Somatic Disorders

SEATTLE – The relative efficacy of three treatments for anorexia nervosa appears to shift with long-term follow-up according to the results of an ongoing analysis of data from a randomized, controlled trial.

The treatment that was the most efficacious at the end of therapy appeared to be the least so at 5 years. But differences among the therapies were much less significant at that point, Virginia V.W. McIntosh, Ph.D., reported at an international conference sponsored by the Academy for Eating Disorders.

Dr. McIntosh, a senior clinical psychologist at the University of Otago, Christchurch, New Zealand, described ongoing analyses of data from a randomized, controlled trial that compared three treatments–cognitive-behavioral therapy (CBT), interpersonal psychotherapy (IPT), and specialist supportive clinical management (SSCM)–among 56 patients with anorexia nervosa.

End-of-treatment results showed that among the 35 patients who completed all sessions, SSCM was superior to both CBT and IPT in terms of global anorexia nervosa status (Am. J. Psychiatry 2005;162:741–7).

One of the new analyses focused on therapist adherence to the protocol for a specific treatment.

Dr. McIntosh and her colleagues measured adherence with a modified version of the Collaborative Study Psychotherapy Rating Scale, which had 28 items unique to IPT, 27 unique to CBT, and 3 unique to SSCM. “I think [adherence] speaks to the distinctiveness of CBT and SSCM, which is important here,” Dr. McIntosh said at the meeting, which was cosponsored by the University of New Mexico.

An additional 14 items overlapped both CBT and SSCM. Those overlap items were items that covered the important elements of weight gain, psychoeducation, and the normalization of eating, she said. An additional 18 items were not specific to any of the therapies and reflected aspects such as alliance and therapy process.

Independent raters listened to the recorded psychotherapy sessions from the trial and rated them for adherence on various subscales: CBT (unique plus overlapping items), CBT-only (unique items), IPT, SSCM (unique plus overlapping items), and a therapy-nonspecific subscale.

Results showed that ratings for the therapy-specific subscales did indeed differ significantly, depending on which therapy the patient had received during a session, Dr. McIntosh reported. Ratings were highest for the corresponding therapy in all cases. For example, the CBT subscale scores were highest for CBT sessions.

In contrast, ratings for the therapy-nonspecific subscale did not differ depending on which therapy the patient had received.

Another new, ongoing analysis of the trial data focused on long-term outcomes. Data at 5 years were available for 45 patients (80% of those initially randomized), Dr. McIntosh said. “The differences at 5 years are much less than the differences at end of treatment,” she reported.

“What we see is that the SSCM group has lost some ground in terms of the proportion with a good outcome, CBT has gained some ground at about the same rate at which SSCM has lost ground, and IPT has gained even more ground,” she said.

As a result, the proportion of patients with a good outcome at the 5-year time point was highest for IPT, intermediate for CBT, and lowest for SSCM.

The trial is comparing CBT, IPT, and SSCM among 56 patients with anorexia nervosa. DR. MCINTOSH

SEATTLE – The relative efficacy of three treatments for anorexia nervosa appears to shift with long-term follow-up according to the results of an ongoing analysis of data from a randomized, controlled trial.

The treatment that was the most efficacious at the end of therapy appeared to be the least so at 5 years. But differences among the therapies were much less significant at that point, Virginia V.W. McIntosh, Ph.D., reported at an international conference sponsored by the Academy for Eating Disorders.

Dr. McIntosh, a senior clinical psychologist at the University of Otago, Christchurch, New Zealand, described ongoing analyses of data from a randomized, controlled trial that compared three treatments–cognitive-behavioral therapy (CBT), interpersonal psychotherapy (IPT), and specialist supportive clinical management (SSCM)–among 56 patients with anorexia nervosa.

End-of-treatment results showed that among the 35 patients who completed all sessions, SSCM was superior to both CBT and IPT in terms of global anorexia nervosa status (Am. J. Psychiatry 2005;162:741–7).

One of the new analyses focused on therapist adherence to the protocol for a specific treatment.

Dr. McIntosh and her colleagues measured adherence with a modified version of the Collaborative Study Psychotherapy Rating Scale, which had 28 items unique to IPT, 27 unique to CBT, and 3 unique to SSCM. “I think [adherence] speaks to the distinctiveness of CBT and SSCM, which is important here,” Dr. McIntosh said at the meeting, which was cosponsored by the University of New Mexico.

An additional 14 items overlapped both CBT and SSCM. Those overlap items were items that covered the important elements of weight gain, psychoeducation, and the normalization of eating, she said. An additional 18 items were not specific to any of the therapies and reflected aspects such as alliance and therapy process.

Independent raters listened to the recorded psychotherapy sessions from the trial and rated them for adherence on various subscales: CBT (unique plus overlapping items), CBT-only (unique items), IPT, SSCM (unique plus overlapping items), and a therapy-nonspecific subscale.

Results showed that ratings for the therapy-specific subscales did indeed differ significantly, depending on which therapy the patient had received during a session, Dr. McIntosh reported. Ratings were highest for the corresponding therapy in all cases. For example, the CBT subscale scores were highest for CBT sessions.

In contrast, ratings for the therapy-nonspecific subscale did not differ depending on which therapy the patient had received.

Another new, ongoing analysis of the trial data focused on long-term outcomes. Data at 5 years were available for 45 patients (80% of those initially randomized), Dr. McIntosh said. “The differences at 5 years are much less than the differences at end of treatment,” she reported.

“What we see is that the SSCM group has lost some ground in terms of the proportion with a good outcome, CBT has gained some ground at about the same rate at which SSCM has lost ground, and IPT has gained even more ground,” she said.

As a result, the proportion of patients with a good outcome at the 5-year time point was highest for IPT, intermediate for CBT, and lowest for SSCM.

The trial is comparing CBT, IPT, and SSCM among 56 patients with anorexia nervosa. DR. MCINTOSH

SEATTLE – The relative efficacy of three treatments for anorexia nervosa appears to shift with long-term follow-up according to the results of an ongoing analysis of data from a randomized, controlled trial.

The treatment that was the most efficacious at the end of therapy appeared to be the least so at 5 years. But differences among the therapies were much less significant at that point, Virginia V.W. McIntosh, Ph.D., reported at an international conference sponsored by the Academy for Eating Disorders.

Dr. McIntosh, a senior clinical psychologist at the University of Otago, Christchurch, New Zealand, described ongoing analyses of data from a randomized, controlled trial that compared three treatments–cognitive-behavioral therapy (CBT), interpersonal psychotherapy (IPT), and specialist supportive clinical management (SSCM)–among 56 patients with anorexia nervosa.

End-of-treatment results showed that among the 35 patients who completed all sessions, SSCM was superior to both CBT and IPT in terms of global anorexia nervosa status (Am. J. Psychiatry 2005;162:741–7).

One of the new analyses focused on therapist adherence to the protocol for a specific treatment.

Dr. McIntosh and her colleagues measured adherence with a modified version of the Collaborative Study Psychotherapy Rating Scale, which had 28 items unique to IPT, 27 unique to CBT, and 3 unique to SSCM. “I think [adherence] speaks to the distinctiveness of CBT and SSCM, which is important here,” Dr. McIntosh said at the meeting, which was cosponsored by the University of New Mexico.

An additional 14 items overlapped both CBT and SSCM. Those overlap items were items that covered the important elements of weight gain, psychoeducation, and the normalization of eating, she said. An additional 18 items were not specific to any of the therapies and reflected aspects such as alliance and therapy process.

Independent raters listened to the recorded psychotherapy sessions from the trial and rated them for adherence on various subscales: CBT (unique plus overlapping items), CBT-only (unique items), IPT, SSCM (unique plus overlapping items), and a therapy-nonspecific subscale.

Results showed that ratings for the therapy-specific subscales did indeed differ significantly, depending on which therapy the patient had received during a session, Dr. McIntosh reported. Ratings were highest for the corresponding therapy in all cases. For example, the CBT subscale scores were highest for CBT sessions.

In contrast, ratings for the therapy-nonspecific subscale did not differ depending on which therapy the patient had received.

Another new, ongoing analysis of the trial data focused on long-term outcomes. Data at 5 years were available for 45 patients (80% of those initially randomized), Dr. McIntosh said. “The differences at 5 years are much less than the differences at end of treatment,” she reported.

“What we see is that the SSCM group has lost some ground in terms of the proportion with a good outcome, CBT has gained some ground at about the same rate at which SSCM has lost ground, and IPT has gained even more ground,” she said.

As a result, the proportion of patients with a good outcome at the 5-year time point was highest for IPT, intermediate for CBT, and lowest for SSCM.

The trial is comparing CBT, IPT, and SSCM among 56 patients with anorexia nervosa. DR. MCINTOSH

COLORADO SPRINGS–Change in sleep duration during midlife is associated in a U-shaped fashion with risk for death more than a decade later, Dr. Francesco Cappuccio reported at a conference of the American Heart Association.

The major driver of increased mortality among individuals at the low end of the sleep duration continuum is an excess of cardiovascular deaths, while in long sleepers the increase in mortality is due to noncardiovascular causes, according to the results of the Whitehall II study, said Dr. Cappuccio of Warwick Medical School, Coventry, England.

Whitehall II is a prospective cohort study of 10,308 white-collar British civil servants who were 35–55 years old when enrolled in the study in 1985–1988. The Whitehall II analysis of the impact of changes in sleep duration included data on baseline sleep patterns in 7,729 participants and changes in those patterns over the next 5 years. Participants then were followed for mortality through 2004.

Cardiovascular mortality was 2.4-fold higher among subjects who slept an average of 6–8 hr/night at baseline but cut their sleep duration to 5 hr/night or less over the next 5 years' follow-up, compared with those who held fast to the 6- to 8-hour pattern. The findings held after adjustment for potential confounding factors including age, gender, employment grade, marital status, blood pressure, body mass index, alcohol intake, smoking status, comorbid illnesses, and physical activity.

In subjects who increased their sleep duration from 7 to 8 hr/night at baseline to 9 or more, there was an adjusted 2.1-fold increase in noncardiovascular mortality.

Short sleep duration is known to be associated with hypertension, weight gain, and diabetes, all of which increase cardiovascular risk. In contrast, the mechanism for the relationship between long sleep and increased mortality is unclear, Dr. Cappuccio added.

COLORADO SPRINGS–Change in sleep duration during midlife is associated in a U-shaped fashion with risk for death more than a decade later, Dr. Francesco Cappuccio reported at a conference of the American Heart Association.

The major driver of increased mortality among individuals at the low end of the sleep duration continuum is an excess of cardiovascular deaths, while in long sleepers the increase in mortality is due to noncardiovascular causes, according to the results of the Whitehall II study, said Dr. Cappuccio of Warwick Medical School, Coventry, England.

Whitehall II is a prospective cohort study of 10,308 white-collar British civil servants who were 35–55 years old when enrolled in the study in 1985–1988. The Whitehall II analysis of the impact of changes in sleep duration included data on baseline sleep patterns in 7,729 participants and changes in those patterns over the next 5 years. Participants then were followed for mortality through 2004.

Cardiovascular mortality was 2.4-fold higher among subjects who slept an average of 6–8 hr/night at baseline but cut their sleep duration to 5 hr/night or less over the next 5 years' follow-up, compared with those who held fast to the 6- to 8-hour pattern. The findings held after adjustment for potential confounding factors including age, gender, employment grade, marital status, blood pressure, body mass index, alcohol intake, smoking status, comorbid illnesses, and physical activity.

In subjects who increased their sleep duration from 7 to 8 hr/night at baseline to 9 or more, there was an adjusted 2.1-fold increase in noncardiovascular mortality.

Short sleep duration is known to be associated with hypertension, weight gain, and diabetes, all of which increase cardiovascular risk. In contrast, the mechanism for the relationship between long sleep and increased mortality is unclear, Dr. Cappuccio added.

COLORADO SPRINGS–Change in sleep duration during midlife is associated in a U-shaped fashion with risk for death more than a decade later, Dr. Francesco Cappuccio reported at a conference of the American Heart Association.

The major driver of increased mortality among individuals at the low end of the sleep duration continuum is an excess of cardiovascular deaths, while in long sleepers the increase in mortality is due to noncardiovascular causes, according to the results of the Whitehall II study, said Dr. Cappuccio of Warwick Medical School, Coventry, England.

Whitehall II is a prospective cohort study of 10,308 white-collar British civil servants who were 35–55 years old when enrolled in the study in 1985–1988. The Whitehall II analysis of the impact of changes in sleep duration included data on baseline sleep patterns in 7,729 participants and changes in those patterns over the next 5 years. Participants then were followed for mortality through 2004.

Cardiovascular mortality was 2.4-fold higher among subjects who slept an average of 6–8 hr/night at baseline but cut their sleep duration to 5 hr/night or less over the next 5 years' follow-up, compared with those who held fast to the 6- to 8-hour pattern. The findings held after adjustment for potential confounding factors including age, gender, employment grade, marital status, blood pressure, body mass index, alcohol intake, smoking status, comorbid illnesses, and physical activity.

In subjects who increased their sleep duration from 7 to 8 hr/night at baseline to 9 or more, there was an adjusted 2.1-fold increase in noncardiovascular mortality.

Short sleep duration is known to be associated with hypertension, weight gain, and diabetes, all of which increase cardiovascular risk. In contrast, the mechanism for the relationship between long sleep and increased mortality is unclear, Dr. Cappuccio added.

ST. LOUIS – Sleep apnea assessment and treatment should be considered an integral part of diabetes management, Susan M. LaRue, R.D., said at the annual meeting of the American Association of Diabetes Educators.

“Sleep apnea is highly prevalent in people with diabetes, people with hypertension and obesity, all of which we see in huge numbers in our patient population,” said Ms. LaRue, a certified diabetes educator with Amylin Pharmaceuticals.

Because sleep apnea is so common among people with diabetes–concomitant with obesity and hypertension–the Scripps' Whittier Institute for Diabetes, La Jolla, Calif., has instituted a “best practice” in which every patient is screened for OSA.

In a study published by Whittier's Dr. Daniel Einhorn and his associates, 72% of 279 adults with type 2 diabetes were found to have some degree of sleep apnea, defined as an apnea-hypopnea index (AHI) of five events or more per hour. Over a third of the patients (36%) had an AHI of at least 15 events per hour, which was associated with a doubling of the risk for the development of hypertension after adjustment for comorbidities (Endocrine Practice 2007;13:355-62).

That study and the symposium in which Ms. LaRue spoke were both sponsored by the ResMed Corp., which manufactures continuous positive airway pressure (CPAP) devices for treatment of OSA.

Diabetes is among several cardiovascular-related conditions that are strongly associated with OSA. Data suggest that OSA is present in about 80% of individuals with drug-resistant hypertension (35% of all hypertension) and in 50% of those with atrial fibrillation.

The mechanism for the association is not known, but theories focus on the increased sympathetic nervous activity resulting from repeated apneas, said Ms. LaRue, formerly with the Whittier Institute.

Treatment with CPAP not only reduces apneic episodes and improves sleep quality, but also appears to improve the cardiovascular and metabolic abnormalities. In a German study of 60 patients with moderate to severe OSA, those given “therapeutic” levels of CPAP for an average of 9 weeks had a 95% reduction in apneas and hypopneas and a decrease in mean arterial blood pressure of 9.9 mm Hg.

That level of decline would be predicted to reduce coronary heart disease event risk by 37% and stroke risk by 56%, the investigators said (Circulation 2003;107:68-73).

ST. LOUIS – Sleep apnea assessment and treatment should be considered an integral part of diabetes management, Susan M. LaRue, R.D., said at the annual meeting of the American Association of Diabetes Educators.

“Sleep apnea is highly prevalent in people with diabetes, people with hypertension and obesity, all of which we see in huge numbers in our patient population,” said Ms. LaRue, a certified diabetes educator with Amylin Pharmaceuticals.

Because sleep apnea is so common among people with diabetes–concomitant with obesity and hypertension–the Scripps' Whittier Institute for Diabetes, La Jolla, Calif., has instituted a “best practice” in which every patient is screened for OSA.

In a study published by Whittier's Dr. Daniel Einhorn and his associates, 72% of 279 adults with type 2 diabetes were found to have some degree of sleep apnea, defined as an apnea-hypopnea index (AHI) of five events or more per hour. Over a third of the patients (36%) had an AHI of at least 15 events per hour, which was associated with a doubling of the risk for the development of hypertension after adjustment for comorbidities (Endocrine Practice 2007;13:355-62).

That study and the symposium in which Ms. LaRue spoke were both sponsored by the ResMed Corp., which manufactures continuous positive airway pressure (CPAP) devices for treatment of OSA.

Diabetes is among several cardiovascular-related conditions that are strongly associated with OSA. Data suggest that OSA is present in about 80% of individuals with drug-resistant hypertension (35% of all hypertension) and in 50% of those with atrial fibrillation.

The mechanism for the association is not known, but theories focus on the increased sympathetic nervous activity resulting from repeated apneas, said Ms. LaRue, formerly with the Whittier Institute.

Treatment with CPAP not only reduces apneic episodes and improves sleep quality, but also appears to improve the cardiovascular and metabolic abnormalities. In a German study of 60 patients with moderate to severe OSA, those given “therapeutic” levels of CPAP for an average of 9 weeks had a 95% reduction in apneas and hypopneas and a decrease in mean arterial blood pressure of 9.9 mm Hg.

That level of decline would be predicted to reduce coronary heart disease event risk by 37% and stroke risk by 56%, the investigators said (Circulation 2003;107:68-73).

ST. LOUIS – Sleep apnea assessment and treatment should be considered an integral part of diabetes management, Susan M. LaRue, R.D., said at the annual meeting of the American Association of Diabetes Educators.

“Sleep apnea is highly prevalent in people with diabetes, people with hypertension and obesity, all of which we see in huge numbers in our patient population,” said Ms. LaRue, a certified diabetes educator with Amylin Pharmaceuticals.

Because sleep apnea is so common among people with diabetes–concomitant with obesity and hypertension–the Scripps' Whittier Institute for Diabetes, La Jolla, Calif., has instituted a “best practice” in which every patient is screened for OSA.

In a study published by Whittier's Dr. Daniel Einhorn and his associates, 72% of 279 adults with type 2 diabetes were found to have some degree of sleep apnea, defined as an apnea-hypopnea index (AHI) of five events or more per hour. Over a third of the patients (36%) had an AHI of at least 15 events per hour, which was associated with a doubling of the risk for the development of hypertension after adjustment for comorbidities (Endocrine Practice 2007;13:355-62).

That study and the symposium in which Ms. LaRue spoke were both sponsored by the ResMed Corp., which manufactures continuous positive airway pressure (CPAP) devices for treatment of OSA.

Diabetes is among several cardiovascular-related conditions that are strongly associated with OSA. Data suggest that OSA is present in about 80% of individuals with drug-resistant hypertension (35% of all hypertension) and in 50% of those with atrial fibrillation.

The mechanism for the association is not known, but theories focus on the increased sympathetic nervous activity resulting from repeated apneas, said Ms. LaRue, formerly with the Whittier Institute.

Treatment with CPAP not only reduces apneic episodes and improves sleep quality, but also appears to improve the cardiovascular and metabolic abnormalities. In a German study of 60 patients with moderate to severe OSA, those given “therapeutic” levels of CPAP for an average of 9 weeks had a 95% reduction in apneas and hypopneas and a decrease in mean arterial blood pressure of 9.9 mm Hg.

That level of decline would be predicted to reduce coronary heart disease event risk by 37% and stroke risk by 56%, the investigators said (Circulation 2003;107:68-73).

The study aimed at assessing what kinds of factors increase the risk of stroke clarifies the relationship between mental health and stroke, according to the lead investigator and his colleagues.

Paul Surtees, Ph.D., and his colleagues conducted a large population study of more than 20,000 residents of Norfolk taking part in the United Kingdom arm of the 10-country European Prospective Investigation Into Cancer.

They found that lower baseline scores on a mental health inventory (indicating greater distress) were associated with an 11% increased risk of stroke over 8 years of follow-up after adjustment for known stroke risk factors. The association indicated a dose-response relationship.

Having a major depressive episode in the 12 months before the baseline mental-health assessment or at any point in their lives was not significantly associated with a greater stroke risk, however (Neurology 2008;70:788–94).

Dr. Surtees and his colleagues found that of the 20,627 study participants aged 41–80, 5% reported having an episode of major depressive disorder (MDD) in the previous 12 months and 15% reported having such an episode any time during their lives. The mean score on the MHI-5 was 55.2 for those who had experienced an MDD episode in the past 12 months, 76.5 for those who had an MDD episode at any time, and 78.5 for participants who reported never having an MDD episode. The researchers identified 595 strokes in 8.5 years of follow-up, 167 of which were fatal.

For every standard deviation lower score on the MHI-5, overall stroke risk increased by 11%, after adjustment for cardiovascular risk factors.

A single standard deviation lower score on MHI-5 resulted in an adjusted hazard ratio of 1.22 for fatal stroke. A significantly elevated risk of stroke was not found among participants who had experienced an MDD episode in last 12 months or in their lives.

The study aimed at assessing what kinds of factors increase the risk of stroke clarifies the relationship between mental health and stroke, according to the lead investigator and his colleagues.

Paul Surtees, Ph.D., and his colleagues conducted a large population study of more than 20,000 residents of Norfolk taking part in the United Kingdom arm of the 10-country European Prospective Investigation Into Cancer.

They found that lower baseline scores on a mental health inventory (indicating greater distress) were associated with an 11% increased risk of stroke over 8 years of follow-up after adjustment for known stroke risk factors. The association indicated a dose-response relationship.

Having a major depressive episode in the 12 months before the baseline mental-health assessment or at any point in their lives was not significantly associated with a greater stroke risk, however (Neurology 2008;70:788–94).

Dr. Surtees and his colleagues found that of the 20,627 study participants aged 41–80, 5% reported having an episode of major depressive disorder (MDD) in the previous 12 months and 15% reported having such an episode any time during their lives. The mean score on the MHI-5 was 55.2 for those who had experienced an MDD episode in the past 12 months, 76.5 for those who had an MDD episode at any time, and 78.5 for participants who reported never having an MDD episode. The researchers identified 595 strokes in 8.5 years of follow-up, 167 of which were fatal.

For every standard deviation lower score on the MHI-5, overall stroke risk increased by 11%, after adjustment for cardiovascular risk factors.

A single standard deviation lower score on MHI-5 resulted in an adjusted hazard ratio of 1.22 for fatal stroke. A significantly elevated risk of stroke was not found among participants who had experienced an MDD episode in last 12 months or in their lives.

The study aimed at assessing what kinds of factors increase the risk of stroke clarifies the relationship between mental health and stroke, according to the lead investigator and his colleagues.

Paul Surtees, Ph.D., and his colleagues conducted a large population study of more than 20,000 residents of Norfolk taking part in the United Kingdom arm of the 10-country European Prospective Investigation Into Cancer.

They found that lower baseline scores on a mental health inventory (indicating greater distress) were associated with an 11% increased risk of stroke over 8 years of follow-up after adjustment for known stroke risk factors. The association indicated a dose-response relationship.

Having a major depressive episode in the 12 months before the baseline mental-health assessment or at any point in their lives was not significantly associated with a greater stroke risk, however (Neurology 2008;70:788–94).

Dr. Surtees and his colleagues found that of the 20,627 study participants aged 41–80, 5% reported having an episode of major depressive disorder (MDD) in the previous 12 months and 15% reported having such an episode any time during their lives. The mean score on the MHI-5 was 55.2 for those who had experienced an MDD episode in the past 12 months, 76.5 for those who had an MDD episode at any time, and 78.5 for participants who reported never having an MDD episode. The researchers identified 595 strokes in 8.5 years of follow-up, 167 of which were fatal.

For every standard deviation lower score on the MHI-5, overall stroke risk increased by 11%, after adjustment for cardiovascular risk factors.

A single standard deviation lower score on MHI-5 resulted in an adjusted hazard ratio of 1.22 for fatal stroke. A significantly elevated risk of stroke was not found among participants who had experienced an MDD episode in last 12 months or in their lives.

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Psychiatry is such a screwed-up field that we cannot retain a language that is scientific and meaningful.

Several months ago I railed against the bastardization of the word “depression.” Now we have a new one, “distress,” which a recent study on causes of stroke equates with emotional distress (see details about the study in article below).

I'm also disturbed–rather than depressed or anxious–by the constant annual effort to rediscover Freud. Rename it, and call it a new finding. Freud said: “Analysis exchanges the pain of neurons for the misery of everyday life.” Was he stealing the idea from Henry David Thoreau, who said, “The mass of men lead lives of quiet desperation”?

I don't use the terms stress and distress to have significant measurable diagnosable meaning. But now, researchers in the United Kingdom have determined that psychological distress is linked to increased risk of stroke (Neurology 2008;70:788–94). I take that to mean that all normal people are at risk for stroke.

Someone has to make very clear to me and the general public what psychological distress means. Is that more than the psychological pain related to the death of a loved one or the loss of a job? For me, stress and distress are lay terms and not psychiatric terms. We need to guard our areas of interest and concern very closely.

Perhaps when the study's authors refer to distress, they are alluding to anxiety. If anxiety, not depression, were linked to increased stroke risk, I would be very interested. Now I think I know why we separated neurology from psychiatry. Emotional disease is nothing about which we should be casual. It is our bread and butter.

About 2 years ago, I became excited about new scientific information suggesting that if a person feels any symptoms that could presage a stroke, he or she should get to a hospital for a CT scan and the medicine that can abort a stroke (if it is not being caused by hemorrhage). The individual should get to a hospital in 15 minutes. Knowing the life-altering and life-endangering nature of stroke, I thought this was a terrific piece of information, but no layperson I know seems to have heard of it. Furthermore, it is highly unlikely that anyone would bypass denial and get to the hospital. Whenever I have a friend or patient tell me about an episode of illness, the story is always exasperating, because the individual first self-diagnoses and delays calling a doctor or rushing off to an emergency department.

My mother became blind as she got older, but I will never forget how it started. I went to Florida for her 75th birthday party, and she complained that her eyesight was getting bad. I asked if she had called the doctor, to which she gave her usual reply, “I didn't want to bother him.” I insisted on going with her to the doctor the next morning, before I was scheduled to fly out. She had hemorrhagic macular degeneration, and I believe she might have had many more years of sight had she seen the value of going to a doctor and getting proper care immediately.

In this context, the U.K. researchers are eager to show that depression, while it often follows a stroke, is not a causative factor. That is important, but one form of human distress is depression. Are we sure that some of those designated as “distressed” were not depressed?

I continue to have great difficulty with researchers and neurologists making psychiatric diagnoses, particularly when the big category is psychological distress, a term of no use or meaning to psychiatrists. No one is free of distress. We are all in conflict about some aspect of our lives. There are lots of categories where we feel confused, fearful of hurting someone, or where we want something we cannot afford or desire sex with someone who is uninterested.

I'm allowing for these conflicts as examples of psychological distress. Or are the authors really talking about some kind of personality disorder in which the patient is always complaining, chronically discontented, or backfilling for things either said or done? Several personality disorders are characterized by psychological distress. The most common is obsessive compulsive disorder, but I'm sure each reader can recall a patient who was always bitching about someone else. It's a very common defense for people to complain about others rather than look at their own role in their unhappiness. My patients with OCD are in terrible pain. Their obsessive thoughts torment them. Is that the distress? The U.K. researchers are talking about every diagnosis in DSM-IV to get the meaning of distress. I think we should try to help them become better diagnosticians of psychiatric disorders. What they have done is demonstrated their stigma and disdain for psychiatry by trivializing distress as a nondescript concept against which to compare depression.

The question posed by the study–Are there psychiatric disorders that help precipitate a stroke?–is an important one. Psychiatrists and neurologists should be working together to either retrospectively or prospectively discover who has strokes.

It seems to me that we should be singling out those who develop arterial sclerosis or other vessel-blocking disorders, testing carotid arteries for blockages, or looking at those who have other evidence of vessel blockage for signs of imminent stroke, weakness, difficulty speaking, etc. Since I obviously am not impressed with the discovery that psychological distress may increase strokes, it means nothing to me. I wouldn't know whom to warn.

In the biopsychosocial world in which we live, a need for greater precision is needed. We analytic types often have been accused of imprecision, guesswork, and flawed theories, and we have, in fact, often lacked the necessary precision that is considered in the biomedical world to be scientific. But as I experience more and more of how the rest of medicine operates, I am amazed by how sloppy others can be in their science! Add to that the institutionalized rudeness of office staff, the lack of concern about the patient's time, and the habitual lack of feedback to the patient and/or the family, and you can begin to understand why I find the misuse of terms and the failure of accurate diagnosis so exasperating.

The use of the anomalous and meaningless word “distress” is obviously one of the nodal points that gets to me. It's worse if you are a physician, because the doctor will often answer my questions with “you know what to do.” If I knew, I wouldn't ask! I assume that he doesn't act the same way with nonphysician patients.

What I'm begging for in this column is a better recognition of the body of knowledge called psychiatry with all of its theories, diagnoses, and treatments. I have resented for decades the stigma against psychiatry practiced by nonpsychiatric physicians, which is passed on by residents to medical students. No matter how hard we fight to erase the stigma, we are stuck with chronic joking and gentle harassment by our colleagues. I believe that much of our thinking is incomprehensible to these men and women who appear to be offended that we seem to know something about how the human mind works and what makes people tick.

I have avoided using the word “castration” in my teaching and scientific talks for years, but today I saw a patient with the residents and students where it was absolutely appropriate. A 56-year-old man with depression and anxiety had severe chronic obstructive pulmonary disease, the result of smoking three packs of cigarettes a day for more than 40 years and drinking two cases of beer a day for decades. Now totally incapacitated, unhappily living with his daughter and son-in-law whom he despises, unable to get out of the house, work or “do” anything, he is depressed, largely because of his unfitness and the death of his wife. Also, he is reliving the death of his mother when he was 7 years old. Today, he is a shadow of his former self: a vibrant husband, father, and construction worker.

This patient is jumping out of his skin to rejoin the living but “doesn't have the energy” and can hardly breathe. Does the pulmonologist, who is recommending a lung transplant, care about any of this, or does he know that his treatment can actually help this man get his life back?

We in psychiatry have to resist glib and often unnecessary research in areas that do not further our work and might start whole new areas of thought that are of no practical use.

Both stroke and depression are important areas for our concern. Knowing the relationship between the two can be helpful to scores of patients. Let's make sure that we don't go along with “scientific” nonsense.

[email protected]

Psychiatry is such a screwed-up field that we cannot retain a language that is scientific and meaningful.

Several months ago I railed against the bastardization of the word “depression.” Now we have a new one, “distress,” which a recent study on causes of stroke equates with emotional distress (see details about the study in article below).

I'm also disturbed–rather than depressed or anxious–by the constant annual effort to rediscover Freud. Rename it, and call it a new finding. Freud said: “Analysis exchanges the pain of neurons for the misery of everyday life.” Was he stealing the idea from Henry David Thoreau, who said, “The mass of men lead lives of quiet desperation”?

I don't use the terms stress and distress to have significant measurable diagnosable meaning. But now, researchers in the United Kingdom have determined that psychological distress is linked to increased risk of stroke (Neurology 2008;70:788–94). I take that to mean that all normal people are at risk for stroke.

Someone has to make very clear to me and the general public what psychological distress means. Is that more than the psychological pain related to the death of a loved one or the loss of a job? For me, stress and distress are lay terms and not psychiatric terms. We need to guard our areas of interest and concern very closely.

Perhaps when the study's authors refer to distress, they are alluding to anxiety. If anxiety, not depression, were linked to increased stroke risk, I would be very interested. Now I think I know why we separated neurology from psychiatry. Emotional disease is nothing about which we should be casual. It is our bread and butter.

About 2 years ago, I became excited about new scientific information suggesting that if a person feels any symptoms that could presage a stroke, he or she should get to a hospital for a CT scan and the medicine that can abort a stroke (if it is not being caused by hemorrhage). The individual should get to a hospital in 15 minutes. Knowing the life-altering and life-endangering nature of stroke, I thought this was a terrific piece of information, but no layperson I know seems to have heard of it. Furthermore, it is highly unlikely that anyone would bypass denial and get to the hospital. Whenever I have a friend or patient tell me about an episode of illness, the story is always exasperating, because the individual first self-diagnoses and delays calling a doctor or rushing off to an emergency department.

My mother became blind as she got older, but I will never forget how it started. I went to Florida for her 75th birthday party, and she complained that her eyesight was getting bad. I asked if she had called the doctor, to which she gave her usual reply, “I didn't want to bother him.” I insisted on going with her to the doctor the next morning, before I was scheduled to fly out. She had hemorrhagic macular degeneration, and I believe she might have had many more years of sight had she seen the value of going to a doctor and getting proper care immediately.

In this context, the U.K. researchers are eager to show that depression, while it often follows a stroke, is not a causative factor. That is important, but one form of human distress is depression. Are we sure that some of those designated as “distressed” were not depressed?

I continue to have great difficulty with researchers and neurologists making psychiatric diagnoses, particularly when the big category is psychological distress, a term of no use or meaning to psychiatrists. No one is free of distress. We are all in conflict about some aspect of our lives. There are lots of categories where we feel confused, fearful of hurting someone, or where we want something we cannot afford or desire sex with someone who is uninterested.

I'm allowing for these conflicts as examples of psychological distress. Or are the authors really talking about some kind of personality disorder in which the patient is always complaining, chronically discontented, or backfilling for things either said or done? Several personality disorders are characterized by psychological distress. The most common is obsessive compulsive disorder, but I'm sure each reader can recall a patient who was always bitching about someone else. It's a very common defense for people to complain about others rather than look at their own role in their unhappiness. My patients with OCD are in terrible pain. Their obsessive thoughts torment them. Is that the distress? The U.K. researchers are talking about every diagnosis in DSM-IV to get the meaning of distress. I think we should try to help them become better diagnosticians of psychiatric disorders. What they have done is demonstrated their stigma and disdain for psychiatry by trivializing distress as a nondescript concept against which to compare depression.

The question posed by the study–Are there psychiatric disorders that help precipitate a stroke?–is an important one. Psychiatrists and neurologists should be working together to either retrospectively or prospectively discover who has strokes.

It seems to me that we should be singling out those who develop arterial sclerosis or other vessel-blocking disorders, testing carotid arteries for blockages, or looking at those who have other evidence of vessel blockage for signs of imminent stroke, weakness, difficulty speaking, etc. Since I obviously am not impressed with the discovery that psychological distress may increase strokes, it means nothing to me. I wouldn't know whom to warn.

In the biopsychosocial world in which we live, a need for greater precision is needed. We analytic types often have been accused of imprecision, guesswork, and flawed theories, and we have, in fact, often lacked the necessary precision that is considered in the biomedical world to be scientific. But as I experience more and more of how the rest of medicine operates, I am amazed by how sloppy others can be in their science! Add to that the institutionalized rudeness of office staff, the lack of concern about the patient's time, and the habitual lack of feedback to the patient and/or the family, and you can begin to understand why I find the misuse of terms and the failure of accurate diagnosis so exasperating.

The use of the anomalous and meaningless word “distress” is obviously one of the nodal points that gets to me. It's worse if you are a physician, because the doctor will often answer my questions with “you know what to do.” If I knew, I wouldn't ask! I assume that he doesn't act the same way with nonphysician patients.

What I'm begging for in this column is a better recognition of the body of knowledge called psychiatry with all of its theories, diagnoses, and treatments. I have resented for decades the stigma against psychiatry practiced by nonpsychiatric physicians, which is passed on by residents to medical students. No matter how hard we fight to erase the stigma, we are stuck with chronic joking and gentle harassment by our colleagues. I believe that much of our thinking is incomprehensible to these men and women who appear to be offended that we seem to know something about how the human mind works and what makes people tick.

I have avoided using the word “castration” in my teaching and scientific talks for years, but today I saw a patient with the residents and students where it was absolutely appropriate. A 56-year-old man with depression and anxiety had severe chronic obstructive pulmonary disease, the result of smoking three packs of cigarettes a day for more than 40 years and drinking two cases of beer a day for decades. Now totally incapacitated, unhappily living with his daughter and son-in-law whom he despises, unable to get out of the house, work or “do” anything, he is depressed, largely because of his unfitness and the death of his wife. Also, he is reliving the death of his mother when he was 7 years old. Today, he is a shadow of his former self: a vibrant husband, father, and construction worker.

This patient is jumping out of his skin to rejoin the living but “doesn't have the energy” and can hardly breathe. Does the pulmonologist, who is recommending a lung transplant, care about any of this, or does he know that his treatment can actually help this man get his life back?

We in psychiatry have to resist glib and often unnecessary research in areas that do not further our work and might start whole new areas of thought that are of no practical use.

Both stroke and depression are important areas for our concern. Knowing the relationship between the two can be helpful to scores of patients. Let's make sure that we don't go along with “scientific” nonsense.

[email protected]

Psychiatry is such a screwed-up field that we cannot retain a language that is scientific and meaningful.

Several months ago I railed against the bastardization of the word “depression.” Now we have a new one, “distress,” which a recent study on causes of stroke equates with emotional distress (see details about the study in article below).

I'm also disturbed–rather than depressed or anxious–by the constant annual effort to rediscover Freud. Rename it, and call it a new finding. Freud said: “Analysis exchanges the pain of neurons for the misery of everyday life.” Was he stealing the idea from Henry David Thoreau, who said, “The mass of men lead lives of quiet desperation”?

I don't use the terms stress and distress to have significant measurable diagnosable meaning. But now, researchers in the United Kingdom have determined that psychological distress is linked to increased risk of stroke (Neurology 2008;70:788–94). I take that to mean that all normal people are at risk for stroke.

Someone has to make very clear to me and the general public what psychological distress means. Is that more than the psychological pain related to the death of a loved one or the loss of a job? For me, stress and distress are lay terms and not psychiatric terms. We need to guard our areas of interest and concern very closely.

Perhaps when the study's authors refer to distress, they are alluding to anxiety. If anxiety, not depression, were linked to increased stroke risk, I would be very interested. Now I think I know why we separated neurology from psychiatry. Emotional disease is nothing about which we should be casual. It is our bread and butter.

About 2 years ago, I became excited about new scientific information suggesting that if a person feels any symptoms that could presage a stroke, he or she should get to a hospital for a CT scan and the medicine that can abort a stroke (if it is not being caused by hemorrhage). The individual should get to a hospital in 15 minutes. Knowing the life-altering and life-endangering nature of stroke, I thought this was a terrific piece of information, but no layperson I know seems to have heard of it. Furthermore, it is highly unlikely that anyone would bypass denial and get to the hospital. Whenever I have a friend or patient tell me about an episode of illness, the story is always exasperating, because the individual first self-diagnoses and delays calling a doctor or rushing off to an emergency department.

My mother became blind as she got older, but I will never forget how it started. I went to Florida for her 75th birthday party, and she complained that her eyesight was getting bad. I asked if she had called the doctor, to which she gave her usual reply, “I didn't want to bother him.” I insisted on going with her to the doctor the next morning, before I was scheduled to fly out. She had hemorrhagic macular degeneration, and I believe she might have had many more years of sight had she seen the value of going to a doctor and getting proper care immediately.

In this context, the U.K. researchers are eager to show that depression, while it often follows a stroke, is not a causative factor. That is important, but one form of human distress is depression. Are we sure that some of those designated as “distressed” were not depressed?

I continue to have great difficulty with researchers and neurologists making psychiatric diagnoses, particularly when the big category is psychological distress, a term of no use or meaning to psychiatrists. No one is free of distress. We are all in conflict about some aspect of our lives. There are lots of categories where we feel confused, fearful of hurting someone, or where we want something we cannot afford or desire sex with someone who is uninterested.

I'm allowing for these conflicts as examples of psychological distress. Or are the authors really talking about some kind of personality disorder in which the patient is always complaining, chronically discontented, or backfilling for things either said or done? Several personality disorders are characterized by psychological distress. The most common is obsessive compulsive disorder, but I'm sure each reader can recall a patient who was always bitching about someone else. It's a very common defense for people to complain about others rather than look at their own role in their unhappiness. My patients with OCD are in terrible pain. Their obsessive thoughts torment them. Is that the distress? The U.K. researchers are talking about every diagnosis in DSM-IV to get the meaning of distress. I think we should try to help them become better diagnosticians of psychiatric disorders. What they have done is demonstrated their stigma and disdain for psychiatry by trivializing distress as a nondescript concept against which to compare depression.

The question posed by the study–Are there psychiatric disorders that help precipitate a stroke?–is an important one. Psychiatrists and neurologists should be working together to either retrospectively or prospectively discover who has strokes.

It seems to me that we should be singling out those who develop arterial sclerosis or other vessel-blocking disorders, testing carotid arteries for blockages, or looking at those who have other evidence of vessel blockage for signs of imminent stroke, weakness, difficulty speaking, etc. Since I obviously am not impressed with the discovery that psychological distress may increase strokes, it means nothing to me. I wouldn't know whom to warn.

In the biopsychosocial world in which we live, a need for greater precision is needed. We analytic types often have been accused of imprecision, guesswork, and flawed theories, and we have, in fact, often lacked the necessary precision that is considered in the biomedical world to be scientific. But as I experience more and more of how the rest of medicine operates, I am amazed by how sloppy others can be in their science! Add to that the institutionalized rudeness of office staff, the lack of concern about the patient's time, and the habitual lack of feedback to the patient and/or the family, and you can begin to understand why I find the misuse of terms and the failure of accurate diagnosis so exasperating.

The use of the anomalous and meaningless word “distress” is obviously one of the nodal points that gets to me. It's worse if you are a physician, because the doctor will often answer my questions with “you know what to do.” If I knew, I wouldn't ask! I assume that he doesn't act the same way with nonphysician patients.

What I'm begging for in this column is a better recognition of the body of knowledge called psychiatry with all of its theories, diagnoses, and treatments. I have resented for decades the stigma against psychiatry practiced by nonpsychiatric physicians, which is passed on by residents to medical students. No matter how hard we fight to erase the stigma, we are stuck with chronic joking and gentle harassment by our colleagues. I believe that much of our thinking is incomprehensible to these men and women who appear to be offended that we seem to know something about how the human mind works and what makes people tick.

I have avoided using the word “castration” in my teaching and scientific talks for years, but today I saw a patient with the residents and students where it was absolutely appropriate. A 56-year-old man with depression and anxiety had severe chronic obstructive pulmonary disease, the result of smoking three packs of cigarettes a day for more than 40 years and drinking two cases of beer a day for decades. Now totally incapacitated, unhappily living with his daughter and son-in-law whom he despises, unable to get out of the house, work or “do” anything, he is depressed, largely because of his unfitness and the death of his wife. Also, he is reliving the death of his mother when he was 7 years old. Today, he is a shadow of his former self: a vibrant husband, father, and construction worker.

This patient is jumping out of his skin to rejoin the living but “doesn't have the energy” and can hardly breathe. Does the pulmonologist, who is recommending a lung transplant, care about any of this, or does he know that his treatment can actually help this man get his life back?

We in psychiatry have to resist glib and often unnecessary research in areas that do not further our work and might start whole new areas of thought that are of no practical use.

Both stroke and depression are important areas for our concern. Knowing the relationship between the two can be helpful to scores of patients. Let's make sure that we don't go along with “scientific” nonsense.

Patients with irritable bowel syndrome have altered brain responses to the anticipation of pain and to pain itself, which might make them more sensitive to painful stimuli, reported Dr. Steven M. Berman and his colleagues from the Center for the Neurobiology of Stress at the University of California, Los Angeles.

During expectation of pain, irritable bowel syndrome patients generate higher levels of tonic noradrenergic activity, producing a bias toward interpretation of network activity as pain, and are inefficient at reducing such activity when discrimination of nonpainful stimulation should be maximized, they said (J. Neurosci. 2008;28:349–59).

Functional magnetic resonance imaging (fMRI) was used to measure the blood oxygen level-dependent response to anticipated and delivered rectal distention in 14 female IBS patients and 12 healthy controls (mean age 36 years). When controls were anticipating a painful stimulus, brain activity decreased in several regions, but there was less of this anticipatory deactivation in the IBS patients.

Visceral distention of the rectum was then performed using a computer-driven pump and rectal balloon. Four to six sessions of 16 inflations were performed. Each inflation was preceded by an anticipatory cue. During rectal distention, increases in activity in the insula, dorsal anterior cingulate cortex, and dorsal brainstem were more extensive in IBS patients than in controls.

The results show that during expectation of experimental abdominal/pelvic discomfort, female IBS patients are more anxious and less able than healthy controls to downregulate activity within the CNS network activated by potentially aversive stimuli, the authors noted.

Patients with irritable bowel syndrome have altered brain responses to the anticipation of pain and to pain itself, which might make them more sensitive to painful stimuli, reported Dr. Steven M. Berman and his colleagues from the Center for the Neurobiology of Stress at the University of California, Los Angeles.

During expectation of pain, irritable bowel syndrome patients generate higher levels of tonic noradrenergic activity, producing a bias toward interpretation of network activity as pain, and are inefficient at reducing such activity when discrimination of nonpainful stimulation should be maximized, they said (J. Neurosci. 2008;28:349–59).

Functional magnetic resonance imaging (fMRI) was used to measure the blood oxygen level-dependent response to anticipated and delivered rectal distention in 14 female IBS patients and 12 healthy controls (mean age 36 years). When controls were anticipating a painful stimulus, brain activity decreased in several regions, but there was less of this anticipatory deactivation in the IBS patients.

Visceral distention of the rectum was then performed using a computer-driven pump and rectal balloon. Four to six sessions of 16 inflations were performed. Each inflation was preceded by an anticipatory cue. During rectal distention, increases in activity in the insula, dorsal anterior cingulate cortex, and dorsal brainstem were more extensive in IBS patients than in controls.

The results show that during expectation of experimental abdominal/pelvic discomfort, female IBS patients are more anxious and less able than healthy controls to downregulate activity within the CNS network activated by potentially aversive stimuli, the authors noted.

Patients with irritable bowel syndrome have altered brain responses to the anticipation of pain and to pain itself, which might make them more sensitive to painful stimuli, reported Dr. Steven M. Berman and his colleagues from the Center for the Neurobiology of Stress at the University of California, Los Angeles.

During expectation of pain, irritable bowel syndrome patients generate higher levels of tonic noradrenergic activity, producing a bias toward interpretation of network activity as pain, and are inefficient at reducing such activity when discrimination of nonpainful stimulation should be maximized, they said (J. Neurosci. 2008;28:349–59).

Functional magnetic resonance imaging (fMRI) was used to measure the blood oxygen level-dependent response to anticipated and delivered rectal distention in 14 female IBS patients and 12 healthy controls (mean age 36 years). When controls were anticipating a painful stimulus, brain activity decreased in several regions, but there was less of this anticipatory deactivation in the IBS patients.

Visceral distention of the rectum was then performed using a computer-driven pump and rectal balloon. Four to six sessions of 16 inflations were performed. Each inflation was preceded by an anticipatory cue. During rectal distention, increases in activity in the insula, dorsal anterior cingulate cortex, and dorsal brainstem were more extensive in IBS patients than in controls.

The results show that during expectation of experimental abdominal/pelvic discomfort, female IBS patients are more anxious and less able than healthy controls to downregulate activity within the CNS network activated by potentially aversive stimuli, the authors noted.

CHICAGO – Sleep apnea was observed in more than half of children with migraine in a study presented at the annual meeting of the American Academy of Neurology.

Polysomnography revealed sleep apnea in 56% of children with migraine, compared with 30% of those with nonmigraine headache in a study of 90 children aged 5–19 years with headache and sleep complaints.

The association between sleep apnea and migraine was significant, with an odds ratio of 2.1, Dr. Martina Vendrame, chief resident, Temple University Hospital, Philadelphia, and colleagues reported.

Two-thirds of the children with migraine also had frequent arousal during sleep.

Children with chronic migraine, defined as 15 days or more of migraine per month, took longer to fall asleep, had a shorter total sleep time, woke more frequently during the night, and had shorter REM and slow-wave sleep.

“Clinicians should ask all children with headaches and their parents about sleep problems,” including snoring, awakenings during sleep, and day-time sleepiness, Dr. Vendrame told reporters during a press briefing at the meeting. If concerns are raised, patients should be referred to ENT specialists for evaluation and treatment of sleep apnea.

Two-thirds of children in the study identified with sleep apnea were evaluated by ENT specialists, and half underwent tonsillectomy. Of these, 80% had some benefit, including reduced migraine frequency, she said.

Dr. Vendrame acknowledged that the presence of headache could contribute to sleep disturbances, as children suffering from headache will often take daytime naps. In addition, it is widely accepted that headache and sleep disorders share common pathophysiologic mechanisms. Previous studies have evaluated the relationship between headache and sleep disturbances, but this is the first to use polysomnography in children, she said.

The study comprised 60 children with migraine, 11 with chronic daily headaches, 6 with tension headaches, and 13 with nonspecific headaches.

Sleep apnea was also noted among 54% of patients with nonspecific headache, and was observed more frequently in those with a higher body mass index.

Children with chronic daily headache had shorter total sleep time, longer sleep latency, shorter REM sleep, and a higher arousal index.

Among the six children with tension headaches, 50% suffered from teeth grinding, versus 2.4% of children with nontension headaches (OR 1.95).

When asked if the study was biased by having a population of children who already had reported headaches and sleep disturbances, Dr. Vendrame said she hopes to repeat the study in a general population of children, in children without headache, and over an extended period of time to minimize the “first night” effect experienced when children are away from home.

The study was conducted at St. Christopher Hospital for Children, Drexel University, Philadelphia; and the authors had no conflicts of interest to disclose.

CHICAGO – Sleep apnea was observed in more than half of children with migraine in a study presented at the annual meeting of the American Academy of Neurology.

Polysomnography revealed sleep apnea in 56% of children with migraine, compared with 30% of those with nonmigraine headache in a study of 90 children aged 5–19 years with headache and sleep complaints.

The association between sleep apnea and migraine was significant, with an odds ratio of 2.1, Dr. Martina Vendrame, chief resident, Temple University Hospital, Philadelphia, and colleagues reported.

Two-thirds of the children with migraine also had frequent arousal during sleep.

Children with chronic migraine, defined as 15 days or more of migraine per month, took longer to fall asleep, had a shorter total sleep time, woke more frequently during the night, and had shorter REM and slow-wave sleep.

“Clinicians should ask all children with headaches and their parents about sleep problems,” including snoring, awakenings during sleep, and day-time sleepiness, Dr. Vendrame told reporters during a press briefing at the meeting. If concerns are raised, patients should be referred to ENT specialists for evaluation and treatment of sleep apnea.

Two-thirds of children in the study identified with sleep apnea were evaluated by ENT specialists, and half underwent tonsillectomy. Of these, 80% had some benefit, including reduced migraine frequency, she said.

Dr. Vendrame acknowledged that the presence of headache could contribute to sleep disturbances, as children suffering from headache will often take daytime naps. In addition, it is widely accepted that headache and sleep disorders share common pathophysiologic mechanisms. Previous studies have evaluated the relationship between headache and sleep disturbances, but this is the first to use polysomnography in children, she said.

The study comprised 60 children with migraine, 11 with chronic daily headaches, 6 with tension headaches, and 13 with nonspecific headaches.

Sleep apnea was also noted among 54% of patients with nonspecific headache, and was observed more frequently in those with a higher body mass index.

Children with chronic daily headache had shorter total sleep time, longer sleep latency, shorter REM sleep, and a higher arousal index.

Among the six children with tension headaches, 50% suffered from teeth grinding, versus 2.4% of children with nontension headaches (OR 1.95).

When asked if the study was biased by having a population of children who already had reported headaches and sleep disturbances, Dr. Vendrame said she hopes to repeat the study in a general population of children, in children without headache, and over an extended period of time to minimize the “first night” effect experienced when children are away from home.

The study was conducted at St. Christopher Hospital for Children, Drexel University, Philadelphia; and the authors had no conflicts of interest to disclose.

CHICAGO – Sleep apnea was observed in more than half of children with migraine in a study presented at the annual meeting of the American Academy of Neurology.

Polysomnography revealed sleep apnea in 56% of children with migraine, compared with 30% of those with nonmigraine headache in a study of 90 children aged 5–19 years with headache and sleep complaints.

The association between sleep apnea and migraine was significant, with an odds ratio of 2.1, Dr. Martina Vendrame, chief resident, Temple University Hospital, Philadelphia, and colleagues reported.

Two-thirds of the children with migraine also had frequent arousal during sleep.

Children with chronic migraine, defined as 15 days or more of migraine per month, took longer to fall asleep, had a shorter total sleep time, woke more frequently during the night, and had shorter REM and slow-wave sleep.

“Clinicians should ask all children with headaches and their parents about sleep problems,” including snoring, awakenings during sleep, and day-time sleepiness, Dr. Vendrame told reporters during a press briefing at the meeting. If concerns are raised, patients should be referred to ENT specialists for evaluation and treatment of sleep apnea.

Two-thirds of children in the study identified with sleep apnea were evaluated by ENT specialists, and half underwent tonsillectomy. Of these, 80% had some benefit, including reduced migraine frequency, she said.

Dr. Vendrame acknowledged that the presence of headache could contribute to sleep disturbances, as children suffering from headache will often take daytime naps. In addition, it is widely accepted that headache and sleep disorders share common pathophysiologic mechanisms. Previous studies have evaluated the relationship between headache and sleep disturbances, but this is the first to use polysomnography in children, she said.

The study comprised 60 children with migraine, 11 with chronic daily headaches, 6 with tension headaches, and 13 with nonspecific headaches.

Sleep apnea was also noted among 54% of patients with nonspecific headache, and was observed more frequently in those with a higher body mass index.

Children with chronic daily headache had shorter total sleep time, longer sleep latency, shorter REM sleep, and a higher arousal index.

Among the six children with tension headaches, 50% suffered from teeth grinding, versus 2.4% of children with nontension headaches (OR 1.95).

When asked if the study was biased by having a population of children who already had reported headaches and sleep disturbances, Dr. Vendrame said she hopes to repeat the study in a general population of children, in children without headache, and over an extended period of time to minimize the “first night” effect experienced when children are away from home.

The study was conducted at St. Christopher Hospital for Children, Drexel University, Philadelphia; and the authors had no conflicts of interest to disclose.

SCOTTSDALE, ARIZ. – Before traveling from California to South Africa, Dr. Alon Y. Avidan prepared for the time change by spending afternoons in his office, out of the sun. After he arrived in South Africa, he awoke between 5 a.m. and 7 a.m. every morning and took a walk for an hour or more in bright sunlight.

“In a few days, I was on South African time,” he told those attending a meeting on sleep medicine sponsored by the American College of Chest Physicians.

Light therapy can be highly effective in correcting jet lag and other circadian rhythm disorders, according to Dr. Avidan, medical director of the University of California, Los Angeles, neurology clinic and associate director of UCLA's sleep disorders center.

Melatonin, a dietary supplement with no approved medical indications, is another useful treatment when delayed sleep is a problem, he said, and ramelteon (Rozerem) shows promise. Although ramelteon is approved only for insomnia, Dr. Avidan said he prescribes it off label to patients with the type of circadian rhythm disorder that causes night owls to complain they can't fall asleep at normal bedtimes or wake up early in the morning.

Often they are tired all day, but not at night, with detriment to their quality of life. “Circadian-related disruption leads to insomnia, hypersomnia, or both,” he said, and it can cause impairment of social, occupational, or other areas of functioning.

Sunlight is the most powerful external time cue for regulating and synchronizing the body's circadian rhythms with the environment, Dr. Avidan said. It promotes wakefulness as input from the retina goes to the suprachiasmatic nucleus (SCN) of the hypothalamus, which contains a circadian pacemaker.

To opposite ends, the pineal gland releases melatonin in response to darkness. Melatonin promotes sleep, but levels of it decrease with aging. Compensating with the dietary supplement has been shown to help advance the circadian clock, according to Dr. Avidan.

For patients with delayed sleep phase, he recommended exposure to bright light–as much as 10,000 amps–in the early morning and taking 0.5 mg of melatonin 5–7 hours before the patient's habitual sleep time, or 12–14 hours before the time a person wishes to awake.

In response to an audience question, Dr. Avidan said several small studies not yet published suggest ramelteon also can advance sleep time. It acts on the melatonin receptors MT1 and MT2, he noted, and described ramelteon as “a true drug.” When using ramelteon off label for a circadian sleep disorder, he prescribes a 4-mg dose (which is half the 8-mg dose approved for insomnia).

Advanced sleep-phase disorder is often seen in poorly lit nursing homes, according to Dr. Avidan. People become sleepy very early in the evening, which causes them to go to bed before 8 p.m. and wake, still sleepy, as early as 3 a.m. or 4 a.m. To delay sleep time and wake time, he recommended exposure to bright lights from 7 p.m. to 9 p.m., but not melatonin because–in addition to promoting sleep–it can exacerbate coronary artery disease in some patients.

Irregular sleep-wake patterns also are seen in nursing homes, he noted. In these cases, although residents accumulate normal sleep time for their age, they do so in three or more irregular periods of sleep. Low doses of melatonin did not help in a multicenter study with Alzheimer's disease patients, according to Dr. Avidan, but 10-mg doses produced a trend toward improvement.

For patients whose weariness is related to working night shifts, Dr. Avidan suggested having the patients align circadian rhythms by wearing dark glasses in the morning, keeping the bedroom dark, going to bed soon after the night shift, and seeking exposure to bright light while working. Other possible interventions include stimulants such as caffeine and modafinil (approved for excessive sleepiness caused by shift work), short-acting hypnotics for insomnia, and melatonin to improve duration of daytime sleep, although it has shown little impact on alertness during night shifts.

Finally, the direction of travel can affect the presentation and treatment of jet lag. People traveling east across two or more time zones will have difficulty falling asleep, whereas those traveling west may struggle to maintain sleep.

In both cases, he said, exposure to and avoidance of light at appropriate times can be “very, very effective.” People traveling west should seek morning light at the new location and avoid exposure to light in the evening. When traveling east, they should do the opposite. “Avoid light in the early morning, and get as much light as possible in the afternoon/early evening,” Dr. Avidan said.

He said it would be advisable to avoid excessive use of caffeine and alcohol in either direction and added that slow-release caffeine has been shown to improve daytime alertness, and melatonin has been shown to foster sleep after an eastbound flight. For specific recommendations geared to time zones of departure and arrival, he recommended using the jet lag calculator in the travel clinic section of www.fleetstreetclinic.com

Dr. Avidan disclosed receiving a consultant fee and serving on the speakers bureau and advisory committee of Takeda Pharmaceuticals, which sells ramelteon in North America. He also listed relationships with Sepracor Inc., GlaxoSmithKline, and Boehringer Ingelheim.

SCOTTSDALE, ARIZ. – Before traveling from California to South Africa, Dr. Alon Y. Avidan prepared for the time change by spending afternoons in his office, out of the sun. After he arrived in South Africa, he awoke between 5 a.m. and 7 a.m. every morning and took a walk for an hour or more in bright sunlight.

“In a few days, I was on South African time,” he told those attending a meeting on sleep medicine sponsored by the American College of Chest Physicians.

Light therapy can be highly effective in correcting jet lag and other circadian rhythm disorders, according to Dr. Avidan, medical director of the University of California, Los Angeles, neurology clinic and associate director of UCLA's sleep disorders center.

Melatonin, a dietary supplement with no approved medical indications, is another useful treatment when delayed sleep is a problem, he said, and ramelteon (Rozerem) shows promise. Although ramelteon is approved only for insomnia, Dr. Avidan said he prescribes it off label to patients with the type of circadian rhythm disorder that causes night owls to complain they can't fall asleep at normal bedtimes or wake up early in the morning.

Often they are tired all day, but not at night, with detriment to their quality of life. “Circadian-related disruption leads to insomnia, hypersomnia, or both,” he said, and it can cause impairment of social, occupational, or other areas of functioning.

Sunlight is the most powerful external time cue for regulating and synchronizing the body's circadian rhythms with the environment, Dr. Avidan said. It promotes wakefulness as input from the retina goes to the suprachiasmatic nucleus (SCN) of the hypothalamus, which contains a circadian pacemaker.

To opposite ends, the pineal gland releases melatonin in response to darkness. Melatonin promotes sleep, but levels of it decrease with aging. Compensating with the dietary supplement has been shown to help advance the circadian clock, according to Dr. Avidan.

For patients with delayed sleep phase, he recommended exposure to bright light–as much as 10,000 amps–in the early morning and taking 0.5 mg of melatonin 5–7 hours before the patient's habitual sleep time, or 12–14 hours before the time a person wishes to awake.

In response to an audience question, Dr. Avidan said several small studies not yet published suggest ramelteon also can advance sleep time. It acts on the melatonin receptors MT1 and MT2, he noted, and described ramelteon as “a true drug.” When using ramelteon off label for a circadian sleep disorder, he prescribes a 4-mg dose (which is half the 8-mg dose approved for insomnia).

Advanced sleep-phase disorder is often seen in poorly lit nursing homes, according to Dr. Avidan. People become sleepy very early in the evening, which causes them to go to bed before 8 p.m. and wake, still sleepy, as early as 3 a.m. or 4 a.m. To delay sleep time and wake time, he recommended exposure to bright lights from 7 p.m. to 9 p.m., but not melatonin because–in addition to promoting sleep–it can exacerbate coronary artery disease in some patients.

Irregular sleep-wake patterns also are seen in nursing homes, he noted. In these cases, although residents accumulate normal sleep time for their age, they do so in three or more irregular periods of sleep. Low doses of melatonin did not help in a multicenter study with Alzheimer's disease patients, according to Dr. Avidan, but 10-mg doses produced a trend toward improvement.

For patients whose weariness is related to working night shifts, Dr. Avidan suggested having the patients align circadian rhythms by wearing dark glasses in the morning, keeping the bedroom dark, going to bed soon after the night shift, and seeking exposure to bright light while working. Other possible interventions include stimulants such as caffeine and modafinil (approved for excessive sleepiness caused by shift work), short-acting hypnotics for insomnia, and melatonin to improve duration of daytime sleep, although it has shown little impact on alertness during night shifts.

Finally, the direction of travel can affect the presentation and treatment of jet lag. People traveling east across two or more time zones will have difficulty falling asleep, whereas those traveling west may struggle to maintain sleep.

In both cases, he said, exposure to and avoidance of light at appropriate times can be “very, very effective.” People traveling west should seek morning light at the new location and avoid exposure to light in the evening. When traveling east, they should do the opposite. “Avoid light in the early morning, and get as much light as possible in the afternoon/early evening,” Dr. Avidan said.

He said it would be advisable to avoid excessive use of caffeine and alcohol in either direction and added that slow-release caffeine has been shown to improve daytime alertness, and melatonin has been shown to foster sleep after an eastbound flight. For specific recommendations geared to time zones of departure and arrival, he recommended using the jet lag calculator in the travel clinic section of www.fleetstreetclinic.com

Dr. Avidan disclosed receiving a consultant fee and serving on the speakers bureau and advisory committee of Takeda Pharmaceuticals, which sells ramelteon in North America. He also listed relationships with Sepracor Inc., GlaxoSmithKline, and Boehringer Ingelheim.

SCOTTSDALE, ARIZ. – Before traveling from California to South Africa, Dr. Alon Y. Avidan prepared for the time change by spending afternoons in his office, out of the sun. After he arrived in South Africa, he awoke between 5 a.m. and 7 a.m. every morning and took a walk for an hour or more in bright sunlight.

“In a few days, I was on South African time,” he told those attending a meeting on sleep medicine sponsored by the American College of Chest Physicians.

Light therapy can be highly effective in correcting jet lag and other circadian rhythm disorders, according to Dr. Avidan, medical director of the University of California, Los Angeles, neurology clinic and associate director of UCLA's sleep disorders center.

Melatonin, a dietary supplement with no approved medical indications, is another useful treatment when delayed sleep is a problem, he said, and ramelteon (Rozerem) shows promise. Although ramelteon is approved only for insomnia, Dr. Avidan said he prescribes it off label to patients with the type of circadian rhythm disorder that causes night owls to complain they can't fall asleep at normal bedtimes or wake up early in the morning.

Often they are tired all day, but not at night, with detriment to their quality of life. “Circadian-related disruption leads to insomnia, hypersomnia, or both,” he said, and it can cause impairment of social, occupational, or other areas of functioning.

Sunlight is the most powerful external time cue for regulating and synchronizing the body's circadian rhythms with the environment, Dr. Avidan said. It promotes wakefulness as input from the retina goes to the suprachiasmatic nucleus (SCN) of the hypothalamus, which contains a circadian pacemaker.

To opposite ends, the pineal gland releases melatonin in response to darkness. Melatonin promotes sleep, but levels of it decrease with aging. Compensating with the dietary supplement has been shown to help advance the circadian clock, according to Dr. Avidan.

For patients with delayed sleep phase, he recommended exposure to bright light–as much as 10,000 amps–in the early morning and taking 0.5 mg of melatonin 5–7 hours before the patient's habitual sleep time, or 12–14 hours before the time a person wishes to awake.

In response to an audience question, Dr. Avidan said several small studies not yet published suggest ramelteon also can advance sleep time. It acts on the melatonin receptors MT1 and MT2, he noted, and described ramelteon as “a true drug.” When using ramelteon off label for a circadian sleep disorder, he prescribes a 4-mg dose (which is half the 8-mg dose approved for insomnia).

Advanced sleep-phase disorder is often seen in poorly lit nursing homes, according to Dr. Avidan. People become sleepy very early in the evening, which causes them to go to bed before 8 p.m. and wake, still sleepy, as early as 3 a.m. or 4 a.m. To delay sleep time and wake time, he recommended exposure to bright lights from 7 p.m. to 9 p.m., but not melatonin because–in addition to promoting sleep–it can exacerbate coronary artery disease in some patients.

Irregular sleep-wake patterns also are seen in nursing homes, he noted. In these cases, although residents accumulate normal sleep time for their age, they do so in three or more irregular periods of sleep. Low doses of melatonin did not help in a multicenter study with Alzheimer's disease patients, according to Dr. Avidan, but 10-mg doses produced a trend toward improvement.

For patients whose weariness is related to working night shifts, Dr. Avidan suggested having the patients align circadian rhythms by wearing dark glasses in the morning, keeping the bedroom dark, going to bed soon after the night shift, and seeking exposure to bright light while working. Other possible interventions include stimulants such as caffeine and modafinil (approved for excessive sleepiness caused by shift work), short-acting hypnotics for insomnia, and melatonin to improve duration of daytime sleep, although it has shown little impact on alertness during night shifts.

Finally, the direction of travel can affect the presentation and treatment of jet lag. People traveling east across two or more time zones will have difficulty falling asleep, whereas those traveling west may struggle to maintain sleep.

In both cases, he said, exposure to and avoidance of light at appropriate times can be “very, very effective.” People traveling west should seek morning light at the new location and avoid exposure to light in the evening. When traveling east, they should do the opposite. “Avoid light in the early morning, and get as much light as possible in the afternoon/early evening,” Dr. Avidan said.

He said it would be advisable to avoid excessive use of caffeine and alcohol in either direction and added that slow-release caffeine has been shown to improve daytime alertness, and melatonin has been shown to foster sleep after an eastbound flight. For specific recommendations geared to time zones of departure and arrival, he recommended using the jet lag calculator in the travel clinic section of www.fleetstreetclinic.com

Dr. Avidan disclosed receiving a consultant fee and serving on the speakers bureau and advisory committee of Takeda Pharmaceuticals, which sells ramelteon in North America. He also listed relationships with Sepracor Inc., GlaxoSmithKline, and Boehringer Ingelheim.

BALTIMORE – African American women with high levels of hostility show increased levels of fasting glucose. In addition, patients' proportion of trunk fat appears to play a role in the association between hostility and glucose metabolism, results from two posters presented at the annual meeting of the American Psychosomatic Society show.

In the first poster, Anastasia Georgiades, Ph.D., a research associate in the department of psychiatry and behavioral science at Duke University, Durham, N.C., and her colleagues recruited 400 healthy, nondiabetic individuals–101 African American women, 118 white women, 82 African American men, and 99 white men. Mean age was 33 years. Hostility was measured using the 27-item Cook Medley hostility questionnaire. Fasting and postprandial glucose and insulin levels were measured with an oral glucose tolerance test.

General linear modeling showed that African American women had consistent positive associations between hostility and fasting glucose, postprandial glucose, and postprandial insulin. In contrast, African American men showed negative associations. Stratified correlation analysis revealed that only African American women showed a significant positive association between hostility and fasting glucose.

The results indicate that hostility may have a greater impact on glucose metabolism in African American women, which could help explain racial and gender-based health disparities.

The second poster study built on these results, showing a consistent hostility/glucose metabolism association among African American women. Dr. Georgiades and her colleagues hypothesized that this relationship might be mediated by trunk fat, given that abdominal fat has been associated with both fasting glucose levels and insulin resistance.

For the study, the researchers recruited 44 African American and 77 white nondiabetic women. The women had either high (greater than 12) or low (less than 9) scores on the 27-item Cook Medley hostility questionnaire. The women underwent several assessments, including an oral fasting glucose tolerance test and dual-energy x-ray absorptiometry (DXA) scan. The researchers included DXA scans because body mass index is a rather imprecise measure of body fat and does not take into account the distribution of body fat. DXA technology gives a highly accurate estimate of percent body fat, and its distribution, Dr. Georgiades said in an interview.

After the researchers controlled for age and race, hostility was significantly associated with greater fasting glucose levels and greater percentage trunk fat but not BMI or fasting insulin for the entire cohort. The association between hostility and fasting glucose was significant for African American women and white women. No significant association was found between race and hostility with respect to fasting glucose. However, there was a significant interaction between race and trunk fat with respect to fasting glucose. In other words, there was a significant correlation between fasting glucose and trunk fat in African American women but not in white women.

“It was clear that the African American women had higher percentage of trunk fat as compared to the [white] women, and that the association between trunk fat and fasting glucose was very strong in African American women, but was not evident in the [white] women,” Dr. Georgiades said.

Controlling for trunk fat reduced the association between hostility and fasting glucose in African American women. A formal test of mediation revealed a significant mediating effect of trunk fat in the association between hostility and fasting glucose among African American women.

“We are not sure exactly why trunk fat mediated the association between hostility and glucose only in African American females. However, a previous study found that African American women have a higher density of β receptor in the fat tissue located around the inner organs as compared to [white] women,” Dr. Georgiades said.

This could potentially make African American women more susceptible to the effects of adrenergic stimulation through stress hormones such as epinephrine and norepinephrine. Epinephrine stimulation of visceral fat tissue has been shown to induce lipolysis, bathing the liver with nonesterified fatty acids, and rendering it insulin resistant.

BALTIMORE – African American women with high levels of hostility show increased levels of fasting glucose. In addition, patients' proportion of trunk fat appears to play a role in the association between hostility and glucose metabolism, results from two posters presented at the annual meeting of the American Psychosomatic Society show.

In the first poster, Anastasia Georgiades, Ph.D., a research associate in the department of psychiatry and behavioral science at Duke University, Durham, N.C., and her colleagues recruited 400 healthy, nondiabetic individuals–101 African American women, 118 white women, 82 African American men, and 99 white men. Mean age was 33 years. Hostility was measured using the 27-item Cook Medley hostility questionnaire. Fasting and postprandial glucose and insulin levels were measured with an oral glucose tolerance test.

General linear modeling showed that African American women had consistent positive associations between hostility and fasting glucose, postprandial glucose, and postprandial insulin. In contrast, African American men showed negative associations. Stratified correlation analysis revealed that only African American women showed a significant positive association between hostility and fasting glucose.

The results indicate that hostility may have a greater impact on glucose metabolism in African American women, which could help explain racial and gender-based health disparities.

The second poster study built on these results, showing a consistent hostility/glucose metabolism association among African American women. Dr. Georgiades and her colleagues hypothesized that this relationship might be mediated by trunk fat, given that abdominal fat has been associated with both fasting glucose levels and insulin resistance.

For the study, the researchers recruited 44 African American and 77 white nondiabetic women. The women had either high (greater than 12) or low (less than 9) scores on the 27-item Cook Medley hostility questionnaire. The women underwent several assessments, including an oral fasting glucose tolerance test and dual-energy x-ray absorptiometry (DXA) scan. The researchers included DXA scans because body mass index is a rather imprecise measure of body fat and does not take into account the distribution of body fat. DXA technology gives a highly accurate estimate of percent body fat, and its distribution, Dr. Georgiades said in an interview.

After the researchers controlled for age and race, hostility was significantly associated with greater fasting glucose levels and greater percentage trunk fat but not BMI or fasting insulin for the entire cohort. The association between hostility and fasting glucose was significant for African American women and white women. No significant association was found between race and hostility with respect to fasting glucose. However, there was a significant interaction between race and trunk fat with respect to fasting glucose. In other words, there was a significant correlation between fasting glucose and trunk fat in African American women but not in white women.

“It was clear that the African American women had higher percentage of trunk fat as compared to the [white] women, and that the association between trunk fat and fasting glucose was very strong in African American women, but was not evident in the [white] women,” Dr. Georgiades said.

Controlling for trunk fat reduced the association between hostility and fasting glucose in African American women. A formal test of mediation revealed a significant mediating effect of trunk fat in the association between hostility and fasting glucose among African American women.

“We are not sure exactly why trunk fat mediated the association between hostility and glucose only in African American females. However, a previous study found that African American women have a higher density of β receptor in the fat tissue located around the inner organs as compared to [white] women,” Dr. Georgiades said.

This could potentially make African American women more susceptible to the effects of adrenergic stimulation through stress hormones such as epinephrine and norepinephrine. Epinephrine stimulation of visceral fat tissue has been shown to induce lipolysis, bathing the liver with nonesterified fatty acids, and rendering it insulin resistant.

BALTIMORE – African American women with high levels of hostility show increased levels of fasting glucose. In addition, patients' proportion of trunk fat appears to play a role in the association between hostility and glucose metabolism, results from two posters presented at the annual meeting of the American Psychosomatic Society show.

In the first poster, Anastasia Georgiades, Ph.D., a research associate in the department of psychiatry and behavioral science at Duke University, Durham, N.C., and her colleagues recruited 400 healthy, nondiabetic individuals–101 African American women, 118 white women, 82 African American men, and 99 white men. Mean age was 33 years. Hostility was measured using the 27-item Cook Medley hostility questionnaire. Fasting and postprandial glucose and insulin levels were measured with an oral glucose tolerance test.

General linear modeling showed that African American women had consistent positive associations between hostility and fasting glucose, postprandial glucose, and postprandial insulin. In contrast, African American men showed negative associations. Stratified correlation analysis revealed that only African American women showed a significant positive association between hostility and fasting glucose.

The results indicate that hostility may have a greater impact on glucose metabolism in African American women, which could help explain racial and gender-based health disparities.

The second poster study built on these results, showing a consistent hostility/glucose metabolism association among African American women. Dr. Georgiades and her colleagues hypothesized that this relationship might be mediated by trunk fat, given that abdominal fat has been associated with both fasting glucose levels and insulin resistance.

For the study, the researchers recruited 44 African American and 77 white nondiabetic women. The women had either high (greater than 12) or low (less than 9) scores on the 27-item Cook Medley hostility questionnaire. The women underwent several assessments, including an oral fasting glucose tolerance test and dual-energy x-ray absorptiometry (DXA) scan. The researchers included DXA scans because body mass index is a rather imprecise measure of body fat and does not take into account the distribution of body fat. DXA technology gives a highly accurate estimate of percent body fat, and its distribution, Dr. Georgiades said in an interview.

After the researchers controlled for age and race, hostility was significantly associated with greater fasting glucose levels and greater percentage trunk fat but not BMI or fasting insulin for the entire cohort. The association between hostility and fasting glucose was significant for African American women and white women. No significant association was found between race and hostility with respect to fasting glucose. However, there was a significant interaction between race and trunk fat with respect to fasting glucose. In other words, there was a significant correlation between fasting glucose and trunk fat in African American women but not in white women.

“It was clear that the African American women had higher percentage of trunk fat as compared to the [white] women, and that the association between trunk fat and fasting glucose was very strong in African American women, but was not evident in the [white] women,” Dr. Georgiades said.

Controlling for trunk fat reduced the association between hostility and fasting glucose in African American women. A formal test of mediation revealed a significant mediating effect of trunk fat in the association between hostility and fasting glucose among African American women.

“We are not sure exactly why trunk fat mediated the association between hostility and glucose only in African American females. However, a previous study found that African American women have a higher density of β receptor in the fat tissue located around the inner organs as compared to [white] women,” Dr. Georgiades said.

This could potentially make African American women more susceptible to the effects of adrenergic stimulation through stress hormones such as epinephrine and norepinephrine. Epinephrine stimulation of visceral fat tissue has been shown to induce lipolysis, bathing the liver with nonesterified fatty acids, and rendering it insulin resistant.

NEW ORLEANS – Increased diastolic blood pressure levels are associated with cognitive impairment, findings from the Reasons for Geographic and Racial Differences in Stroke study suggest.

More than 27,800 participants from REGARDS–a long-term, ongoing study designed to investigate the reasons why stroke-related mortality is more common in portions of the southeastern United States (the “stroke belt”) and among blacks–were included in the analysis.

The patients were evaluated in an effort to identify associations between blood pressure indices and cognitive function, as well as any potential interactions between blood pressure indices and age in cognitive function, and any possible racial differences in the relationship between blood pressure and cognition, Dr. Georgios Tsivgoulis, lead author in this portion of the study, reported at the International Stroke Conference 2008.

Findings from previous studies have been conflicting in regard to such interactions, but in this very large cohort of patients, the relationship between diastolic blood pressure levels and cognitive impairment persisted even after adjusting for a host of demographic characteristics, environmental factors, vascular risk factors, health behaviors, and depressive symptoms (odds ratio, 1.08 per 10 mm Hg change for cognitive impairment with increased diastolic blood pressure), said Dr. Tsivgoulis of the University of Alabama at Birmingham.

No interactions were seen between blood pressure and age in impaired cognitive function, nor were racial differences noted in the associations between blood pressure and cognitive status, he said at the conference, which was sponsored by the American Stroke Association.

Study participants were at least 45 years of age (mean age, 66 years in the current cohort), and lived in various areas across the United States, with oversampling in the stroke belt. Whites and blacks, as well as men and women, were equally represented.

These preliminary results did not give enough information to determine the reason for the existence of the “stroke belt,” and Dr. Tsivgoulis didn't speculate on that in his presentation.

Cognitive status was assessed using the 6-item screen derived from the Mini-Mental State Examination. Patients with a score of 4 or less were considered to have cognitive impairment. Cognitive status was validated against other cognitive measures for the diagnosis of dementia, and depression was assessed using the Center for Epidemiologic Studies Depression 4-item scale.

The finding of a linear and cross-sectional association between higher diastolic blood pressure and impaired cognitive status suggests that the careful monitoring and control of elevated blood pressure could contribute to the preservation of cognitive function, Dr. Tsivgoulis concluded.

The study was funded by the National Institute of Neurological Disorders and Stroke.

NEW ORLEANS – Increased diastolic blood pressure levels are associated with cognitive impairment, findings from the Reasons for Geographic and Racial Differences in Stroke study suggest.

More than 27,800 participants from REGARDS–a long-term, ongoing study designed to investigate the reasons why stroke-related mortality is more common in portions of the southeastern United States (the “stroke belt”) and among blacks–were included in the analysis.

The patients were evaluated in an effort to identify associations between blood pressure indices and cognitive function, as well as any potential interactions between blood pressure indices and age in cognitive function, and any possible racial differences in the relationship between blood pressure and cognition, Dr. Georgios Tsivgoulis, lead author in this portion of the study, reported at the International Stroke Conference 2008.

Findings from previous studies have been conflicting in regard to such interactions, but in this very large cohort of patients, the relationship between diastolic blood pressure levels and cognitive impairment persisted even after adjusting for a host of demographic characteristics, environmental factors, vascular risk factors, health behaviors, and depressive symptoms (odds ratio, 1.08 per 10 mm Hg change for cognitive impairment with increased diastolic blood pressure), said Dr. Tsivgoulis of the University of Alabama at Birmingham.

No interactions were seen between blood pressure and age in impaired cognitive function, nor were racial differences noted in the associations between blood pressure and cognitive status, he said at the conference, which was sponsored by the American Stroke Association.

Study participants were at least 45 years of age (mean age, 66 years in the current cohort), and lived in various areas across the United States, with oversampling in the stroke belt. Whites and blacks, as well as men and women, were equally represented.

These preliminary results did not give enough information to determine the reason for the existence of the “stroke belt,” and Dr. Tsivgoulis didn't speculate on that in his presentation.

Cognitive status was assessed using the 6-item screen derived from the Mini-Mental State Examination. Patients with a score of 4 or less were considered to have cognitive impairment. Cognitive status was validated against other cognitive measures for the diagnosis of dementia, and depression was assessed using the Center for Epidemiologic Studies Depression 4-item scale.

The finding of a linear and cross-sectional association between higher diastolic blood pressure and impaired cognitive status suggests that the careful monitoring and control of elevated blood pressure could contribute to the preservation of cognitive function, Dr. Tsivgoulis concluded.

The study was funded by the National Institute of Neurological Disorders and Stroke.

NEW ORLEANS – Increased diastolic blood pressure levels are associated with cognitive impairment, findings from the Reasons for Geographic and Racial Differences in Stroke study suggest.

More than 27,800 participants from REGARDS–a long-term, ongoing study designed to investigate the reasons why stroke-related mortality is more common in portions of the southeastern United States (the “stroke belt”) and among blacks–were included in the analysis.

The patients were evaluated in an effort to identify associations between blood pressure indices and cognitive function, as well as any potential interactions between blood pressure indices and age in cognitive function, and any possible racial differences in the relationship between blood pressure and cognition, Dr. Georgios Tsivgoulis, lead author in this portion of the study, reported at the International Stroke Conference 2008.

Findings from previous studies have been conflicting in regard to such interactions, but in this very large cohort of patients, the relationship between diastolic blood pressure levels and cognitive impairment persisted even after adjusting for a host of demographic characteristics, environmental factors, vascular risk factors, health behaviors, and depressive symptoms (odds ratio, 1.08 per 10 mm Hg change for cognitive impairment with increased diastolic blood pressure), said Dr. Tsivgoulis of the University of Alabama at Birmingham.

No interactions were seen between blood pressure and age in impaired cognitive function, nor were racial differences noted in the associations between blood pressure and cognitive status, he said at the conference, which was sponsored by the American Stroke Association.

Study participants were at least 45 years of age (mean age, 66 years in the current cohort), and lived in various areas across the United States, with oversampling in the stroke belt. Whites and blacks, as well as men and women, were equally represented.

These preliminary results did not give enough information to determine the reason for the existence of the “stroke belt,” and Dr. Tsivgoulis didn't speculate on that in his presentation.

Cognitive status was assessed using the 6-item screen derived from the Mini-Mental State Examination. Patients with a score of 4 or less were considered to have cognitive impairment. Cognitive status was validated against other cognitive measures for the diagnosis of dementia, and depression was assessed using the Center for Epidemiologic Studies Depression 4-item scale.

The finding of a linear and cross-sectional association between higher diastolic blood pressure and impaired cognitive status suggests that the careful monitoring and control of elevated blood pressure could contribute to the preservation of cognitive function, Dr. Tsivgoulis concluded.

The study was funded by the National Institute of Neurological Disorders and Stroke.