow to the pathogenesis of the eating disorder, she noted.

Although more research is needed to clarify the relationship between the cooccurring conditions, the demonstrated link between the two may help clinicians more readily identify bulimia patients at risk for lingering obsessive-compulsive symptoms, Dr. Morgan said.

TORONTO – Comorbid obsessive and compulsive behaviors persist in women with bulimia nervosa, even after the abnormal eating patterns associated with the condition have been successfully treated, Dr. Jessica C. Morgan said at the annual meeting of the American Psychiatric Association.

This finding suggests that elevated obsessive and compulsive ratings may reflect a persistent trait characteristic in individuals who develop the eating disorder–a discovery that “could lead to new treatment strategies for managing anxiety symptoms in at-risk individuals, particularly those in the recovery stages of bulimia,” said Dr. Morgan of the department of psychiatry at Dartmouth Medical School in Hanover, N.H.

Because previous studies have linked obsessive and compulsive behaviors to the primary symptoms of bulimia, Dr. Morgan and her colleagues sought to determine whether remission from bulimia had an impact on co-occurring obsessive-compulsive symptoms.

Using subject self-ratings on the Maudsley Obsessive-Compulsive Inventory (MOCI), the investigators compared the obsessive-compulsive characteristics of 25 women with active bulimia, 21 of whom were in recovery from bulimia, and 28 healthy controls–all of whom were medication free at the time of the assessment. The investigators also looked at participants' mean scores on the Eating Attitudes Test (EAT), which assesses disordered eating attitudes, and the Spielberger Trait Anxiety Inventory (STAI), which tests for anxiety disorders.

“As we had expected, the MOCI scores for the bulimia group were significantly elevated, compared to those of the controls,” said Dr. Morgan, noting that the respective scores were 5.4 vs. 2.5 on the 30-item true-false questionnaire designed to assess overt rituals and their related obsessions. “The recovery group had similarly elevated MOCI scores [5.5],” she said, which suggests that those aspects of the disease associated with obsessive-compulsive behaviors were not affected by treatment.

In contrast, the EAT and STAI scores for the women in recovery were significantly reduced, compared with those of the women with active bulimia, “although they were still significantly higher than what we observed in the control group,” Dr. Morgan said.

The persistence of obsessive-compulsive symptoms after recovery from bulimia not only suggests that such behaviors may be trait related in affected individuals, but also raises the possibility that the behaviors contribute somehow to the pathogenesis of the eating disorder, she noted.

Although more research is needed to clarify the relationship between the cooccurring conditions, the demonstrated link between the two may help clinicians more readily identify bulimia patients at risk for lingering obsessive-compulsive symptoms, Dr. Morgan said.

SAN FRANCISCO – A high risk for sleep apnea was common in women with polycystic ovary syndrome and was linked to high fasting insulin levels, Dr. Esra Tasali reported at a conference sponsored by the American Diabetes Association.

Among the women with normal glucose tolerance, insulin levels in response to oral glucose were twice as high in women at high risk for sleep apnea, compared with those at low risk. This finding suggests that sleep apnea might worsen the metabolic consequences of insulin resistance, accelerating the conversion from normal to impaired glucose tolerance, Dr. Tasali said.

Although the study does not establish causation, Dr. Tasali recommended that women with polycystic ovary syndrome (PCOS) be systematically evaluated for sleep apnea, as its treatment might improve glucose metabolism.

A high risk for sleep apnea was observed in 30 of 40 women with PCOS, and 92% of the women had sleep problems, according to Dr. Tasali and her colleagues at the University of Chicago (J. Clin. Endocrinol. Metab. 2006;91:36–42).

Of the 40 women, 32 had previously been given an oral glucose tolerance test. Glucose tolerance was normal in 19 women. In 22 women at high sleep apnea risk, average fasting insulin levels were significantly higher (168 pmol/L) than they were in the 10 women at low apnea risk (97 pmol/L). Among the 13 women with impaired glucose tolerance, glucose and insulin levels did not differ depending on the level of apnea risk.

Another cohort of eight women with PCOS underwent overnight polysomnography for symptoms suggestive of obstructive sleep apnea. Mean sleep efficiency was 80% in the women with PCOS, compared with 92% in a control group of age-matched, nonobese women. The women with PCOS also had significantly longer mean sleep latency (41 minutes vs. 10 minutes), and significantly shorter total sleep time (323 minutes vs. 442 minutes, a difference of almost 2 hours).

“Sleep apnea might be an intrinsic component of the metabolic disturbances that appear with” PCOS, Dr. Tasali said.

Furthermore, severity of sleep apnea as measured by the apnea-hypopnea index, and the degree of oxygen desaturations during rapid-eye-movement sleep, accounted for more than 90% of the variability in measures of glucose tolerance including hemoglobin A_1c levels.

Dr. Tasali had no conflict of interest to report regarding her presentation.

Women withPCOS should be evaluated for sleep apnea, as its treatment might improve glucose metabolism. DR. TASALI

SAN FRANCISCO – A high risk for sleep apnea was common in women with polycystic ovary syndrome and was linked to high fasting insulin levels, Dr. Esra Tasali reported at a conference sponsored by the American Diabetes Association.

Among the women with normal glucose tolerance, insulin levels in response to oral glucose were twice as high in women at high risk for sleep apnea, compared with those at low risk. This finding suggests that sleep apnea might worsen the metabolic consequences of insulin resistance, accelerating the conversion from normal to impaired glucose tolerance, Dr. Tasali said.

Although the study does not establish causation, Dr. Tasali recommended that women with polycystic ovary syndrome (PCOS) be systematically evaluated for sleep apnea, as its treatment might improve glucose metabolism.

A high risk for sleep apnea was observed in 30 of 40 women with PCOS, and 92% of the women had sleep problems, according to Dr. Tasali and her colleagues at the University of Chicago (J. Clin. Endocrinol. Metab. 2006;91:36–42).

Of the 40 women, 32 had previously been given an oral glucose tolerance test. Glucose tolerance was normal in 19 women. In 22 women at high sleep apnea risk, average fasting insulin levels were significantly higher (168 pmol/L) than they were in the 10 women at low apnea risk (97 pmol/L). Among the 13 women with impaired glucose tolerance, glucose and insulin levels did not differ depending on the level of apnea risk.

Another cohort of eight women with PCOS underwent overnight polysomnography for symptoms suggestive of obstructive sleep apnea. Mean sleep efficiency was 80% in the women with PCOS, compared with 92% in a control group of age-matched, nonobese women. The women with PCOS also had significantly longer mean sleep latency (41 minutes vs. 10 minutes), and significantly shorter total sleep time (323 minutes vs. 442 minutes, a difference of almost 2 hours).

“Sleep apnea might be an intrinsic component of the metabolic disturbances that appear with” PCOS, Dr. Tasali said.

Furthermore, severity of sleep apnea as measured by the apnea-hypopnea index, and the degree of oxygen desaturations during rapid-eye-movement sleep, accounted for more than 90% of the variability in measures of glucose tolerance including hemoglobin A_1c levels.

Dr. Tasali had no conflict of interest to report regarding her presentation.

Women withPCOS should be evaluated for sleep apnea, as its treatment might improve glucose metabolism. DR. TASALI

SAN FRANCISCO – A high risk for sleep apnea was common in women with polycystic ovary syndrome and was linked to high fasting insulin levels, Dr. Esra Tasali reported at a conference sponsored by the American Diabetes Association.

Among the women with normal glucose tolerance, insulin levels in response to oral glucose were twice as high in women at high risk for sleep apnea, compared with those at low risk. This finding suggests that sleep apnea might worsen the metabolic consequences of insulin resistance, accelerating the conversion from normal to impaired glucose tolerance, Dr. Tasali said.

Although the study does not establish causation, Dr. Tasali recommended that women with polycystic ovary syndrome (PCOS) be systematically evaluated for sleep apnea, as its treatment might improve glucose metabolism.

A high risk for sleep apnea was observed in 30 of 40 women with PCOS, and 92% of the women had sleep problems, according to Dr. Tasali and her colleagues at the University of Chicago (J. Clin. Endocrinol. Metab. 2006;91:36–42).

Of the 40 women, 32 had previously been given an oral glucose tolerance test. Glucose tolerance was normal in 19 women. In 22 women at high sleep apnea risk, average fasting insulin levels were significantly higher (168 pmol/L) than they were in the 10 women at low apnea risk (97 pmol/L). Among the 13 women with impaired glucose tolerance, glucose and insulin levels did not differ depending on the level of apnea risk.

Another cohort of eight women with PCOS underwent overnight polysomnography for symptoms suggestive of obstructive sleep apnea. Mean sleep efficiency was 80% in the women with PCOS, compared with 92% in a control group of age-matched, nonobese women. The women with PCOS also had significantly longer mean sleep latency (41 minutes vs. 10 minutes), and significantly shorter total sleep time (323 minutes vs. 442 minutes, a difference of almost 2 hours).

“Sleep apnea might be an intrinsic component of the metabolic disturbances that appear with” PCOS, Dr. Tasali said.

Furthermore, severity of sleep apnea as measured by the apnea-hypopnea index, and the degree of oxygen desaturations during rapid-eye-movement sleep, accounted for more than 90% of the variability in measures of glucose tolerance including hemoglobin A_1c levels.

Dr. Tasali had no conflict of interest to report regarding her presentation.

Women withPCOS should be evaluated for sleep apnea, as its treatment might improve glucose metabolism. DR. TASALI

LOS ANGELES – An educational tool kit designed to improve patient-physician interactions during visits for irritable bowel syndrome had a greater impact on global symptom relief than did any medication ever studied for the enigmatic disorder.

Dr. Brennan M. Spiegel and associates at the University of California, Los Angeles, tested the tool kit in a randomized study of 73 patients with irritable bowel syndrome (IBS) symptoms who attended the gastrointestinal disease catchment clinic for the VA Greater Los Angeles Health Care System.

Follow-up surveys 3 months later found that patients assigned to the physician-patient intervention group were far more likely than were those who received standard care to say they had achieved relief of their global symptoms (20 of 36 patients, or 56%, compared with 5 of 34 patients, or 15%.)

The intervention effect size of 0.75 “exceeds the largest effect size demonstrated in pharmaceutical studies for IBS,” Dr. Spiegel said at the annual Digestive Disease Week.

Although studies of alosetron using similar outcome measures had effect sizes between 0.2 and 0.5, “this does not mean … that these agents are not effective. It does suggest that medical therapy alone may be suboptimal if it is not delivered in the context of a supportive and informative physician/patient interaction,” he said.

The multifactorial intervention consisted of a five-part tool kit that included:

▸ A waiting room questionnaire to document the patient's primary concerns, fears, and opinions about what might be causing IBS symptoms.

▸ A laminated flash card for the physician that includes key components of an effective discussion of IBS, including reminders to ask about psychosocial elements of the disease, descriptions of IBS in lay language, and the fact that IBS is not a life-threatening disease.

▸ A worksheet and diagram of the brain and gut that the physician could use to depict a simple explanation of the complex neural circuitry linking the two.

▸ A multimedia patient educational kit, including a self-empowerment video, an explanation of the brain-gut axis in lay language, information about support groups, a dietary card, and educational materials about IBS from the National Institutes of Health.

▸ A letter, sent 1 month following the office visit, asking the patient, “How are you doing?” and providing information about how to contact the physician if symptoms had not improved. This correspondence also included more educational information about IBS.

Physicians were free to use or ignore the patient's questionnaire, the flash card, and worksheet during the office visit; however most found that it actually “streamlined” the visit, Dr. Spiegel said.

Similarly, patients could read or dispose of the educational materials provided. Some told study investigators that they found the worksheet very important, while others primarily relied on the diet cards they found in the take-home educational kit.

Whatever elements did the trick, the intervention clearly had an impact on patients, with significant differences seen in global IBS symptoms, satisfaction, and perceptions of their physicians' interpersonal skills.

Ironically, the same physicians saw IBS patients assigned to the intervention group or to usual care.

When independent observers assessed physicians' notes from the visits, they found “very large differences” between the intervention and standard care groups in terms of observations concerning patients' quality of life and extraintestinal symptoms such as anxiety or depression. None of the physician notes documenting visits with control group patients mentioned patients' fears and concerns or disease education efforts, while these elements appeared in their notes regarding 23% and 54% of intervention patient visits, respectively.

Dr. Spiegel prefaced the report on his findings by acknowledging the deep frustration many physicians feel in dealing with patients with IBS, since the disease is common and expensive, symptom expression is heterogeneous, the disease model is incomplete, and highly effective treatment options are scarce.

This frustration can spill over into office visits that leave neither party satisfied.

“Patients often feel uninformed after they have left the office and physicians often do a poor job of predicting patients' severity when patients and physicians fill out the same questionnaire,” he said.

LOS ANGELES – An educational tool kit designed to improve patient-physician interactions during visits for irritable bowel syndrome had a greater impact on global symptom relief than did any medication ever studied for the enigmatic disorder.

Dr. Brennan M. Spiegel and associates at the University of California, Los Angeles, tested the tool kit in a randomized study of 73 patients with irritable bowel syndrome (IBS) symptoms who attended the gastrointestinal disease catchment clinic for the VA Greater Los Angeles Health Care System.

Follow-up surveys 3 months later found that patients assigned to the physician-patient intervention group were far more likely than were those who received standard care to say they had achieved relief of their global symptoms (20 of 36 patients, or 56%, compared with 5 of 34 patients, or 15%.)

The intervention effect size of 0.75 “exceeds the largest effect size demonstrated in pharmaceutical studies for IBS,” Dr. Spiegel said at the annual Digestive Disease Week.

Although studies of alosetron using similar outcome measures had effect sizes between 0.2 and 0.5, “this does not mean … that these agents are not effective. It does suggest that medical therapy alone may be suboptimal if it is not delivered in the context of a supportive and informative physician/patient interaction,” he said.

The multifactorial intervention consisted of a five-part tool kit that included:

▸ A waiting room questionnaire to document the patient's primary concerns, fears, and opinions about what might be causing IBS symptoms.

▸ A laminated flash card for the physician that includes key components of an effective discussion of IBS, including reminders to ask about psychosocial elements of the disease, descriptions of IBS in lay language, and the fact that IBS is not a life-threatening disease.

▸ A worksheet and diagram of the brain and gut that the physician could use to depict a simple explanation of the complex neural circuitry linking the two.

▸ A multimedia patient educational kit, including a self-empowerment video, an explanation of the brain-gut axis in lay language, information about support groups, a dietary card, and educational materials about IBS from the National Institutes of Health.

▸ A letter, sent 1 month following the office visit, asking the patient, “How are you doing?” and providing information about how to contact the physician if symptoms had not improved. This correspondence also included more educational information about IBS.

Physicians were free to use or ignore the patient's questionnaire, the flash card, and worksheet during the office visit; however most found that it actually “streamlined” the visit, Dr. Spiegel said.

Similarly, patients could read or dispose of the educational materials provided. Some told study investigators that they found the worksheet very important, while others primarily relied on the diet cards they found in the take-home educational kit.

Whatever elements did the trick, the intervention clearly had an impact on patients, with significant differences seen in global IBS symptoms, satisfaction, and perceptions of their physicians' interpersonal skills.

Ironically, the same physicians saw IBS patients assigned to the intervention group or to usual care.

When independent observers assessed physicians' notes from the visits, they found “very large differences” between the intervention and standard care groups in terms of observations concerning patients' quality of life and extraintestinal symptoms such as anxiety or depression. None of the physician notes documenting visits with control group patients mentioned patients' fears and concerns or disease education efforts, while these elements appeared in their notes regarding 23% and 54% of intervention patient visits, respectively.

Dr. Spiegel prefaced the report on his findings by acknowledging the deep frustration many physicians feel in dealing with patients with IBS, since the disease is common and expensive, symptom expression is heterogeneous, the disease model is incomplete, and highly effective treatment options are scarce.

This frustration can spill over into office visits that leave neither party satisfied.

“Patients often feel uninformed after they have left the office and physicians often do a poor job of predicting patients' severity when patients and physicians fill out the same questionnaire,” he said.

LOS ANGELES – An educational tool kit designed to improve patient-physician interactions during visits for irritable bowel syndrome had a greater impact on global symptom relief than did any medication ever studied for the enigmatic disorder.

Dr. Brennan M. Spiegel and associates at the University of California, Los Angeles, tested the tool kit in a randomized study of 73 patients with irritable bowel syndrome (IBS) symptoms who attended the gastrointestinal disease catchment clinic for the VA Greater Los Angeles Health Care System.

Follow-up surveys 3 months later found that patients assigned to the physician-patient intervention group were far more likely than were those who received standard care to say they had achieved relief of their global symptoms (20 of 36 patients, or 56%, compared with 5 of 34 patients, or 15%.)

The intervention effect size of 0.75 “exceeds the largest effect size demonstrated in pharmaceutical studies for IBS,” Dr. Spiegel said at the annual Digestive Disease Week.

Although studies of alosetron using similar outcome measures had effect sizes between 0.2 and 0.5, “this does not mean … that these agents are not effective. It does suggest that medical therapy alone may be suboptimal if it is not delivered in the context of a supportive and informative physician/patient interaction,” he said.

The multifactorial intervention consisted of a five-part tool kit that included:

▸ A waiting room questionnaire to document the patient's primary concerns, fears, and opinions about what might be causing IBS symptoms.

▸ A laminated flash card for the physician that includes key components of an effective discussion of IBS, including reminders to ask about psychosocial elements of the disease, descriptions of IBS in lay language, and the fact that IBS is not a life-threatening disease.

▸ A worksheet and diagram of the brain and gut that the physician could use to depict a simple explanation of the complex neural circuitry linking the two.

▸ A multimedia patient educational kit, including a self-empowerment video, an explanation of the brain-gut axis in lay language, information about support groups, a dietary card, and educational materials about IBS from the National Institutes of Health.

▸ A letter, sent 1 month following the office visit, asking the patient, “How are you doing?” and providing information about how to contact the physician if symptoms had not improved. This correspondence also included more educational information about IBS.

Physicians were free to use or ignore the patient's questionnaire, the flash card, and worksheet during the office visit; however most found that it actually “streamlined” the visit, Dr. Spiegel said.

Similarly, patients could read or dispose of the educational materials provided. Some told study investigators that they found the worksheet very important, while others primarily relied on the diet cards they found in the take-home educational kit.

Whatever elements did the trick, the intervention clearly had an impact on patients, with significant differences seen in global IBS symptoms, satisfaction, and perceptions of their physicians' interpersonal skills.

Ironically, the same physicians saw IBS patients assigned to the intervention group or to usual care.

When independent observers assessed physicians' notes from the visits, they found “very large differences” between the intervention and standard care groups in terms of observations concerning patients' quality of life and extraintestinal symptoms such as anxiety or depression. None of the physician notes documenting visits with control group patients mentioned patients' fears and concerns or disease education efforts, while these elements appeared in their notes regarding 23% and 54% of intervention patient visits, respectively.

Dr. Spiegel prefaced the report on his findings by acknowledging the deep frustration many physicians feel in dealing with patients with IBS, since the disease is common and expensive, symptom expression is heterogeneous, the disease model is incomplete, and highly effective treatment options are scarce.

This frustration can spill over into office visits that leave neither party satisfied.

“Patients often feel uninformed after they have left the office and physicians often do a poor job of predicting patients' severity when patients and physicians fill out the same questionnaire,” he said.

TORONTO – Fluoxetine failed to prevent relapse of anorexia nervosa in the largest controlled medication trial to date exploring the issue, Dr. B. Timothy Walsh reported at the annual meeting of the American Psychiatric Association.

“Antidepressants don't offer patients with anorexia nervosa very much,” said Dr. Walsh, director of the eating disorders research unit of the New York State Psychiatric Institute, New York City. “We can't say for sure that an antidepressant other than fluoxetine wouldn't have an effect, but it would surprise me.”

The study represents yet another failure to find an efficacious medical treatment for anorexia. These failures imply that anorexia is unlike any other psychiatric condition, Dr. Walsh said.

“Interventions that are useful for other sorts of possibly related disorders don't work terribly well for anorexia nervosa,” he said. The only evidence-based treatment for anorexia is cognitive-behavioral therapy (CBT), which helps, but “not a lot,” he added.

The investigators, whose results were later published, compared fluoxetine with placebo in a clinical trial involving 93 patients who had completed intensive treatment and maintained a body mass index (BMI) of at least 19 kg/m

Subjects were randomly assigned to receive 20 mg daily of fluoxetine (49 patients), with a goal of increasing to 60 mg, or placebo (44 patients). They were monitored by a psychiatrist for dosing, adverse effects, and general medical status. They also received CBT.

The subjects underwent assessments of depression, anxiety, self-esteem, and quality of life every month. They were followed for 50 weeks, or until they either relapsed, defined as falling back to a BMI of 16.5 for 2 weeks, or dropped out of the study.

At 25 weeks, 48% of the 49 fluoxetine-treated subjects had either dropped out or relapsed, versus 39% of the placebo controls. At 50 weeks, 58% of the fluoxetine-treated subjects and 55% of the controls had either dropped out or relapsed.

To pick up on any possible benefit of the drug, Dr. Walsh and his colleagues also considered just those who relapsed, and those who relapsed plus those who clinically appeared to be in trouble when they dropped out–either because their BMI had dropped to 17 or because they had begun binging and purging again, at least twice a week.

At 50 weeks, 27% of the fluoxetine-treated patients and 29% of the placebo controls were documented relapsers.

Considering as failures both those with documented relapse and those who clinically appeared to be not doing well when they dropped out, the percentages were 49% fluoxetine and 51% placebo.

Dr. Walsh said he also looked only at those with depression, and at those who purged or restricted food only, and treatment still made no difference in those particular patients. “However we cut it, we can find no evidence that fluoxetine prolongs time to relapse following successful initial treatment, and we've looked pretty hard,” Dr. Walsh said.

In an editorial comment accompanying the published report, Dr. Scott J. Crow of the University of Minnesota, Minneapolis, said, “While the results of previous relapse prevention trials have been mixed, the report by Walsh and colleagues has many strengths and appears convincingly negative” (JAMA 2006;295:2659–60).

The study amply demonstrates that antidepressant therapy, “a fairly common treatment practice for this illness,” provides no benefit, Dr. Crow noted.

Additional reporting was done by contributing writer Mary Ann Moon.

'We can find no evidence that fluoxetine prolongs time to relapse … and we've looked pretty hard.' DR. WALSH

TORONTO – Fluoxetine failed to prevent relapse of anorexia nervosa in the largest controlled medication trial to date exploring the issue, Dr. B. Timothy Walsh reported at the annual meeting of the American Psychiatric Association.

“Antidepressants don't offer patients with anorexia nervosa very much,” said Dr. Walsh, director of the eating disorders research unit of the New York State Psychiatric Institute, New York City. “We can't say for sure that an antidepressant other than fluoxetine wouldn't have an effect, but it would surprise me.”

The study represents yet another failure to find an efficacious medical treatment for anorexia. These failures imply that anorexia is unlike any other psychiatric condition, Dr. Walsh said.

“Interventions that are useful for other sorts of possibly related disorders don't work terribly well for anorexia nervosa,” he said. The only evidence-based treatment for anorexia is cognitive-behavioral therapy (CBT), which helps, but “not a lot,” he added.

The investigators, whose results were later published, compared fluoxetine with placebo in a clinical trial involving 93 patients who had completed intensive treatment and maintained a body mass index (BMI) of at least 19 kg/m

Subjects were randomly assigned to receive 20 mg daily of fluoxetine (49 patients), with a goal of increasing to 60 mg, or placebo (44 patients). They were monitored by a psychiatrist for dosing, adverse effects, and general medical status. They also received CBT.

The subjects underwent assessments of depression, anxiety, self-esteem, and quality of life every month. They were followed for 50 weeks, or until they either relapsed, defined as falling back to a BMI of 16.5 for 2 weeks, or dropped out of the study.

At 25 weeks, 48% of the 49 fluoxetine-treated subjects had either dropped out or relapsed, versus 39% of the placebo controls. At 50 weeks, 58% of the fluoxetine-treated subjects and 55% of the controls had either dropped out or relapsed.

To pick up on any possible benefit of the drug, Dr. Walsh and his colleagues also considered just those who relapsed, and those who relapsed plus those who clinically appeared to be in trouble when they dropped out–either because their BMI had dropped to 17 or because they had begun binging and purging again, at least twice a week.

At 50 weeks, 27% of the fluoxetine-treated patients and 29% of the placebo controls were documented relapsers.

Considering as failures both those with documented relapse and those who clinically appeared to be not doing well when they dropped out, the percentages were 49% fluoxetine and 51% placebo.

Dr. Walsh said he also looked only at those with depression, and at those who purged or restricted food only, and treatment still made no difference in those particular patients. “However we cut it, we can find no evidence that fluoxetine prolongs time to relapse following successful initial treatment, and we've looked pretty hard,” Dr. Walsh said.

In an editorial comment accompanying the published report, Dr. Scott J. Crow of the University of Minnesota, Minneapolis, said, “While the results of previous relapse prevention trials have been mixed, the report by Walsh and colleagues has many strengths and appears convincingly negative” (JAMA 2006;295:2659–60).

The study amply demonstrates that antidepressant therapy, “a fairly common treatment practice for this illness,” provides no benefit, Dr. Crow noted.

Additional reporting was done by contributing writer Mary Ann Moon.

'We can find no evidence that fluoxetine prolongs time to relapse … and we've looked pretty hard.' DR. WALSH

TORONTO – Fluoxetine failed to prevent relapse of anorexia nervosa in the largest controlled medication trial to date exploring the issue, Dr. B. Timothy Walsh reported at the annual meeting of the American Psychiatric Association.

“Antidepressants don't offer patients with anorexia nervosa very much,” said Dr. Walsh, director of the eating disorders research unit of the New York State Psychiatric Institute, New York City. “We can't say for sure that an antidepressant other than fluoxetine wouldn't have an effect, but it would surprise me.”

The study represents yet another failure to find an efficacious medical treatment for anorexia. These failures imply that anorexia is unlike any other psychiatric condition, Dr. Walsh said.

“Interventions that are useful for other sorts of possibly related disorders don't work terribly well for anorexia nervosa,” he said. The only evidence-based treatment for anorexia is cognitive-behavioral therapy (CBT), which helps, but “not a lot,” he added.

The investigators, whose results were later published, compared fluoxetine with placebo in a clinical trial involving 93 patients who had completed intensive treatment and maintained a body mass index (BMI) of at least 19 kg/m

Subjects were randomly assigned to receive 20 mg daily of fluoxetine (49 patients), with a goal of increasing to 60 mg, or placebo (44 patients). They were monitored by a psychiatrist for dosing, adverse effects, and general medical status. They also received CBT.

The subjects underwent assessments of depression, anxiety, self-esteem, and quality of life every month. They were followed for 50 weeks, or until they either relapsed, defined as falling back to a BMI of 16.5 for 2 weeks, or dropped out of the study.

At 25 weeks, 48% of the 49 fluoxetine-treated subjects had either dropped out or relapsed, versus 39% of the placebo controls. At 50 weeks, 58% of the fluoxetine-treated subjects and 55% of the controls had either dropped out or relapsed.

To pick up on any possible benefit of the drug, Dr. Walsh and his colleagues also considered just those who relapsed, and those who relapsed plus those who clinically appeared to be in trouble when they dropped out–either because their BMI had dropped to 17 or because they had begun binging and purging again, at least twice a week.

At 50 weeks, 27% of the fluoxetine-treated patients and 29% of the placebo controls were documented relapsers.

Considering as failures both those with documented relapse and those who clinically appeared to be not doing well when they dropped out, the percentages were 49% fluoxetine and 51% placebo.

Dr. Walsh said he also looked only at those with depression, and at those who purged or restricted food only, and treatment still made no difference in those particular patients. “However we cut it, we can find no evidence that fluoxetine prolongs time to relapse following successful initial treatment, and we've looked pretty hard,” Dr. Walsh said.

In an editorial comment accompanying the published report, Dr. Scott J. Crow of the University of Minnesota, Minneapolis, said, “While the results of previous relapse prevention trials have been mixed, the report by Walsh and colleagues has many strengths and appears convincingly negative” (JAMA 2006;295:2659–60).

The study amply demonstrates that antidepressant therapy, “a fairly common treatment practice for this illness,” provides no benefit, Dr. Crow noted.

Additional reporting was done by contributing writer Mary Ann Moon.

'We can find no evidence that fluoxetine prolongs time to relapse … and we've looked pretty hard.' DR. WALSH

WASHINGTON – Tight glycemic control early in the course of type 1 diabetes does not result in later cognitive decline, according to new findings from two studies with an average of 18 years of follow-up data.

“Because of the length of follow-up and extent of cognitive testing, this study strongly supports the safety of intensive diabetes therapy,” Dr. Alan M. Jacobson said at the annual scientific sessions of the American Diabetes Association.

The results should allay the serious concerns that have been raised about whether tight glycemic control might lead to more severe hypoglycemic episodes and subsequent decreased cognitive ability, said Dr. Jacobson, head of the behavioral and mental health research section at the Joslin Diabetes Center, Boston.

But the recurrent, severe hypoglycemic events that are more likely to occur with tight glycemic control could still possibly have a negative cognitive effect on older adults, very young children, or those with a longer disease duration, he added.

The results from the multicenter, randomized Diabetes Control and Complications Trial (DCCT) and its continuation in the long-term observational Epidemiology of Diabetes Interventions and Complications (EDIC) study showed that patients who received intensive glycemic control during the DCCT did not have any differences in cognition, compared with conventional treatment, as measured by an extensive test battery involving eight cognitive domains (problem solving, learning, immediate memory, delayed recall, spatial information, attention, psychomotor efficiency, and motor speed), Dr. Jacobson reported.

The 18 years of combined follow-up make the DCCT and the EDIC the largest, longest-term prospective study that has implemented a cognitive assessment of patients with any clinical condition, he said.

Among patients in either group, there were no differences in cognitive functioning in those who had no hypoglycemic episodes, one to five episodes, or more than five episodes.

Control of HbA_1c (glycosylated hemoglobin) values to less than 7.9% similarly showed no significant effects, except in sparing patients from small reductions in psychomotor efficiency and in improving motor speed. The “very modest” declines in psychomotor efficiency and motor speed that were associated with higher HbA_1c values (7.9% or greater) were “consistent with emerging literature on the effects of persistent hyperglycemia on mental and motor slowing,” Dr. Jacobson said.

The results did not change when the investigators removed 28 patients with potentially confounding illnesses–strokes, decreased vision, renal insufficiency–from the analysis, except that patients who had prior tight glycemic control in the DCCT had a significantly lower decline in psychomotor efficiency than did patients who received conventional treatment.

All of the analyses were adjusted to account for the confounding variables of baseline age, gender, years of education, length of follow-up, and the number of cognitive tests taken. (Patients took different numbers of tests because they entered the DCCT at different times.)

The initial results at the end of the DCCT showed that maintenance of near normal glycemic control reduced the risk of developing–or the progression of–microvascular complications.

After 10 years of additional follow-up in the EDIC study, the patients who had prior intensive treatment still had reduced progression of retinopathy, nephropathy, neuropathy, and cardiovascular events.

As patients in the intensive treatment arm of the DCCT finished the trial and entered the EDIC study, they did not maintain the same level of glycemic control during the ensuing years, whereas individuals who were in the conventional treatment arm of the DCCT received training on how to maintain tight glycemic control and soon began doing so on their own. Both groups had a mean HbA_1c value of 7.8% at the end of 12 years of follow-up in the EDIC study, which includes more than 90% of the original DCCT patients.

At the end of those 12 years, a significantly greater percentage of the 583 patients who were in the intensive treatment arm of the DCCT had one or more severe hypoglycemic events leading to coma or seizures than did the 553 patients who received conventional treatment (44%, or 258 patients with 880 events, vs. 34%, or 187 patients with 452 events).

Most (97%) of the participants were white and were 27 years old on average when they entered the DCCT, where they received a mean of 6.5 years of intervention; they were 45 years old on average after 12 years of follow-up in the EDIC trial. At the last follow-up, all of the participants were adults and about 50% were employed as professionals.

The patients in the study were “unusually healthy and subject to careful follow-up, which may suggest that those in worse control may show worse cognitive outcomes,” he said.

WASHINGTON – Tight glycemic control early in the course of type 1 diabetes does not result in later cognitive decline, according to new findings from two studies with an average of 18 years of follow-up data.

“Because of the length of follow-up and extent of cognitive testing, this study strongly supports the safety of intensive diabetes therapy,” Dr. Alan M. Jacobson said at the annual scientific sessions of the American Diabetes Association.

The results should allay the serious concerns that have been raised about whether tight glycemic control might lead to more severe hypoglycemic episodes and subsequent decreased cognitive ability, said Dr. Jacobson, head of the behavioral and mental health research section at the Joslin Diabetes Center, Boston.

But the recurrent, severe hypoglycemic events that are more likely to occur with tight glycemic control could still possibly have a negative cognitive effect on older adults, very young children, or those with a longer disease duration, he added.

The results from the multicenter, randomized Diabetes Control and Complications Trial (DCCT) and its continuation in the long-term observational Epidemiology of Diabetes Interventions and Complications (EDIC) study showed that patients who received intensive glycemic control during the DCCT did not have any differences in cognition, compared with conventional treatment, as measured by an extensive test battery involving eight cognitive domains (problem solving, learning, immediate memory, delayed recall, spatial information, attention, psychomotor efficiency, and motor speed), Dr. Jacobson reported.

The 18 years of combined follow-up make the DCCT and the EDIC the largest, longest-term prospective study that has implemented a cognitive assessment of patients with any clinical condition, he said.

Among patients in either group, there were no differences in cognitive functioning in those who had no hypoglycemic episodes, one to five episodes, or more than five episodes.

Control of HbA_1c (glycosylated hemoglobin) values to less than 7.9% similarly showed no significant effects, except in sparing patients from small reductions in psychomotor efficiency and in improving motor speed. The “very modest” declines in psychomotor efficiency and motor speed that were associated with higher HbA_1c values (7.9% or greater) were “consistent with emerging literature on the effects of persistent hyperglycemia on mental and motor slowing,” Dr. Jacobson said.

The results did not change when the investigators removed 28 patients with potentially confounding illnesses–strokes, decreased vision, renal insufficiency–from the analysis, except that patients who had prior tight glycemic control in the DCCT had a significantly lower decline in psychomotor efficiency than did patients who received conventional treatment.

All of the analyses were adjusted to account for the confounding variables of baseline age, gender, years of education, length of follow-up, and the number of cognitive tests taken. (Patients took different numbers of tests because they entered the DCCT at different times.)

The initial results at the end of the DCCT showed that maintenance of near normal glycemic control reduced the risk of developing–or the progression of–microvascular complications.

After 10 years of additional follow-up in the EDIC study, the patients who had prior intensive treatment still had reduced progression of retinopathy, nephropathy, neuropathy, and cardiovascular events.

As patients in the intensive treatment arm of the DCCT finished the trial and entered the EDIC study, they did not maintain the same level of glycemic control during the ensuing years, whereas individuals who were in the conventional treatment arm of the DCCT received training on how to maintain tight glycemic control and soon began doing so on their own. Both groups had a mean HbA_1c value of 7.8% at the end of 12 years of follow-up in the EDIC study, which includes more than 90% of the original DCCT patients.

At the end of those 12 years, a significantly greater percentage of the 583 patients who were in the intensive treatment arm of the DCCT had one or more severe hypoglycemic events leading to coma or seizures than did the 553 patients who received conventional treatment (44%, or 258 patients with 880 events, vs. 34%, or 187 patients with 452 events).

Most (97%) of the participants were white and were 27 years old on average when they entered the DCCT, where they received a mean of 6.5 years of intervention; they were 45 years old on average after 12 years of follow-up in the EDIC trial. At the last follow-up, all of the participants were adults and about 50% were employed as professionals.

The patients in the study were “unusually healthy and subject to careful follow-up, which may suggest that those in worse control may show worse cognitive outcomes,” he said.

WASHINGTON – Tight glycemic control early in the course of type 1 diabetes does not result in later cognitive decline, according to new findings from two studies with an average of 18 years of follow-up data.

“Because of the length of follow-up and extent of cognitive testing, this study strongly supports the safety of intensive diabetes therapy,” Dr. Alan M. Jacobson said at the annual scientific sessions of the American Diabetes Association.

The results should allay the serious concerns that have been raised about whether tight glycemic control might lead to more severe hypoglycemic episodes and subsequent decreased cognitive ability, said Dr. Jacobson, head of the behavioral and mental health research section at the Joslin Diabetes Center, Boston.

But the recurrent, severe hypoglycemic events that are more likely to occur with tight glycemic control could still possibly have a negative cognitive effect on older adults, very young children, or those with a longer disease duration, he added.

The results from the multicenter, randomized Diabetes Control and Complications Trial (DCCT) and its continuation in the long-term observational Epidemiology of Diabetes Interventions and Complications (EDIC) study showed that patients who received intensive glycemic control during the DCCT did not have any differences in cognition, compared with conventional treatment, as measured by an extensive test battery involving eight cognitive domains (problem solving, learning, immediate memory, delayed recall, spatial information, attention, psychomotor efficiency, and motor speed), Dr. Jacobson reported.

The 18 years of combined follow-up make the DCCT and the EDIC the largest, longest-term prospective study that has implemented a cognitive assessment of patients with any clinical condition, he said.

Among patients in either group, there were no differences in cognitive functioning in those who had no hypoglycemic episodes, one to five episodes, or more than five episodes.

Control of HbA_1c (glycosylated hemoglobin) values to less than 7.9% similarly showed no significant effects, except in sparing patients from small reductions in psychomotor efficiency and in improving motor speed. The “very modest” declines in psychomotor efficiency and motor speed that were associated with higher HbA_1c values (7.9% or greater) were “consistent with emerging literature on the effects of persistent hyperglycemia on mental and motor slowing,” Dr. Jacobson said.

The results did not change when the investigators removed 28 patients with potentially confounding illnesses–strokes, decreased vision, renal insufficiency–from the analysis, except that patients who had prior tight glycemic control in the DCCT had a significantly lower decline in psychomotor efficiency than did patients who received conventional treatment.

All of the analyses were adjusted to account for the confounding variables of baseline age, gender, years of education, length of follow-up, and the number of cognitive tests taken. (Patients took different numbers of tests because they entered the DCCT at different times.)

The initial results at the end of the DCCT showed that maintenance of near normal glycemic control reduced the risk of developing–or the progression of–microvascular complications.

After 10 years of additional follow-up in the EDIC study, the patients who had prior intensive treatment still had reduced progression of retinopathy, nephropathy, neuropathy, and cardiovascular events.

As patients in the intensive treatment arm of the DCCT finished the trial and entered the EDIC study, they did not maintain the same level of glycemic control during the ensuing years, whereas individuals who were in the conventional treatment arm of the DCCT received training on how to maintain tight glycemic control and soon began doing so on their own. Both groups had a mean HbA_1c value of 7.8% at the end of 12 years of follow-up in the EDIC study, which includes more than 90% of the original DCCT patients.

At the end of those 12 years, a significantly greater percentage of the 583 patients who were in the intensive treatment arm of the DCCT had one or more severe hypoglycemic events leading to coma or seizures than did the 553 patients who received conventional treatment (44%, or 258 patients with 880 events, vs. 34%, or 187 patients with 452 events).

Most (97%) of the participants were white and were 27 years old on average when they entered the DCCT, where they received a mean of 6.5 years of intervention; they were 45 years old on average after 12 years of follow-up in the EDIC trial. At the last follow-up, all of the participants were adults and about 50% were employed as professionals.

The patients in the study were “unusually healthy and subject to careful follow-up, which may suggest that those in worse control may show worse cognitive outcomes,” he said.

WASHINGTON – Which comes first, diabetes or depression?

The data on this temporal relationship are mixed. While findings from previous studies suggest that depression precedes diabetes, findings from another investigation, presented at the annual scientific sessions of the American Diabetes Association, propose that no time correlation exists between the two diagnoses.

This chicken-or-egg question is important because depression has a reported prevalence ranging from 11% to 33% in patients with diabetes, which is twice as high as it is in people without diabetes, said Dr. Lawrence S. Phillips, professor of medicine in the division of endocrinology and metabolism at Emory University, Atlanta.

Dr. Phillips and his colleagues conducted a cross-sectional study of 573 people (about half were white and half were African American) who said that they did not have diabetes. Each person received a 75-g oral glucose tolerance test after an 8-hour overnight fast, and screening for depression with a well-validated tool, the Patient Health Questionnaire.

Normal glucose tolerance (NGT) occurred in 65% of the participants while 15% had impaired fasting glucose (IFG), 8% had impaired glucose tolerance (IGT), 8% had both IFG and IGT, and 4% had diabetes. Some participants had received (11%) or were currently receiving (12%) treatment for depression.

PHQ scores rose in a statistically significant trend from being low among those who never underwent treatment for depression to being higher in people who received depression treatment in the past and highest in individuals who were currently receiving depression treatment.

But there was no relationship between the different categories of glucose tolerance and PHQ score, the prevalence of any depressive syndrome or major depressive disorder, or the severity of depression, Dr. Phillips said.

In multivariate analyses, higher body mass index and current receipt of depression treatment significantly increased the risk of having any depressive syndrome, but this risk was not increased within any category of glucose tolerance.

One audience member asked Dr. Phillips how he viewed the results of his study in light of the fact that a poster presented at last year's ADA meeting found that patients with IGT in the Diabetes Prevention Program had a significantly increased risk for depression, suggesting depression may have preceded IGT.

“It's certainly possible that among people who are depressed, there are neuroendocrine changes that lead to diabetes. There's certainly room in human biology for both processes,” Dr. Phillips said.

But he argued that the situation in which depression precedes the development of diabetes is unlikely given the lack of an association between depression and unrecognized IGT in his study and the fact that patients in the Diabetes Prevention Program were told that they had IGT and were at risk for diabetes, which could possibly have had a negative psychosocial effect.

Firm conclusions favoring either side of the issue, however, may have to wait for research into the dynamics of neurohormonal changes, which are believed to underlie some of the association between depression and the development of diabetes, said Dr. Sherita Hill Golden of the division of endocrinology and metabolism at Johns Hopkins University, Baltimore.

Melancholic depression is known to increase the activation of the hypothalamic pituitary adrenal (HPA) axis, which leads to a simultaneous activation of the sympathetic nervous system, Dr. Golden said.

In the tightly regulated feedback loop of the HPA axis, the hypothalamus produces corticotropin-releasing hormone (CRH) that stimulates the pituitary gland to release adrenocorticotropin hormone (ACTH), which stimulates the adrenal gland to release cortisol. Cortisol levels then in turn regulate the production and release of CRH.

There is evidence to suggest that subclinical hypercortisolism, defined as having two of three abnormalities in HPA axis function (increased 24-hour urine free cortisol, failure of the dexamethasone suppression test, and decreased levels of ACTH), may contribute to the development of type 2 diabetes, Dr. Golden said.

One study of 12 patients with adrenal incidentalomas and subclinical hypercortisolism found that such patients had a higher prevalence of insulin resistance, impaired glucose tolerance, and type 2 diabetes, as well as greater central adiposity, than did 29 patients with a nonfunctioning adrenal incidentaloma and no subclinical hypercortisolism (J. Clin. Endocrinol. Metab. 2002;87:998–1003).

Dr. Golden's own research has centered on determining which measures of neuroendocrine activity provide the most reliable results, and understanding how that activity correlates with metabolic parameters. Preliminary results of an extensive 3-day series of tests in 15 healthy African American women have indicated that static measures of HPA axis activity, such as salivary cortisol sampling, do not correlate well with more dynamic measurements, such as 24-hour urine-free cortisol levels. Other analyses in the patient group suggested that CT scan measurements of adrenal gland volume and the results of dexamethasone suppression testing are correlated strongly with body mass index, high-density lipoprotein cholesterol, and systolic blood pressure.

The results of studies measuring the effect of neuroendocrine changes on metabolic parameters are beginning to suggest that “modification of the neurohormonal response may provide a novel approach to the primary prevention of type 2 diabetes,” Dr. Golden said.

WASHINGTON – Which comes first, diabetes or depression?

The data on this temporal relationship are mixed. While findings from previous studies suggest that depression precedes diabetes, findings from another investigation, presented at the annual scientific sessions of the American Diabetes Association, propose that no time correlation exists between the two diagnoses.

This chicken-or-egg question is important because depression has a reported prevalence ranging from 11% to 33% in patients with diabetes, which is twice as high as it is in people without diabetes, said Dr. Lawrence S. Phillips, professor of medicine in the division of endocrinology and metabolism at Emory University, Atlanta.

Dr. Phillips and his colleagues conducted a cross-sectional study of 573 people (about half were white and half were African American) who said that they did not have diabetes. Each person received a 75-g oral glucose tolerance test after an 8-hour overnight fast, and screening for depression with a well-validated tool, the Patient Health Questionnaire.

Normal glucose tolerance (NGT) occurred in 65% of the participants while 15% had impaired fasting glucose (IFG), 8% had impaired glucose tolerance (IGT), 8% had both IFG and IGT, and 4% had diabetes. Some participants had received (11%) or were currently receiving (12%) treatment for depression.

PHQ scores rose in a statistically significant trend from being low among those who never underwent treatment for depression to being higher in people who received depression treatment in the past and highest in individuals who were currently receiving depression treatment.

But there was no relationship between the different categories of glucose tolerance and PHQ score, the prevalence of any depressive syndrome or major depressive disorder, or the severity of depression, Dr. Phillips said.

In multivariate analyses, higher body mass index and current receipt of depression treatment significantly increased the risk of having any depressive syndrome, but this risk was not increased within any category of glucose tolerance.

One audience member asked Dr. Phillips how he viewed the results of his study in light of the fact that a poster presented at last year's ADA meeting found that patients with IGT in the Diabetes Prevention Program had a significantly increased risk for depression, suggesting depression may have preceded IGT.

“It's certainly possible that among people who are depressed, there are neuroendocrine changes that lead to diabetes. There's certainly room in human biology for both processes,” Dr. Phillips said.

But he argued that the situation in which depression precedes the development of diabetes is unlikely given the lack of an association between depression and unrecognized IGT in his study and the fact that patients in the Diabetes Prevention Program were told that they had IGT and were at risk for diabetes, which could possibly have had a negative psychosocial effect.

Firm conclusions favoring either side of the issue, however, may have to wait for research into the dynamics of neurohormonal changes, which are believed to underlie some of the association between depression and the development of diabetes, said Dr. Sherita Hill Golden of the division of endocrinology and metabolism at Johns Hopkins University, Baltimore.

Melancholic depression is known to increase the activation of the hypothalamic pituitary adrenal (HPA) axis, which leads to a simultaneous activation of the sympathetic nervous system, Dr. Golden said.

In the tightly regulated feedback loop of the HPA axis, the hypothalamus produces corticotropin-releasing hormone (CRH) that stimulates the pituitary gland to release adrenocorticotropin hormone (ACTH), which stimulates the adrenal gland to release cortisol. Cortisol levels then in turn regulate the production and release of CRH.

There is evidence to suggest that subclinical hypercortisolism, defined as having two of three abnormalities in HPA axis function (increased 24-hour urine free cortisol, failure of the dexamethasone suppression test, and decreased levels of ACTH), may contribute to the development of type 2 diabetes, Dr. Golden said.

One study of 12 patients with adrenal incidentalomas and subclinical hypercortisolism found that such patients had a higher prevalence of insulin resistance, impaired glucose tolerance, and type 2 diabetes, as well as greater central adiposity, than did 29 patients with a nonfunctioning adrenal incidentaloma and no subclinical hypercortisolism (J. Clin. Endocrinol. Metab. 2002;87:998–1003).

Dr. Golden's own research has centered on determining which measures of neuroendocrine activity provide the most reliable results, and understanding how that activity correlates with metabolic parameters. Preliminary results of an extensive 3-day series of tests in 15 healthy African American women have indicated that static measures of HPA axis activity, such as salivary cortisol sampling, do not correlate well with more dynamic measurements, such as 24-hour urine-free cortisol levels. Other analyses in the patient group suggested that CT scan measurements of adrenal gland volume and the results of dexamethasone suppression testing are correlated strongly with body mass index, high-density lipoprotein cholesterol, and systolic blood pressure.

The results of studies measuring the effect of neuroendocrine changes on metabolic parameters are beginning to suggest that “modification of the neurohormonal response may provide a novel approach to the primary prevention of type 2 diabetes,” Dr. Golden said.

WASHINGTON – Which comes first, diabetes or depression?

The data on this temporal relationship are mixed. While findings from previous studies suggest that depression precedes diabetes, findings from another investigation, presented at the annual scientific sessions of the American Diabetes Association, propose that no time correlation exists between the two diagnoses.

This chicken-or-egg question is important because depression has a reported prevalence ranging from 11% to 33% in patients with diabetes, which is twice as high as it is in people without diabetes, said Dr. Lawrence S. Phillips, professor of medicine in the division of endocrinology and metabolism at Emory University, Atlanta.

Dr. Phillips and his colleagues conducted a cross-sectional study of 573 people (about half were white and half were African American) who said that they did not have diabetes. Each person received a 75-g oral glucose tolerance test after an 8-hour overnight fast, and screening for depression with a well-validated tool, the Patient Health Questionnaire.

Normal glucose tolerance (NGT) occurred in 65% of the participants while 15% had impaired fasting glucose (IFG), 8% had impaired glucose tolerance (IGT), 8% had both IFG and IGT, and 4% had diabetes. Some participants had received (11%) or were currently receiving (12%) treatment for depression.

PHQ scores rose in a statistically significant trend from being low among those who never underwent treatment for depression to being higher in people who received depression treatment in the past and highest in individuals who were currently receiving depression treatment.

But there was no relationship between the different categories of glucose tolerance and PHQ score, the prevalence of any depressive syndrome or major depressive disorder, or the severity of depression, Dr. Phillips said.

In multivariate analyses, higher body mass index and current receipt of depression treatment significantly increased the risk of having any depressive syndrome, but this risk was not increased within any category of glucose tolerance.

One audience member asked Dr. Phillips how he viewed the results of his study in light of the fact that a poster presented at last year's ADA meeting found that patients with IGT in the Diabetes Prevention Program had a significantly increased risk for depression, suggesting depression may have preceded IGT.

“It's certainly possible that among people who are depressed, there are neuroendocrine changes that lead to diabetes. There's certainly room in human biology for both processes,” Dr. Phillips said.

But he argued that the situation in which depression precedes the development of diabetes is unlikely given the lack of an association between depression and unrecognized IGT in his study and the fact that patients in the Diabetes Prevention Program were told that they had IGT and were at risk for diabetes, which could possibly have had a negative psychosocial effect.

Firm conclusions favoring either side of the issue, however, may have to wait for research into the dynamics of neurohormonal changes, which are believed to underlie some of the association between depression and the development of diabetes, said Dr. Sherita Hill Golden of the division of endocrinology and metabolism at Johns Hopkins University, Baltimore.

Melancholic depression is known to increase the activation of the hypothalamic pituitary adrenal (HPA) axis, which leads to a simultaneous activation of the sympathetic nervous system, Dr. Golden said.

In the tightly regulated feedback loop of the HPA axis, the hypothalamus produces corticotropin-releasing hormone (CRH) that stimulates the pituitary gland to release adrenocorticotropin hormone (ACTH), which stimulates the adrenal gland to release cortisol. Cortisol levels then in turn regulate the production and release of CRH.

There is evidence to suggest that subclinical hypercortisolism, defined as having two of three abnormalities in HPA axis function (increased 24-hour urine free cortisol, failure of the dexamethasone suppression test, and decreased levels of ACTH), may contribute to the development of type 2 diabetes, Dr. Golden said.

One study of 12 patients with adrenal incidentalomas and subclinical hypercortisolism found that such patients had a higher prevalence of insulin resistance, impaired glucose tolerance, and type 2 diabetes, as well as greater central adiposity, than did 29 patients with a nonfunctioning adrenal incidentaloma and no subclinical hypercortisolism (J. Clin. Endocrinol. Metab. 2002;87:998–1003).

Dr. Golden's own research has centered on determining which measures of neuroendocrine activity provide the most reliable results, and understanding how that activity correlates with metabolic parameters. Preliminary results of an extensive 3-day series of tests in 15 healthy African American women have indicated that static measures of HPA axis activity, such as salivary cortisol sampling, do not correlate well with more dynamic measurements, such as 24-hour urine-free cortisol levels. Other analyses in the patient group suggested that CT scan measurements of adrenal gland volume and the results of dexamethasone suppression testing are correlated strongly with body mass index, high-density lipoprotein cholesterol, and systolic blood pressure.

The results of studies measuring the effect of neuroendocrine changes on metabolic parameters are beginning to suggest that “modification of the neurohormonal response may provide a novel approach to the primary prevention of type 2 diabetes,” Dr. Golden said.

SAN JUAN, P.R. – Low heart rate variability is significantly associated with an increased risk of death in depressed versus nondepressed patients after an acute myocardial infarction, Robert M. Carney, Ph.D., said at the annual meeting of the American College of Psychiatrists.

Depression is common among patients with a recent, acute myocardial infarction (MI)–incidence of major depression ranges from 15% to 23% in the literature. Other researchers found that low 24-hour heart rate variability is a strong predictor of cardiac mortality in patients with a recent MI (Ann. Noninvasive Electrocardiol. 2005;10:88–101). Heart rate variability was as robust a predictor as ventricular dysfunction or the size of the infarction in this review article.

The aim of the current study was to determine whether 24-hour heart rate variability is lower in depressed patients, and if so, whether this finding explains why depression reduces cardiovascular mortality after an MI, said Dr. Carney, professor of psychiatry and director of the behavioral medicine center at Washington University, St. Louis.

He and his associates assessed 305 depressed patients (135 with major depression and 170 with minor depression) with 24-hour ambulatory ECG readings 1–3 weeks post MI. Another group of 366 nondepressed, post-MI patients was included for comparison.

The investigators measured frequency domain heart rate variability using very-low-frequency (VLF) power spectral analysis. “VLF reflects parasympathetic modulation and is one of the best predictors of post-MI mortality,” Dr. Carney said.

Dr. Carney and his associates found a difference in log of VLF power (LnVLF) measurements: 6.32 in the depressed group, compared with 6.59 in the nondepressed patients.

“This was statistically significant, but is it clinically significant?” Dr. Carney asked.

In the study, 16% of depressed patients and 7% of nondepressed controls had a VLF below 180 squared milliseconds. The estimated probability of survival over 30 months of follow-up was statistically lower among depressed patients.

“So low heart rate variability is a significant and important factor post MI,” Dr. Carney said.

After adjustment for other risk factors, including left ventricular ejection fraction, smoking, older age, and diabetes, the low heart rate variability hazard ratio “goes from 3.1 to 2.8–a tiny difference,” he said.

“About 27% of the mortality risk in these patients can be accounted for by low heart rate variability,” Dr. Carney said. “So there are other things that are important here–including platelet function and inflammation.”

The literature is conflicting about whether treatment of depression provides a beneficial increase in heart rate variability. For example, 10 studies with tricyclic antidepressants yielded mixed results, Dr. Carney said, “and the six SSRI studies are more confusing.” Three SSRI studies reported increased heart rate variability, and three reported no change. Studies with other antidepressants offer no clear answer, either. No change in heart rate variability was seen in a nefazodone study, while lower heart rate variability was observed in a bupropion study and a venlafaxine trial.

Dr. Carney assessed the effect of psychotherapy among depressed congestive heart disease (CHD) patients. After 12 sessions of cognitive-behavioral therapy, mean heart rate decreased 5 beats/min and root mean squared successive difference increased. There were no changes in other heart rate variability indices.

“Heart rate variability may be improved through medication, exercise, and cardiac risk factor modification,” Dr. Carney emphasized.

“Regardless, depression in cardiac patients should be treated to improve quality of life, because we know we can do that,” he said.

SAN JUAN, P.R. – Low heart rate variability is significantly associated with an increased risk of death in depressed versus nondepressed patients after an acute myocardial infarction, Robert M. Carney, Ph.D., said at the annual meeting of the American College of Psychiatrists.

Depression is common among patients with a recent, acute myocardial infarction (MI)–incidence of major depression ranges from 15% to 23% in the literature. Other researchers found that low 24-hour heart rate variability is a strong predictor of cardiac mortality in patients with a recent MI (Ann. Noninvasive Electrocardiol. 2005;10:88–101). Heart rate variability was as robust a predictor as ventricular dysfunction or the size of the infarction in this review article.

The aim of the current study was to determine whether 24-hour heart rate variability is lower in depressed patients, and if so, whether this finding explains why depression reduces cardiovascular mortality after an MI, said Dr. Carney, professor of psychiatry and director of the behavioral medicine center at Washington University, St. Louis.

He and his associates assessed 305 depressed patients (135 with major depression and 170 with minor depression) with 24-hour ambulatory ECG readings 1–3 weeks post MI. Another group of 366 nondepressed, post-MI patients was included for comparison.

The investigators measured frequency domain heart rate variability using very-low-frequency (VLF) power spectral analysis. “VLF reflects parasympathetic modulation and is one of the best predictors of post-MI mortality,” Dr. Carney said.

Dr. Carney and his associates found a difference in log of VLF power (LnVLF) measurements: 6.32 in the depressed group, compared with 6.59 in the nondepressed patients.

“This was statistically significant, but is it clinically significant?” Dr. Carney asked.

In the study, 16% of depressed patients and 7% of nondepressed controls had a VLF below 180 squared milliseconds. The estimated probability of survival over 30 months of follow-up was statistically lower among depressed patients.

“So low heart rate variability is a significant and important factor post MI,” Dr. Carney said.

After adjustment for other risk factors, including left ventricular ejection fraction, smoking, older age, and diabetes, the low heart rate variability hazard ratio “goes from 3.1 to 2.8–a tiny difference,” he said.

“About 27% of the mortality risk in these patients can be accounted for by low heart rate variability,” Dr. Carney said. “So there are other things that are important here–including platelet function and inflammation.”

The literature is conflicting about whether treatment of depression provides a beneficial increase in heart rate variability. For example, 10 studies with tricyclic antidepressants yielded mixed results, Dr. Carney said, “and the six SSRI studies are more confusing.” Three SSRI studies reported increased heart rate variability, and three reported no change. Studies with other antidepressants offer no clear answer, either. No change in heart rate variability was seen in a nefazodone study, while lower heart rate variability was observed in a bupropion study and a venlafaxine trial.

Dr. Carney assessed the effect of psychotherapy among depressed congestive heart disease (CHD) patients. After 12 sessions of cognitive-behavioral therapy, mean heart rate decreased 5 beats/min and root mean squared successive difference increased. There were no changes in other heart rate variability indices.

“Heart rate variability may be improved through medication, exercise, and cardiac risk factor modification,” Dr. Carney emphasized.

“Regardless, depression in cardiac patients should be treated to improve quality of life, because we know we can do that,” he said.

SAN JUAN, P.R. – Low heart rate variability is significantly associated with an increased risk of death in depressed versus nondepressed patients after an acute myocardial infarction, Robert M. Carney, Ph.D., said at the annual meeting of the American College of Psychiatrists.

Depression is common among patients with a recent, acute myocardial infarction (MI)–incidence of major depression ranges from 15% to 23% in the literature. Other researchers found that low 24-hour heart rate variability is a strong predictor of cardiac mortality in patients with a recent MI (Ann. Noninvasive Electrocardiol. 2005;10:88–101). Heart rate variability was as robust a predictor as ventricular dysfunction or the size of the infarction in this review article.

The aim of the current study was to determine whether 24-hour heart rate variability is lower in depressed patients, and if so, whether this finding explains why depression reduces cardiovascular mortality after an MI, said Dr. Carney, professor of psychiatry and director of the behavioral medicine center at Washington University, St. Louis.

He and his associates assessed 305 depressed patients (135 with major depression and 170 with minor depression) with 24-hour ambulatory ECG readings 1–3 weeks post MI. Another group of 366 nondepressed, post-MI patients was included for comparison.

The investigators measured frequency domain heart rate variability using very-low-frequency (VLF) power spectral analysis. “VLF reflects parasympathetic modulation and is one of the best predictors of post-MI mortality,” Dr. Carney said.

Dr. Carney and his associates found a difference in log of VLF power (LnVLF) measurements: 6.32 in the depressed group, compared with 6.59 in the nondepressed patients.

“This was statistically significant, but is it clinically significant?” Dr. Carney asked.

In the study, 16% of depressed patients and 7% of nondepressed controls had a VLF below 180 squared milliseconds. The estimated probability of survival over 30 months of follow-up was statistically lower among depressed patients.

“So low heart rate variability is a significant and important factor post MI,” Dr. Carney said.

After adjustment for other risk factors, including left ventricular ejection fraction, smoking, older age, and diabetes, the low heart rate variability hazard ratio “goes from 3.1 to 2.8–a tiny difference,” he said.

“About 27% of the mortality risk in these patients can be accounted for by low heart rate variability,” Dr. Carney said. “So there are other things that are important here–including platelet function and inflammation.”

The literature is conflicting about whether treatment of depression provides a beneficial increase in heart rate variability. For example, 10 studies with tricyclic antidepressants yielded mixed results, Dr. Carney said, “and the six SSRI studies are more confusing.” Three SSRI studies reported increased heart rate variability, and three reported no change. Studies with other antidepressants offer no clear answer, either. No change in heart rate variability was seen in a nefazodone study, while lower heart rate variability was observed in a bupropion study and a venlafaxine trial.

Dr. Carney assessed the effect of psychotherapy among depressed congestive heart disease (CHD) patients. After 12 sessions of cognitive-behavioral therapy, mean heart rate decreased 5 beats/min and root mean squared successive difference increased. There were no changes in other heart rate variability indices.

“Heart rate variability may be improved through medication, exercise, and cardiac risk factor modification,” Dr. Carney emphasized.

“Regardless, depression in cardiac patients should be treated to improve quality of life, because we know we can do that,” he said.

DENVER – Depression that occurred in adults after acute myocardial infarction decreased in severity during the first 6 months after the cardiac event, but then stabilized over the next several years, Kenneth E. Freedland, Ph.D., reported in a poster presented at the annual meeting of the American Psychosomatic Society.

Dr. Freedland, a member of the psychiatry department at Washington University, St. Louis, and his colleagues reviewed data on 1,086 adults who were randomized to the usual care arm of the Enhancing Recovery in Coronary Heart Disease (ENRICHD) study, a multicenter trial sponsored by the National Institutes of Health that was designed to evaluate depression interventions in MI patients.

The patients' mean age was 43 years, 44% were female, and 35% were minorities. In addition, 55% were high school graduates, 19% were college graduates, and 26% had less than a high school education. About 60% of the patients had a history of major depression before the MI.

The patients completed a Beck Depression Inventory (BDI) at the start of the study, and again at 6-month intervals for an average follow-up period of 26 months. The average baseline BDI score was 15.3; baseline BDI scores were lowest among older patients, non-Hispanic white patients, and patients without a history of major depression, and highest among women and patients who were taking antidepressants.

Antidepressant use was associated with worse depression in the overall ENRICHD study, so its impact in this analysis must be interpreted with caution, the investigators noted.

Overall, the severity of depression decreased during the first 6 months after the MI, but depression scores then stabilized during the follow-up period, which lasted as long as 4 years for some patients. The average decrease in BDI score was −0.85 during months 0–6, compared with −0.07 during months 6–54.

Female gender, minority status, younger age, and lower levels of education were significantly associated with higher levels of depression immediately after MI, but younger female patients showed the fastest improvements in depressive symptoms over time. Additional analysis is needed to determine patterns among these subgroups, the researchers noted.

DENVER – Depression that occurred in adults after acute myocardial infarction decreased in severity during the first 6 months after the cardiac event, but then stabilized over the next several years, Kenneth E. Freedland, Ph.D., reported in a poster presented at the annual meeting of the American Psychosomatic Society.

Dr. Freedland, a member of the psychiatry department at Washington University, St. Louis, and his colleagues reviewed data on 1,086 adults who were randomized to the usual care arm of the Enhancing Recovery in Coronary Heart Disease (ENRICHD) study, a multicenter trial sponsored by the National Institutes of Health that was designed to evaluate depression interventions in MI patients.

The patients' mean age was 43 years, 44% were female, and 35% were minorities. In addition, 55% were high school graduates, 19% were college graduates, and 26% had less than a high school education. About 60% of the patients had a history of major depression before the MI.

The patients completed a Beck Depression Inventory (BDI) at the start of the study, and again at 6-month intervals for an average follow-up period of 26 months. The average baseline BDI score was 15.3; baseline BDI scores were lowest among older patients, non-Hispanic white patients, and patients without a history of major depression, and highest among women and patients who were taking antidepressants.

Antidepressant use was associated with worse depression in the overall ENRICHD study, so its impact in this analysis must be interpreted with caution, the investigators noted.

Overall, the severity of depression decreased during the first 6 months after the MI, but depression scores then stabilized during the follow-up period, which lasted as long as 4 years for some patients. The average decrease in BDI score was −0.85 during months 0–6, compared with −0.07 during months 6–54.

Female gender, minority status, younger age, and lower levels of education were significantly associated with higher levels of depression immediately after MI, but younger female patients showed the fastest improvements in depressive symptoms over time. Additional analysis is needed to determine patterns among these subgroups, the researchers noted.

DENVER – Depression that occurred in adults after acute myocardial infarction decreased in severity during the first 6 months after the cardiac event, but then stabilized over the next several years, Kenneth E. Freedland, Ph.D., reported in a poster presented at the annual meeting of the American Psychosomatic Society.

Dr. Freedland, a member of the psychiatry department at Washington University, St. Louis, and his colleagues reviewed data on 1,086 adults who were randomized to the usual care arm of the Enhancing Recovery in Coronary Heart Disease (ENRICHD) study, a multicenter trial sponsored by the National Institutes of Health that was designed to evaluate depression interventions in MI patients.

The patients' mean age was 43 years, 44% were female, and 35% were minorities. In addition, 55% were high school graduates, 19% were college graduates, and 26% had less than a high school education. About 60% of the patients had a history of major depression before the MI.

The patients completed a Beck Depression Inventory (BDI) at the start of the study, and again at 6-month intervals for an average follow-up period of 26 months. The average baseline BDI score was 15.3; baseline BDI scores were lowest among older patients, non-Hispanic white patients, and patients without a history of major depression, and highest among women and patients who were taking antidepressants.

Antidepressant use was associated with worse depression in the overall ENRICHD study, so its impact in this analysis must be interpreted with caution, the investigators noted.

Overall, the severity of depression decreased during the first 6 months after the MI, but depression scores then stabilized during the follow-up period, which lasted as long as 4 years for some patients. The average decrease in BDI score was −0.85 during months 0–6, compared with −0.07 during months 6–54.

Female gender, minority status, younger age, and lower levels of education were significantly associated with higher levels of depression immediately after MI, but younger female patients showed the fastest improvements in depressive symptoms over time. Additional analysis is needed to determine patterns among these subgroups, the researchers noted.

Older white men who have an optimistic nature have about half the risk of dying from cardiovascular causes as their less optimistic peers, according to Dr. Erik J. Giltay of the Institute of Mental Health, Delft, the Netherlands, and his associates.

The researchers used data from a large, prospective study of cardiovascular disease (CVD) in healthy, middle-aged Dutch men to examine a possible link with dispositional optimism. Their study differed from previous research in that it adjusted for classic CVD risk factors, socioeconomic characteristics, and depression.

Dispositional optimism was defined as having “generalized positive expectancies for one's future.” It was measured using a four-item questionnaire in which subjects rated their agreement with the following statements: “I still expect much from life,” “I do not look forward to what lies ahead for me in the years to come,” “My days seem to be passing by slowly,” and “I am still full of plans.”

A total of 545 healthy men aged 64–84 years in 1985 began the study and were followed up at 5-year intervals until 2000. During that time, 373 (68.4%) died, including 187 (50.1%) who died of cardiovascular causes.

“Compared with men in the lowest tertile of dispositional optimism, those in the top tertile had a 55% lower multivariate-adjusted hazard ratio of cardiovascular mortality,” the investigators said (Arch. Intern. Med. 2006;166:431–6).

Optimism was not related to CVD risk factors such as body mass index, hypertension, diabetes, or HDL cholesterol levels. It also proved to be a relatively constant personality trait through the years.

“Our results demonstrate a strong and consistent association between dispositional optimism and an about 50% lower risk of cardiovascular mortality in elderly men during 15 years of follow-up,” Dr. Giltay and his associates said.

“A low subjectively perceived level of optimism should be added to the list of independent risk markers for cardiovascular mortality in elderly men,” they said. The study findings may not be generalizable to women or to other ethnic groups, as all of the subjects were white men, the researchers noted.

Older white men who have an optimistic nature have about half the risk of dying from cardiovascular causes as their less optimistic peers, according to Dr. Erik J. Giltay of the Institute of Mental Health, Delft, the Netherlands, and his associates.

The researchers used data from a large, prospective study of cardiovascular disease (CVD) in healthy, middle-aged Dutch men to examine a possible link with dispositional optimism. Their study differed from previous research in that it adjusted for classic CVD risk factors, socioeconomic characteristics, and depression.

Dispositional optimism was defined as having “generalized positive expectancies for one's future.” It was measured using a four-item questionnaire in which subjects rated their agreement with the following statements: “I still expect much from life,” “I do not look forward to what lies ahead for me in the years to come,” “My days seem to be passing by slowly,” and “I am still full of plans.”

A total of 545 healthy men aged 64–84 years in 1985 began the study and were followed up at 5-year intervals until 2000. During that time, 373 (68.4%) died, including 187 (50.1%) who died of cardiovascular causes.

“Compared with men in the lowest tertile of dispositional optimism, those in the top tertile had a 55% lower multivariate-adjusted hazard ratio of cardiovascular mortality,” the investigators said (Arch. Intern. Med. 2006;166:431–6).

Optimism was not related to CVD risk factors such as body mass index, hypertension, diabetes, or HDL cholesterol levels. It also proved to be a relatively constant personality trait through the years.

“Our results demonstrate a strong and consistent association between dispositional optimism and an about 50% lower risk of cardiovascular mortality in elderly men during 15 years of follow-up,” Dr. Giltay and his associates said.

“A low subjectively perceived level of optimism should be added to the list of independent risk markers for cardiovascular mortality in elderly men,” they said. The study findings may not be generalizable to women or to other ethnic groups, as all of the subjects were white men, the researchers noted.

Older white men who have an optimistic nature have about half the risk of dying from cardiovascular causes as their less optimistic peers, according to Dr. Erik J. Giltay of the Institute of Mental Health, Delft, the Netherlands, and his associates.

The researchers used data from a large, prospective study of cardiovascular disease (CVD) in healthy, middle-aged Dutch men to examine a possible link with dispositional optimism. Their study differed from previous research in that it adjusted for classic CVD risk factors, socioeconomic characteristics, and depression.

Dispositional optimism was defined as having “generalized positive expectancies for one's future.” It was measured using a four-item questionnaire in which subjects rated their agreement with the following statements: “I still expect much from life,” “I do not look forward to what lies ahead for me in the years to come,” “My days seem to be passing by slowly,” and “I am still full of plans.”

A total of 545 healthy men aged 64–84 years in 1985 began the study and were followed up at 5-year intervals until 2000. During that time, 373 (68.4%) died, including 187 (50.1%) who died of cardiovascular causes.

“Compared with men in the lowest tertile of dispositional optimism, those in the top tertile had a 55% lower multivariate-adjusted hazard ratio of cardiovascular mortality,” the investigators said (Arch. Intern. Med. 2006;166:431–6).

Optimism was not related to CVD risk factors such as body mass index, hypertension, diabetes, or HDL cholesterol levels. It also proved to be a relatively constant personality trait through the years.

“Our results demonstrate a strong and consistent association between dispositional optimism and an about 50% lower risk of cardiovascular mortality in elderly men during 15 years of follow-up,” Dr. Giltay and his associates said.

“A low subjectively perceived level of optimism should be added to the list of independent risk markers for cardiovascular mortality in elderly men,” they said. The study findings may not be generalizable to women or to other ethnic groups, as all of the subjects were white men, the researchers noted.