Somatic Disorders

TUCSON, ARIZ. – Complementary herbal and nutritional therapies can play an important role in an integrated psychiatric practice, Dr. Iris R. Bell said at a psychopharmacology conference sponsored by the University of Arizona.

Disputes remain about the lack of randomized trials supporting the use of complementary and alternative medicine (CAM). But evidence continues to mount about the benefits of CAM therapy that is individualized to a patient's specific needs and preferences.

The use of broad-based nutritional supplements has been reported to ameliorate psychiatric symptoms such as mood swings, depression, and aggression in a variety of patients, including young criminal offenders. The mechanisms by which these changes occur are not established. But the supplements may provide the nutritional support needed to improve brain chemistry and promote better use of traditional medications, said Dr. Bell, a professor at the university and director of research for its integrative medicine program.

Activated forms of pyridoxine, niacin, iron, and tetrahydrobiopterin are cofactors for the enzymes tyrosine hydroxylase and tryptophan 5-hydroxylase, which participate in brain biosynthesis of catecholamines and serotonin. It has been shown that patients with the melancholic form of depression have low levels of folate and respond poorly to fluoxetine, in part because they don't have adequate neurotransmitters to use it, she said.

Studies of high-dose antioxidant supplements by themselves, such as vitamin E alone in Parkinson's disease, may have failed because the vitamin needs other components of its biochemical network, such as vitamin C and other nutrients, to regenerate antioxidant forms from prooxidant forms of the vitamin, Dr. Bell said. Folate, B₁₂, and B₆ vitamin supplements are now being used together as a low-risk strategy to lower homocysteine levels in Alzheimer's patients. Studies suggest that elevated homocysteine is an independent risk factor for Alzheimer's disease and a variety of vascular diseases. “We may have a more preventive role to play than we thought,” she said.

Ginkgo biloba has produced mixed results in patients with dementia and should be used with caution in those patients on concomitant warfarin or other anticoagulant agents, Dr. Bell said.

Small controlled studies have shown that kava kava can reduce anxiety over a 4-week period, but Dr. Bell said she is uncomfortable recommending its because of the potential for serious liver damage from the forms available in Western countries.

The folk remedy passion flower has been helpful in generalized anxiety and when used in combination with clonidine to reduce mental symptoms in opiate addicts. “It might provide an added benefit to get them through acute withdrawal, but it's not a long-term solution,” Dr. Bell said.

TUCSON, ARIZ. – Complementary herbal and nutritional therapies can play an important role in an integrated psychiatric practice, Dr. Iris R. Bell said at a psychopharmacology conference sponsored by the University of Arizona.

Disputes remain about the lack of randomized trials supporting the use of complementary and alternative medicine (CAM). But evidence continues to mount about the benefits of CAM therapy that is individualized to a patient's specific needs and preferences.

The use of broad-based nutritional supplements has been reported to ameliorate psychiatric symptoms such as mood swings, depression, and aggression in a variety of patients, including young criminal offenders. The mechanisms by which these changes occur are not established. But the supplements may provide the nutritional support needed to improve brain chemistry and promote better use of traditional medications, said Dr. Bell, a professor at the university and director of research for its integrative medicine program.

Activated forms of pyridoxine, niacin, iron, and tetrahydrobiopterin are cofactors for the enzymes tyrosine hydroxylase and tryptophan 5-hydroxylase, which participate in brain biosynthesis of catecholamines and serotonin. It has been shown that patients with the melancholic form of depression have low levels of folate and respond poorly to fluoxetine, in part because they don't have adequate neurotransmitters to use it, she said.

Studies of high-dose antioxidant supplements by themselves, such as vitamin E alone in Parkinson's disease, may have failed because the vitamin needs other components of its biochemical network, such as vitamin C and other nutrients, to regenerate antioxidant forms from prooxidant forms of the vitamin, Dr. Bell said. Folate, B₁₂, and B₆ vitamin supplements are now being used together as a low-risk strategy to lower homocysteine levels in Alzheimer's patients. Studies suggest that elevated homocysteine is an independent risk factor for Alzheimer's disease and a variety of vascular diseases. “We may have a more preventive role to play than we thought,” she said.

Ginkgo biloba has produced mixed results in patients with dementia and should be used with caution in those patients on concomitant warfarin or other anticoagulant agents, Dr. Bell said.

Small controlled studies have shown that kava kava can reduce anxiety over a 4-week period, but Dr. Bell said she is uncomfortable recommending its because of the potential for serious liver damage from the forms available in Western countries.

The folk remedy passion flower has been helpful in generalized anxiety and when used in combination with clonidine to reduce mental symptoms in opiate addicts. “It might provide an added benefit to get them through acute withdrawal, but it's not a long-term solution,” Dr. Bell said.

TUCSON, ARIZ. – Complementary herbal and nutritional therapies can play an important role in an integrated psychiatric practice, Dr. Iris R. Bell said at a psychopharmacology conference sponsored by the University of Arizona.

Disputes remain about the lack of randomized trials supporting the use of complementary and alternative medicine (CAM). But evidence continues to mount about the benefits of CAM therapy that is individualized to a patient's specific needs and preferences.

The use of broad-based nutritional supplements has been reported to ameliorate psychiatric symptoms such as mood swings, depression, and aggression in a variety of patients, including young criminal offenders. The mechanisms by which these changes occur are not established. But the supplements may provide the nutritional support needed to improve brain chemistry and promote better use of traditional medications, said Dr. Bell, a professor at the university and director of research for its integrative medicine program.

Activated forms of pyridoxine, niacin, iron, and tetrahydrobiopterin are cofactors for the enzymes tyrosine hydroxylase and tryptophan 5-hydroxylase, which participate in brain biosynthesis of catecholamines and serotonin. It has been shown that patients with the melancholic form of depression have low levels of folate and respond poorly to fluoxetine, in part because they don't have adequate neurotransmitters to use it, she said.

Studies of high-dose antioxidant supplements by themselves, such as vitamin E alone in Parkinson's disease, may have failed because the vitamin needs other components of its biochemical network, such as vitamin C and other nutrients, to regenerate antioxidant forms from prooxidant forms of the vitamin, Dr. Bell said. Folate, B₁₂, and B₆ vitamin supplements are now being used together as a low-risk strategy to lower homocysteine levels in Alzheimer's patients. Studies suggest that elevated homocysteine is an independent risk factor for Alzheimer's disease and a variety of vascular diseases. “We may have a more preventive role to play than we thought,” she said.

Ginkgo biloba has produced mixed results in patients with dementia and should be used with caution in those patients on concomitant warfarin or other anticoagulant agents, Dr. Bell said.

Small controlled studies have shown that kava kava can reduce anxiety over a 4-week period, but Dr. Bell said she is uncomfortable recommending its because of the potential for serious liver damage from the forms available in Western countries.

The folk remedy passion flower has been helpful in generalized anxiety and when used in combination with clonidine to reduce mental symptoms in opiate addicts. “It might provide an added benefit to get them through acute withdrawal, but it's not a long-term solution,” Dr. Bell said.

SAN JUAN, P.R. – Women who experience stressful life events, especially trauma, together with depression have a shorter time to breast cancer progression than women with no such history, Dr. David Spiegel said at the annual meeting of the American College of Psychiatrists.

Based on this study, which is under review, screening women with breast cancer for depression and stressful and/or traumatic life events might be worthwhile, said Dr. Spiegel, Willson Professor at Stanford (Calif.) University.

In a second study he conducted with Janine Giese-Davis, Ph.D., antidepressant treatment improved survival in this population. Improving depression might improve breast cancer prognosis independent of other risk factors that affect survival, such as metastatic spread of disease, he said.

So what is the connection? The combination of trauma and depression may dysregulate the hypothalamic-pituitary-adrenal (HPA) axis and lead to more stress among women with breast cancer. “Our breast cancer patients look more like depressed patients than healthy people, which means they may share some aspect of HPA dysregulation,” Dr. Spiegel said.

Stressful life events can diminish a person's ability to handle subsequent challenges, including cancer. Diminished physical capability, changes in social environment and family roles, difficult treatments, fear, pain, and facing mortality can all cause stress in women with breast cancer.

“Cancer is a chronic and severe stressor with constant reminders because of its effects on the body,” said Dr. Spiegel, who is also a member of the university's comprehensive cancer center.

Chronic stress causes changes to brain structures and the endocrine system, according to neuroimaging and other studies in humans and animals. Specifically, researchers have found that stress alters the size and/or activation of the hippocampus and amygdala.

“A smaller amygdala and hippocampus do not buffer a patient from the effects of stressful life situations as well,” he said.

Other researchers determined that serious life events increase risk of cancer (Am. J. Epidemiol. 2003;157:415–23).

This prospective study included 10,808 women in Finland surveyed in 1981 about adverse life events. A total of 180 incident cases of breast cancer occurred between 1982 and 1996. Participants who reported any single event had a slightly elevated risk of breast cancer compared with controls (hazard ratio, 1.07). The risk increased with a major event (1.35), death of close relative or friend (1.36), death of husband (2.00), and divorce or separation (2.26). “The findings suggest a role for life events in breast cancer etiology through hormonal or other mechanisms,” the researchers wrote.

“We looked at our own data, and those with an early stress, especially early trauma, have a shorter time to progression of breast cancer from diagnosis compared to women with no such history,” Dr. Spiegel said.

Stress is not the only culprit. “A shorter disease-free interval has also been shown with depression,” and the study he conducted with Dr. Giese-Davis showed that “if you treat depression, you can improve survival,” he said.

Stress can also adversely affect the endocrine system. People with posttraumatic stress disorder or depression tend to have constant levels of cortisol throughout the day. Normally, cortisol levels increase and decrease according to a circadian rhythm. “Waking up is stressful–think of getting up this morning,” Dr. Spiegel said, “and in healthy individuals, cortisol levels are five times higher in the morning compared to at bedtime.”

He and another group of investigators have published data showing that these abnormal cortisol patterns predict shorter survival with breast cancer (J. Natl. Cancer Inst. 2000;92:994–1000).

When a person attending the meeting asked about changes in catecholamine levels, Dr. Spiegel said, “We did not measure that–cortisol is easier to measure.”

Dr. Spiegel said that patients with relatively flat cortisol slopes have fewer natural killer cells. As breast cancer progresses, natural killer cell levels tend to decrease “so it's a salient finding, because this component of the immune system is linked to cancer progression.

“We are trying to construct a model that links a history of stress or trauma to progression of cancer,” he said.

'Our breast cancer patients look more like depressed patients than healthy people.' DR. SPIEGEL

SAN JUAN, P.R. – Women who experience stressful life events, especially trauma, together with depression have a shorter time to breast cancer progression than women with no such history, Dr. David Spiegel said at the annual meeting of the American College of Psychiatrists.

Based on this study, which is under review, screening women with breast cancer for depression and stressful and/or traumatic life events might be worthwhile, said Dr. Spiegel, Willson Professor at Stanford (Calif.) University.

In a second study he conducted with Janine Giese-Davis, Ph.D., antidepressant treatment improved survival in this population. Improving depression might improve breast cancer prognosis independent of other risk factors that affect survival, such as metastatic spread of disease, he said.

So what is the connection? The combination of trauma and depression may dysregulate the hypothalamic-pituitary-adrenal (HPA) axis and lead to more stress among women with breast cancer. “Our breast cancer patients look more like depressed patients than healthy people, which means they may share some aspect of HPA dysregulation,” Dr. Spiegel said.

Stressful life events can diminish a person's ability to handle subsequent challenges, including cancer. Diminished physical capability, changes in social environment and family roles, difficult treatments, fear, pain, and facing mortality can all cause stress in women with breast cancer.

“Cancer is a chronic and severe stressor with constant reminders because of its effects on the body,” said Dr. Spiegel, who is also a member of the university's comprehensive cancer center.

Chronic stress causes changes to brain structures and the endocrine system, according to neuroimaging and other studies in humans and animals. Specifically, researchers have found that stress alters the size and/or activation of the hippocampus and amygdala.

“A smaller amygdala and hippocampus do not buffer a patient from the effects of stressful life situations as well,” he said.

Other researchers determined that serious life events increase risk of cancer (Am. J. Epidemiol. 2003;157:415–23).

This prospective study included 10,808 women in Finland surveyed in 1981 about adverse life events. A total of 180 incident cases of breast cancer occurred between 1982 and 1996. Participants who reported any single event had a slightly elevated risk of breast cancer compared with controls (hazard ratio, 1.07). The risk increased with a major event (1.35), death of close relative or friend (1.36), death of husband (2.00), and divorce or separation (2.26). “The findings suggest a role for life events in breast cancer etiology through hormonal or other mechanisms,” the researchers wrote.

“We looked at our own data, and those with an early stress, especially early trauma, have a shorter time to progression of breast cancer from diagnosis compared to women with no such history,” Dr. Spiegel said.

Stress is not the only culprit. “A shorter disease-free interval has also been shown with depression,” and the study he conducted with Dr. Giese-Davis showed that “if you treat depression, you can improve survival,” he said.

Stress can also adversely affect the endocrine system. People with posttraumatic stress disorder or depression tend to have constant levels of cortisol throughout the day. Normally, cortisol levels increase and decrease according to a circadian rhythm. “Waking up is stressful–think of getting up this morning,” Dr. Spiegel said, “and in healthy individuals, cortisol levels are five times higher in the morning compared to at bedtime.”

He and another group of investigators have published data showing that these abnormal cortisol patterns predict shorter survival with breast cancer (J. Natl. Cancer Inst. 2000;92:994–1000).

When a person attending the meeting asked about changes in catecholamine levels, Dr. Spiegel said, “We did not measure that–cortisol is easier to measure.”

Dr. Spiegel said that patients with relatively flat cortisol slopes have fewer natural killer cells. As breast cancer progresses, natural killer cell levels tend to decrease “so it's a salient finding, because this component of the immune system is linked to cancer progression.

“We are trying to construct a model that links a history of stress or trauma to progression of cancer,” he said.

'Our breast cancer patients look more like depressed patients than healthy people.' DR. SPIEGEL

SAN JUAN, P.R. – Women who experience stressful life events, especially trauma, together with depression have a shorter time to breast cancer progression than women with no such history, Dr. David Spiegel said at the annual meeting of the American College of Psychiatrists.

Based on this study, which is under review, screening women with breast cancer for depression and stressful and/or traumatic life events might be worthwhile, said Dr. Spiegel, Willson Professor at Stanford (Calif.) University.

In a second study he conducted with Janine Giese-Davis, Ph.D., antidepressant treatment improved survival in this population. Improving depression might improve breast cancer prognosis independent of other risk factors that affect survival, such as metastatic spread of disease, he said.

So what is the connection? The combination of trauma and depression may dysregulate the hypothalamic-pituitary-adrenal (HPA) axis and lead to more stress among women with breast cancer. “Our breast cancer patients look more like depressed patients than healthy people, which means they may share some aspect of HPA dysregulation,” Dr. Spiegel said.

Stressful life events can diminish a person's ability to handle subsequent challenges, including cancer. Diminished physical capability, changes in social environment and family roles, difficult treatments, fear, pain, and facing mortality can all cause stress in women with breast cancer.

“Cancer is a chronic and severe stressor with constant reminders because of its effects on the body,” said Dr. Spiegel, who is also a member of the university's comprehensive cancer center.

Chronic stress causes changes to brain structures and the endocrine system, according to neuroimaging and other studies in humans and animals. Specifically, researchers have found that stress alters the size and/or activation of the hippocampus and amygdala.

“A smaller amygdala and hippocampus do not buffer a patient from the effects of stressful life situations as well,” he said.

Other researchers determined that serious life events increase risk of cancer (Am. J. Epidemiol. 2003;157:415–23).

This prospective study included 10,808 women in Finland surveyed in 1981 about adverse life events. A total of 180 incident cases of breast cancer occurred between 1982 and 1996. Participants who reported any single event had a slightly elevated risk of breast cancer compared with controls (hazard ratio, 1.07). The risk increased with a major event (1.35), death of close relative or friend (1.36), death of husband (2.00), and divorce or separation (2.26). “The findings suggest a role for life events in breast cancer etiology through hormonal or other mechanisms,” the researchers wrote.

“We looked at our own data, and those with an early stress, especially early trauma, have a shorter time to progression of breast cancer from diagnosis compared to women with no such history,” Dr. Spiegel said.

Stress is not the only culprit. “A shorter disease-free interval has also been shown with depression,” and the study he conducted with Dr. Giese-Davis showed that “if you treat depression, you can improve survival,” he said.

Stress can also adversely affect the endocrine system. People with posttraumatic stress disorder or depression tend to have constant levels of cortisol throughout the day. Normally, cortisol levels increase and decrease according to a circadian rhythm. “Waking up is stressful–think of getting up this morning,” Dr. Spiegel said, “and in healthy individuals, cortisol levels are five times higher in the morning compared to at bedtime.”

He and another group of investigators have published data showing that these abnormal cortisol patterns predict shorter survival with breast cancer (J. Natl. Cancer Inst. 2000;92:994–1000).

When a person attending the meeting asked about changes in catecholamine levels, Dr. Spiegel said, “We did not measure that–cortisol is easier to measure.”

Dr. Spiegel said that patients with relatively flat cortisol slopes have fewer natural killer cells. As breast cancer progresses, natural killer cell levels tend to decrease “so it's a salient finding, because this component of the immune system is linked to cancer progression.

“We are trying to construct a model that links a history of stress or trauma to progression of cancer,” he said.

'Our breast cancer patients look more like depressed patients than healthy people.' DR. SPIEGEL

NEW YORK – There is mounting evidence that stress and the way in which patients with psoriasis view themselves or perceive themselves to be seen affects the way that they respond to treatment, Dr. Christopher Griffiths said at a dermatology symposium sponsored by Cornell University.

“While the exact etiology of psoriasis remains unknown, there is a strong environmental component to the disease, including stress, especially in the genetically predisposed with the HLA-Cw6 gene,” said Dr. Griffiths of the dermatology center at Hope Hospital, University of Manchester (England), the largest center for psoriasis research and treatment in the world.

Psoriasis occurs in about 2% of the population. Whether stress causes psoriasis or psoriasis is the origin of stress is still a point of contention. Studies have shown that psoriasis ranks just ahead of chronic lung disease and depression when it comes to the impact reported on the daily lives of patients, with 46% reporting an impact on their daily lives, versus 44% and 35% with chronic lung disease and depression, respectively. Approximately 60% of patients with psoriasis report that stressful life events may either trigger or exacerbate their condition, Dr. Griffiths said.

With 53% of patients strongly affected by how they view themselves and 28% by how they see themselves viewed by others, “psoriasis strongly affects how patients see themselves and how they think others see them,” he said.

“Patients with psoriasis are constantly looking for environmental cues which might be signs of how others are viewing them,” Dr. Griffiths noted.

A study using the Penn State Worry Questionnaire to measure whether worry affected 88 patients' (57 males, 31 females) response to PUVA therapy showed a correlation between worry and treatment efficacy. Patients who were high or pathologic worriers were less likely to show a response to PUVA therapy than were patients in the normal or low worry categories. “Those patients who did respond took twice as long to respond to PUVA treatment if they were higher on the worry scale,” Dr. Griffiths said.

The average age of patients in the study was 43 years.

Dr. Griffiths also reported that managing psoriasis symptoms with adjuncts such as behavioral therapy measurably enhances response to standard therapy.

Psoriasis patients always look for environmental cues that might be signs of how others are viewing them. DR. GRIFFITHS

NEW YORK – There is mounting evidence that stress and the way in which patients with psoriasis view themselves or perceive themselves to be seen affects the way that they respond to treatment, Dr. Christopher Griffiths said at a dermatology symposium sponsored by Cornell University.

“While the exact etiology of psoriasis remains unknown, there is a strong environmental component to the disease, including stress, especially in the genetically predisposed with the HLA-Cw6 gene,” said Dr. Griffiths of the dermatology center at Hope Hospital, University of Manchester (England), the largest center for psoriasis research and treatment in the world.

Psoriasis occurs in about 2% of the population. Whether stress causes psoriasis or psoriasis is the origin of stress is still a point of contention. Studies have shown that psoriasis ranks just ahead of chronic lung disease and depression when it comes to the impact reported on the daily lives of patients, with 46% reporting an impact on their daily lives, versus 44% and 35% with chronic lung disease and depression, respectively. Approximately 60% of patients with psoriasis report that stressful life events may either trigger or exacerbate their condition, Dr. Griffiths said.

With 53% of patients strongly affected by how they view themselves and 28% by how they see themselves viewed by others, “psoriasis strongly affects how patients see themselves and how they think others see them,” he said.

“Patients with psoriasis are constantly looking for environmental cues which might be signs of how others are viewing them,” Dr. Griffiths noted.

A study using the Penn State Worry Questionnaire to measure whether worry affected 88 patients' (57 males, 31 females) response to PUVA therapy showed a correlation between worry and treatment efficacy. Patients who were high or pathologic worriers were less likely to show a response to PUVA therapy than were patients in the normal or low worry categories. “Those patients who did respond took twice as long to respond to PUVA treatment if they were higher on the worry scale,” Dr. Griffiths said.

The average age of patients in the study was 43 years.

Dr. Griffiths also reported that managing psoriasis symptoms with adjuncts such as behavioral therapy measurably enhances response to standard therapy.

Psoriasis patients always look for environmental cues that might be signs of how others are viewing them. DR. GRIFFITHS

NEW YORK – There is mounting evidence that stress and the way in which patients with psoriasis view themselves or perceive themselves to be seen affects the way that they respond to treatment, Dr. Christopher Griffiths said at a dermatology symposium sponsored by Cornell University.

“While the exact etiology of psoriasis remains unknown, there is a strong environmental component to the disease, including stress, especially in the genetically predisposed with the HLA-Cw6 gene,” said Dr. Griffiths of the dermatology center at Hope Hospital, University of Manchester (England), the largest center for psoriasis research and treatment in the world.

Psoriasis occurs in about 2% of the population. Whether stress causes psoriasis or psoriasis is the origin of stress is still a point of contention. Studies have shown that psoriasis ranks just ahead of chronic lung disease and depression when it comes to the impact reported on the daily lives of patients, with 46% reporting an impact on their daily lives, versus 44% and 35% with chronic lung disease and depression, respectively. Approximately 60% of patients with psoriasis report that stressful life events may either trigger or exacerbate their condition, Dr. Griffiths said.

With 53% of patients strongly affected by how they view themselves and 28% by how they see themselves viewed by others, “psoriasis strongly affects how patients see themselves and how they think others see them,” he said.

“Patients with psoriasis are constantly looking for environmental cues which might be signs of how others are viewing them,” Dr. Griffiths noted.

A study using the Penn State Worry Questionnaire to measure whether worry affected 88 patients' (57 males, 31 females) response to PUVA therapy showed a correlation between worry and treatment efficacy. Patients who were high or pathologic worriers were less likely to show a response to PUVA therapy than were patients in the normal or low worry categories. “Those patients who did respond took twice as long to respond to PUVA treatment if they were higher on the worry scale,” Dr. Griffiths said.

The average age of patients in the study was 43 years.

Dr. Griffiths also reported that managing psoriasis symptoms with adjuncts such as behavioral therapy measurably enhances response to standard therapy.

Psoriasis patients always look for environmental cues that might be signs of how others are viewing them. DR. GRIFFITHS

MIAMI – People with anxiety often present with insomnia, but evidence suggests that untreated insomnia might precipitate anxiety disorders, according to a presentation at the annual conference of the Anxiety Disorders Association of America.

“We know as psychiatrists that anxiety disorders produce insomnia. But now we have evidence that insomnia is a risk factor for future psychiatric disorders, in particular, anxiety disorder,” Dr. John W. Winkelman said.

Anxiety disorders are the most common psychiatric disorders, affecting more than 19 million Americans per year (N. Engl. J. Med. 2005;353:803–10). In addition, insomnia is the most common sleep disorder–an estimated 10%–15% of the general population has chronic insomnia (J. Clin. Psychiatry 2005;66[Suppl. 9]:14–7).

“By no other mechanism, these would have a significant overlap, but it's not just coincidence,” said Dr. Winkelman of the Sleep Health Center, Brigham and Women's Hospital, Boston.

“Often, patients with insomnia are referred to us by a primary care provider with the assumption that there is a psychiatric disorder, but 60% do not have one,” Dr. Winkelman said. “But if they do, anxiety disorders are the most common.”

Differential diagnosis between insomnia and anxiety can be challenging because of substantial overlap in presenting symptoms. Worry, agitation, irritability, loss of appetite, impaired concentration, loss of interest, sleep disturbance, hopelessness, and fatigue are examples. These shared signs “might tell us something about the underlying physiology,” he said.

Insomnia is a presenting symptom of anxiety disorders (Clin. Ther. 2000;22[Suppl A]:A3–19). Insomnia can also be a side effect of anxiety treatment or a residual symptom after treatment (Biol. Psychiatry 1995;37:85–98). Both subjective and objective studies in generalized anxiety disorder (GAD) document increased sleep latency, decreased sleep efficiency, and decreased total sleep time, he said.

“In PTSD, things get even uglier,” he said. Hypervigilance is a diagnostic criterion for posttraumatic stress disorder. Most patients will have sleep problems, including nightmares and difficulty with sleep onset and duration. “However, objectively, we have not been able to demonstrate worse sleep in people with PTSD in sleep lab studies.”

Some patients with insomnia develop conditioned fear of the sleep environment. Typically, this “insomnia phobia” begins with repeated episodes of acute insomnia, and is maintained by negative associations that produce anxiety and hyperarousal. “From my perspective, this is an anxiety disorder,” Dr. Winkelman said. “Perpetuating factors increase in strength, and this is where we see patients.”

Whole brain hypermetabolism is present during both wake and sleep in insomniacs, he said. “There is a relationship between cognitive arousal and insomnia–we can't prove it is causal yet–but it is why cognitive-behavioral therapy is effective.”

Cognitive-behavioral therapy, or CBT, helps people with insomnia fall asleep faster and stay asleep, Dr. Winkelman said, but it does not extend total sleep time. CBT gives people more confidence that they can sleep. Although CBT has a role, he added, “For the subset of people with very severe insomnia, I would start with medication to quell the situation first.” He suggested use of benzodiazepines rather than antidepressants because the latter can significantly alter sleep architecture.

And insomnia might precipitate an anxiety disorder. In one study, researchers found that persistent insomnia lasting at least a year was associated with new onset of an anxiety disorder (Gen. Hosp. Psychiatry 1997;19:245–50).

These studies are only suggestive, Dr. Winkelman said, and data are not strong enough yet to establish a causal relationship. In the meantime, he said, “we should aggressively treat insomnia. It's not just a minor quality of life issue.”

MIAMI – People with anxiety often present with insomnia, but evidence suggests that untreated insomnia might precipitate anxiety disorders, according to a presentation at the annual conference of the Anxiety Disorders Association of America.

“We know as psychiatrists that anxiety disorders produce insomnia. But now we have evidence that insomnia is a risk factor for future psychiatric disorders, in particular, anxiety disorder,” Dr. John W. Winkelman said.

Anxiety disorders are the most common psychiatric disorders, affecting more than 19 million Americans per year (N. Engl. J. Med. 2005;353:803–10). In addition, insomnia is the most common sleep disorder–an estimated 10%–15% of the general population has chronic insomnia (J. Clin. Psychiatry 2005;66[Suppl. 9]:14–7).

“By no other mechanism, these would have a significant overlap, but it's not just coincidence,” said Dr. Winkelman of the Sleep Health Center, Brigham and Women's Hospital, Boston.

“Often, patients with insomnia are referred to us by a primary care provider with the assumption that there is a psychiatric disorder, but 60% do not have one,” Dr. Winkelman said. “But if they do, anxiety disorders are the most common.”

Differential diagnosis between insomnia and anxiety can be challenging because of substantial overlap in presenting symptoms. Worry, agitation, irritability, loss of appetite, impaired concentration, loss of interest, sleep disturbance, hopelessness, and fatigue are examples. These shared signs “might tell us something about the underlying physiology,” he said.

Insomnia is a presenting symptom of anxiety disorders (Clin. Ther. 2000;22[Suppl A]:A3–19). Insomnia can also be a side effect of anxiety treatment or a residual symptom after treatment (Biol. Psychiatry 1995;37:85–98). Both subjective and objective studies in generalized anxiety disorder (GAD) document increased sleep latency, decreased sleep efficiency, and decreased total sleep time, he said.

“In PTSD, things get even uglier,” he said. Hypervigilance is a diagnostic criterion for posttraumatic stress disorder. Most patients will have sleep problems, including nightmares and difficulty with sleep onset and duration. “However, objectively, we have not been able to demonstrate worse sleep in people with PTSD in sleep lab studies.”

Some patients with insomnia develop conditioned fear of the sleep environment. Typically, this “insomnia phobia” begins with repeated episodes of acute insomnia, and is maintained by negative associations that produce anxiety and hyperarousal. “From my perspective, this is an anxiety disorder,” Dr. Winkelman said. “Perpetuating factors increase in strength, and this is where we see patients.”

Whole brain hypermetabolism is present during both wake and sleep in insomniacs, he said. “There is a relationship between cognitive arousal and insomnia–we can't prove it is causal yet–but it is why cognitive-behavioral therapy is effective.”

Cognitive-behavioral therapy, or CBT, helps people with insomnia fall asleep faster and stay asleep, Dr. Winkelman said, but it does not extend total sleep time. CBT gives people more confidence that they can sleep. Although CBT has a role, he added, “For the subset of people with very severe insomnia, I would start with medication to quell the situation first.” He suggested use of benzodiazepines rather than antidepressants because the latter can significantly alter sleep architecture.

And insomnia might precipitate an anxiety disorder. In one study, researchers found that persistent insomnia lasting at least a year was associated with new onset of an anxiety disorder (Gen. Hosp. Psychiatry 1997;19:245–50).

These studies are only suggestive, Dr. Winkelman said, and data are not strong enough yet to establish a causal relationship. In the meantime, he said, “we should aggressively treat insomnia. It's not just a minor quality of life issue.”

MIAMI – People with anxiety often present with insomnia, but evidence suggests that untreated insomnia might precipitate anxiety disorders, according to a presentation at the annual conference of the Anxiety Disorders Association of America.

“We know as psychiatrists that anxiety disorders produce insomnia. But now we have evidence that insomnia is a risk factor for future psychiatric disorders, in particular, anxiety disorder,” Dr. John W. Winkelman said.

Anxiety disorders are the most common psychiatric disorders, affecting more than 19 million Americans per year (N. Engl. J. Med. 2005;353:803–10). In addition, insomnia is the most common sleep disorder–an estimated 10%–15% of the general population has chronic insomnia (J. Clin. Psychiatry 2005;66[Suppl. 9]:14–7).

“By no other mechanism, these would have a significant overlap, but it's not just coincidence,” said Dr. Winkelman of the Sleep Health Center, Brigham and Women's Hospital, Boston.

“Often, patients with insomnia are referred to us by a primary care provider with the assumption that there is a psychiatric disorder, but 60% do not have one,” Dr. Winkelman said. “But if they do, anxiety disorders are the most common.”

Differential diagnosis between insomnia and anxiety can be challenging because of substantial overlap in presenting symptoms. Worry, agitation, irritability, loss of appetite, impaired concentration, loss of interest, sleep disturbance, hopelessness, and fatigue are examples. These shared signs “might tell us something about the underlying physiology,” he said.

Insomnia is a presenting symptom of anxiety disorders (Clin. Ther. 2000;22[Suppl A]:A3–19). Insomnia can also be a side effect of anxiety treatment or a residual symptom after treatment (Biol. Psychiatry 1995;37:85–98). Both subjective and objective studies in generalized anxiety disorder (GAD) document increased sleep latency, decreased sleep efficiency, and decreased total sleep time, he said.

“In PTSD, things get even uglier,” he said. Hypervigilance is a diagnostic criterion for posttraumatic stress disorder. Most patients will have sleep problems, including nightmares and difficulty with sleep onset and duration. “However, objectively, we have not been able to demonstrate worse sleep in people with PTSD in sleep lab studies.”

Some patients with insomnia develop conditioned fear of the sleep environment. Typically, this “insomnia phobia” begins with repeated episodes of acute insomnia, and is maintained by negative associations that produce anxiety and hyperarousal. “From my perspective, this is an anxiety disorder,” Dr. Winkelman said. “Perpetuating factors increase in strength, and this is where we see patients.”

Whole brain hypermetabolism is present during both wake and sleep in insomniacs, he said. “There is a relationship between cognitive arousal and insomnia–we can't prove it is causal yet–but it is why cognitive-behavioral therapy is effective.”

Cognitive-behavioral therapy, or CBT, helps people with insomnia fall asleep faster and stay asleep, Dr. Winkelman said, but it does not extend total sleep time. CBT gives people more confidence that they can sleep. Although CBT has a role, he added, “For the subset of people with very severe insomnia, I would start with medication to quell the situation first.” He suggested use of benzodiazepines rather than antidepressants because the latter can significantly alter sleep architecture.

And insomnia might precipitate an anxiety disorder. In one study, researchers found that persistent insomnia lasting at least a year was associated with new onset of an anxiety disorder (Gen. Hosp. Psychiatry 1997;19:245–50).

These studies are only suggestive, Dr. Winkelman said, and data are not strong enough yet to establish a causal relationship. In the meantime, he said, “we should aggressively treat insomnia. It's not just a minor quality of life issue.”

NEW YORK – Compelling research supports the link between psychological stress and specific skin and allergic disorders, Dr. Rosalind J. Wright said at a dermatology symposium sponsored by Cornell University.

“There is huge biological plausibility to think that there is this psycho-neuro-cutaneous-immunology link to suggest that there is interconnection between these systems, and one important effector organ is the skin,” said Dr. Wright of the department of society, human development, and health at Harvard School of Public Health, Boston.

Atopic dermatitis shows dysregulation of the responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis. “Studies done across the age spectrum show that inpatients with atopic dermatitis seem to have a blunted cortisol response to different types of challenges” when compared with nonatopic dermatitis patients, said Dr. Wright, also of Brigham and Women's Hospital.

Atopic dermatitis is known to start in early childhood. The early experiences shape the stress vulnerability of the older child and adult later in life. “Not only early childhood, but even prenatal exposure to stress is a very critical period of development,” she said.

“There is huge plasticity of the HPA axis early in life. Early experiences in rat experiments–and this has been done in humans as well–also with respect to prenatal stress, show programming of the HPA response in the child postnatally. In animal experiments, social buffering of newborns by the mother seems to dampen the cortisol response,” Dr. Wright said.

In human studies, there seems to be a parallel response. Exposing mothers to stress has been demonstrated to alter the immune function of their children, she noted.

A National Institutes of Health-funded prospective birth cohort study involving a total of 499 mothers recruited at Brigham and Women's at the time of giving birth used asthma to evaluate the external influence of elevated stress on the development of children's immune systems. The patients were genetically predisposed for atopic dermatitis and allergic dermatoses. The question that the investigators hoped to answer was whether stress primed the immune system toward a T helper cell-type pattern of immune response, as is typically seen in allergic dermatoses.

Families with a predisposition to allergic response were followed prospectively every 2 months to see if the children had any clinical manifestations of atopic disease.. “Results indicated that higher caregiver stress predicted a phenotype of early asthma,” Dr. Wright said. Dose-response relationship was seen between a measure of perceived stress over time and the clinical manifestations of wheeze.

Serum IgE, which is a marker for susceptibility to atopic dermatitis, was measured in the blood of children, and high-stress households were associated with elevated levels of IgE expression in their children.

When children were evaluated up to age 6 years, a correlation between stress and eczema was also demonstrated.

“We need to get back to treating the whole patient,” Dr. Wright urged. As a physician, she has seen emotional response and stress affecting the disease process and clinical response to treatment in her patients and said she is fortunate to be able to send patients to the Mind-Body Institute at Beth Israel Deaconess Center in Boston to learn relaxation therapies.

NEW YORK – Compelling research supports the link between psychological stress and specific skin and allergic disorders, Dr. Rosalind J. Wright said at a dermatology symposium sponsored by Cornell University.

“There is huge biological plausibility to think that there is this psycho-neuro-cutaneous-immunology link to suggest that there is interconnection between these systems, and one important effector organ is the skin,” said Dr. Wright of the department of society, human development, and health at Harvard School of Public Health, Boston.

Atopic dermatitis shows dysregulation of the responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis. “Studies done across the age spectrum show that inpatients with atopic dermatitis seem to have a blunted cortisol response to different types of challenges” when compared with nonatopic dermatitis patients, said Dr. Wright, also of Brigham and Women's Hospital.

Atopic dermatitis is known to start in early childhood. The early experiences shape the stress vulnerability of the older child and adult later in life. “Not only early childhood, but even prenatal exposure to stress is a very critical period of development,” she said.

“There is huge plasticity of the HPA axis early in life. Early experiences in rat experiments–and this has been done in humans as well–also with respect to prenatal stress, show programming of the HPA response in the child postnatally. In animal experiments, social buffering of newborns by the mother seems to dampen the cortisol response,” Dr. Wright said.

In human studies, there seems to be a parallel response. Exposing mothers to stress has been demonstrated to alter the immune function of their children, she noted.

A National Institutes of Health-funded prospective birth cohort study involving a total of 499 mothers recruited at Brigham and Women's at the time of giving birth used asthma to evaluate the external influence of elevated stress on the development of children's immune systems. The patients were genetically predisposed for atopic dermatitis and allergic dermatoses. The question that the investigators hoped to answer was whether stress primed the immune system toward a T helper cell-type pattern of immune response, as is typically seen in allergic dermatoses.

Families with a predisposition to allergic response were followed prospectively every 2 months to see if the children had any clinical manifestations of atopic disease.. “Results indicated that higher caregiver stress predicted a phenotype of early asthma,” Dr. Wright said. Dose-response relationship was seen between a measure of perceived stress over time and the clinical manifestations of wheeze.

Serum IgE, which is a marker for susceptibility to atopic dermatitis, was measured in the blood of children, and high-stress households were associated with elevated levels of IgE expression in their children.

When children were evaluated up to age 6 years, a correlation between stress and eczema was also demonstrated.

“We need to get back to treating the whole patient,” Dr. Wright urged. As a physician, she has seen emotional response and stress affecting the disease process and clinical response to treatment in her patients and said she is fortunate to be able to send patients to the Mind-Body Institute at Beth Israel Deaconess Center in Boston to learn relaxation therapies.

NEW YORK – Compelling research supports the link between psychological stress and specific skin and allergic disorders, Dr. Rosalind J. Wright said at a dermatology symposium sponsored by Cornell University.

“There is huge biological plausibility to think that there is this psycho-neuro-cutaneous-immunology link to suggest that there is interconnection between these systems, and one important effector organ is the skin,” said Dr. Wright of the department of society, human development, and health at Harvard School of Public Health, Boston.

Atopic dermatitis shows dysregulation of the responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis. “Studies done across the age spectrum show that inpatients with atopic dermatitis seem to have a blunted cortisol response to different types of challenges” when compared with nonatopic dermatitis patients, said Dr. Wright, also of Brigham and Women's Hospital.

Atopic dermatitis is known to start in early childhood. The early experiences shape the stress vulnerability of the older child and adult later in life. “Not only early childhood, but even prenatal exposure to stress is a very critical period of development,” she said.

“There is huge plasticity of the HPA axis early in life. Early experiences in rat experiments–and this has been done in humans as well–also with respect to prenatal stress, show programming of the HPA response in the child postnatally. In animal experiments, social buffering of newborns by the mother seems to dampen the cortisol response,” Dr. Wright said.

In human studies, there seems to be a parallel response. Exposing mothers to stress has been demonstrated to alter the immune function of their children, she noted.

A National Institutes of Health-funded prospective birth cohort study involving a total of 499 mothers recruited at Brigham and Women's at the time of giving birth used asthma to evaluate the external influence of elevated stress on the development of children's immune systems. The patients were genetically predisposed for atopic dermatitis and allergic dermatoses. The question that the investigators hoped to answer was whether stress primed the immune system toward a T helper cell-type pattern of immune response, as is typically seen in allergic dermatoses.

Families with a predisposition to allergic response were followed prospectively every 2 months to see if the children had any clinical manifestations of atopic disease.. “Results indicated that higher caregiver stress predicted a phenotype of early asthma,” Dr. Wright said. Dose-response relationship was seen between a measure of perceived stress over time and the clinical manifestations of wheeze.

Serum IgE, which is a marker for susceptibility to atopic dermatitis, was measured in the blood of children, and high-stress households were associated with elevated levels of IgE expression in their children.

When children were evaluated up to age 6 years, a correlation between stress and eczema was also demonstrated.

“We need to get back to treating the whole patient,” Dr. Wright urged. As a physician, she has seen emotional response and stress affecting the disease process and clinical response to treatment in her patients and said she is fortunate to be able to send patients to the Mind-Body Institute at Beth Israel Deaconess Center in Boston to learn relaxation therapies.

SAN DIEGO – Increased levels of C-reactive protein and other markers of perioperative inflammatory response are associated with neurocognitive decline following cardiac surgery, Dr. Basel Ramlawi said at a congress sponsored by the Association for Academic Surgery and the Society of University Surgeons.

Dr. Ramlawi and his associates prospectively evaluated 41 patients who underwent coronary artery bypass graft and/or valve procedures that used cardiopulmonary bypass. The patients' mean age was 67 years. All patients had neurocognitive testing preoperatively, postoperatively at day 4, and at 3 months. The validated tests took 45 minutes to administer and covered memory, executive function, naming, attention, fluency, and premorbid intelligence, said Dr. Ramlawi of the division of cardiothoracic surgery at Harvard Medical School, Boston. Neurocognitive decline was defined as performing one standard deviation from baseline on at least 25% of tasks.

Participants also underwent serum testing preoperatively, postoperatively at 6 hours, and at 4 days. Levels of C-reactive protein (CRP) and of interleukin 1β, IL-6, and IL-10 were assessed, and an increase of serum tau protein after surgery was used as a marker of axonal central nervous system damage.

Of the 41 patients, 7 (17%) developed neurocognitive decline. Baseline characteristics and predictors of neurocognitive decline such as age, education level, and perioperative temperature did not differ significantly between patients with and without postoperative neurocognitive decline.

However, patients who experienced postoperative neurocognitive decline had significantly greater increases of CRP, IL-1β, and IL-10 than those who had no decline.

In addition, the level of tau protein was increased 78% in patients with neurocognitive decline, compared with 29% in their counterparts who did not show a decline.

“There exists a significant association [between] the magnitude and persistence of the perioperative inflammatory response and neurocognitive decline in this cohort,” Dr. Ramlawi said. “This association is likely mediated by axonal damage.”

According to the medical literature, the incidence of neurocognitive decline is 20%–60% in the first 2 weeks after cardiac surgery. “It can range from 5% to 40% for periods up to 5 years after surgery,” he said, adding that the etiology of this complication is not known.

“It is likely a multifactorial problem,” Dr. Ramlawi said. “Several theories have been assessed. The most obvious one is ischemia. Any microemboli might cause this.”

Other possible factors include anesthesia, perioperative hypothermia, and low level of education.

“While there have been certain markers of brain injury following cardiopulmonary bypass, very few have been associated with clinical outcomes and neurocognitive decline,” he said. “Tau protein, on the other hand, assesses axonal damage and has not been [studied] in cardiac surgery before.”

SAN DIEGO – Increased levels of C-reactive protein and other markers of perioperative inflammatory response are associated with neurocognitive decline following cardiac surgery, Dr. Basel Ramlawi said at a congress sponsored by the Association for Academic Surgery and the Society of University Surgeons.

Dr. Ramlawi and his associates prospectively evaluated 41 patients who underwent coronary artery bypass graft and/or valve procedures that used cardiopulmonary bypass. The patients' mean age was 67 years. All patients had neurocognitive testing preoperatively, postoperatively at day 4, and at 3 months. The validated tests took 45 minutes to administer and covered memory, executive function, naming, attention, fluency, and premorbid intelligence, said Dr. Ramlawi of the division of cardiothoracic surgery at Harvard Medical School, Boston. Neurocognitive decline was defined as performing one standard deviation from baseline on at least 25% of tasks.

Participants also underwent serum testing preoperatively, postoperatively at 6 hours, and at 4 days. Levels of C-reactive protein (CRP) and of interleukin 1β, IL-6, and IL-10 were assessed, and an increase of serum tau protein after surgery was used as a marker of axonal central nervous system damage.

Of the 41 patients, 7 (17%) developed neurocognitive decline. Baseline characteristics and predictors of neurocognitive decline such as age, education level, and perioperative temperature did not differ significantly between patients with and without postoperative neurocognitive decline.

However, patients who experienced postoperative neurocognitive decline had significantly greater increases of CRP, IL-1β, and IL-10 than those who had no decline.

In addition, the level of tau protein was increased 78% in patients with neurocognitive decline, compared with 29% in their counterparts who did not show a decline.

“There exists a significant association [between] the magnitude and persistence of the perioperative inflammatory response and neurocognitive decline in this cohort,” Dr. Ramlawi said. “This association is likely mediated by axonal damage.”

According to the medical literature, the incidence of neurocognitive decline is 20%–60% in the first 2 weeks after cardiac surgery. “It can range from 5% to 40% for periods up to 5 years after surgery,” he said, adding that the etiology of this complication is not known.

“It is likely a multifactorial problem,” Dr. Ramlawi said. “Several theories have been assessed. The most obvious one is ischemia. Any microemboli might cause this.”

Other possible factors include anesthesia, perioperative hypothermia, and low level of education.

“While there have been certain markers of brain injury following cardiopulmonary bypass, very few have been associated with clinical outcomes and neurocognitive decline,” he said. “Tau protein, on the other hand, assesses axonal damage and has not been [studied] in cardiac surgery before.”

SAN DIEGO – Increased levels of C-reactive protein and other markers of perioperative inflammatory response are associated with neurocognitive decline following cardiac surgery, Dr. Basel Ramlawi said at a congress sponsored by the Association for Academic Surgery and the Society of University Surgeons.

Dr. Ramlawi and his associates prospectively evaluated 41 patients who underwent coronary artery bypass graft and/or valve procedures that used cardiopulmonary bypass. The patients' mean age was 67 years. All patients had neurocognitive testing preoperatively, postoperatively at day 4, and at 3 months. The validated tests took 45 minutes to administer and covered memory, executive function, naming, attention, fluency, and premorbid intelligence, said Dr. Ramlawi of the division of cardiothoracic surgery at Harvard Medical School, Boston. Neurocognitive decline was defined as performing one standard deviation from baseline on at least 25% of tasks.

Participants also underwent serum testing preoperatively, postoperatively at 6 hours, and at 4 days. Levels of C-reactive protein (CRP) and of interleukin 1β, IL-6, and IL-10 were assessed, and an increase of serum tau protein after surgery was used as a marker of axonal central nervous system damage.

Of the 41 patients, 7 (17%) developed neurocognitive decline. Baseline characteristics and predictors of neurocognitive decline such as age, education level, and perioperative temperature did not differ significantly between patients with and without postoperative neurocognitive decline.

However, patients who experienced postoperative neurocognitive decline had significantly greater increases of CRP, IL-1β, and IL-10 than those who had no decline.

In addition, the level of tau protein was increased 78% in patients with neurocognitive decline, compared with 29% in their counterparts who did not show a decline.

“There exists a significant association [between] the magnitude and persistence of the perioperative inflammatory response and neurocognitive decline in this cohort,” Dr. Ramlawi said. “This association is likely mediated by axonal damage.”

According to the medical literature, the incidence of neurocognitive decline is 20%–60% in the first 2 weeks after cardiac surgery. “It can range from 5% to 40% for periods up to 5 years after surgery,” he said, adding that the etiology of this complication is not known.

“It is likely a multifactorial problem,” Dr. Ramlawi said. “Several theories have been assessed. The most obvious one is ischemia. Any microemboli might cause this.”

Other possible factors include anesthesia, perioperative hypothermia, and low level of education.

“While there have been certain markers of brain injury following cardiopulmonary bypass, very few have been associated with clinical outcomes and neurocognitive decline,” he said. “Tau protein, on the other hand, assesses axonal damage and has not been [studied] in cardiac surgery before.”

SAN FRANCISCO – Rape appears to initiate a host of neuroinflammatory changes that could predispose the victim to later inflammatory disease, Maureen Groer, Ph.D., said at the annual meeting of the Society of Behavioral Medicine.

“Victims of rape experience more headaches, chronic pain, gastrointestinal disorders, breast cancer, and arthritis–many of which have an inflammatory component,” said Dr. Groer, a registered nurse at the University of South Florida, Tampa. “About a third of them also develop posttraumatic stress disorder, which is also associated with an increase in inflammatory disorders.

“I would suggest that this could be explained by psychoneuroimmunology, in which stressors appear to provoke an immune response that can lead to damage of normal tissues if it is prolonged.”

To examine the relationship between rape and inflammatory response, Dr. Groer compared lymphocyte counts and cytokine and hormone levels in a group of 16 healthy control women who had low self-reported stress with those in a group of 15 victims of recent, first-time rape. Blood was collected from the rape victims within 72 hours of their assault (most within 24 hours). The rape victims' mean age was 30 years; that of the control group was 24 years. None of the women were living in domestic abuse or violent situations.

Serum analysis revealed that levels of CD8 cytotoxic cells were significantly higher in rape victims than in controls (10% vs. 6%), and CD19 percentages were significantly lower in rape victims compared with controls (6% vs. 20%).

Compared with controls, rape victims also expressed much higher levels of interferon-γ (10 times higher), interleukin-10 (four times higher), interleukin-6 (five times higher), and C-reactive protein (three times higher). These data suggest an acute inflammatory process.

Nurses who examined the rape victims also noted victims' behavior as controlled (quiet and withdrawn) or uncontrolled (angry or lashing out). Most of the victims were controlled; control correlated with lower CD4 counts, reduced CD4/CD8 ratios, and lower lymphocyte proliferation. “This suggests a state of T-cell suppression,” Dr. Groer said. “The inflammatory response system may dominate and deplete the adaptive resources of the women, and provoke a pathophysiologic state leading to multiple adverse health outcomes.”

SAN FRANCISCO – Rape appears to initiate a host of neuroinflammatory changes that could predispose the victim to later inflammatory disease, Maureen Groer, Ph.D., said at the annual meeting of the Society of Behavioral Medicine.

“Victims of rape experience more headaches, chronic pain, gastrointestinal disorders, breast cancer, and arthritis–many of which have an inflammatory component,” said Dr. Groer, a registered nurse at the University of South Florida, Tampa. “About a third of them also develop posttraumatic stress disorder, which is also associated with an increase in inflammatory disorders.

“I would suggest that this could be explained by psychoneuroimmunology, in which stressors appear to provoke an immune response that can lead to damage of normal tissues if it is prolonged.”

To examine the relationship between rape and inflammatory response, Dr. Groer compared lymphocyte counts and cytokine and hormone levels in a group of 16 healthy control women who had low self-reported stress with those in a group of 15 victims of recent, first-time rape. Blood was collected from the rape victims within 72 hours of their assault (most within 24 hours). The rape victims' mean age was 30 years; that of the control group was 24 years. None of the women were living in domestic abuse or violent situations.

Serum analysis revealed that levels of CD8 cytotoxic cells were significantly higher in rape victims than in controls (10% vs. 6%), and CD19 percentages were significantly lower in rape victims compared with controls (6% vs. 20%).

Compared with controls, rape victims also expressed much higher levels of interferon-γ (10 times higher), interleukin-10 (four times higher), interleukin-6 (five times higher), and C-reactive protein (three times higher). These data suggest an acute inflammatory process.

Nurses who examined the rape victims also noted victims' behavior as controlled (quiet and withdrawn) or uncontrolled (angry or lashing out). Most of the victims were controlled; control correlated with lower CD4 counts, reduced CD4/CD8 ratios, and lower lymphocyte proliferation. “This suggests a state of T-cell suppression,” Dr. Groer said. “The inflammatory response system may dominate and deplete the adaptive resources of the women, and provoke a pathophysiologic state leading to multiple adverse health outcomes.”

SAN FRANCISCO – Rape appears to initiate a host of neuroinflammatory changes that could predispose the victim to later inflammatory disease, Maureen Groer, Ph.D., said at the annual meeting of the Society of Behavioral Medicine.

“Victims of rape experience more headaches, chronic pain, gastrointestinal disorders, breast cancer, and arthritis–many of which have an inflammatory component,” said Dr. Groer, a registered nurse at the University of South Florida, Tampa. “About a third of them also develop posttraumatic stress disorder, which is also associated with an increase in inflammatory disorders.

“I would suggest that this could be explained by psychoneuroimmunology, in which stressors appear to provoke an immune response that can lead to damage of normal tissues if it is prolonged.”

To examine the relationship between rape and inflammatory response, Dr. Groer compared lymphocyte counts and cytokine and hormone levels in a group of 16 healthy control women who had low self-reported stress with those in a group of 15 victims of recent, first-time rape. Blood was collected from the rape victims within 72 hours of their assault (most within 24 hours). The rape victims' mean age was 30 years; that of the control group was 24 years. None of the women were living in domestic abuse or violent situations.

Serum analysis revealed that levels of CD8 cytotoxic cells were significantly higher in rape victims than in controls (10% vs. 6%), and CD19 percentages were significantly lower in rape victims compared with controls (6% vs. 20%).

Compared with controls, rape victims also expressed much higher levels of interferon-γ (10 times higher), interleukin-10 (four times higher), interleukin-6 (five times higher), and C-reactive protein (three times higher). These data suggest an acute inflammatory process.

Nurses who examined the rape victims also noted victims' behavior as controlled (quiet and withdrawn) or uncontrolled (angry or lashing out). Most of the victims were controlled; control correlated with lower CD4 counts, reduced CD4/CD8 ratios, and lower lymphocyte proliferation. “This suggests a state of T-cell suppression,” Dr. Groer said. “The inflammatory response system may dominate and deplete the adaptive resources of the women, and provoke a pathophysiologic state leading to multiple adverse health outcomes.”

SAN JUAN, P.R. – Growing evidence points to an association between inflammation and depression, according to a presentation at the annual meeting of the American College of Psychiatrists.

For example, depressed patients have elevated inflammatory markers–such as interleukin-6 and C-reactive protein. In fact, the levels of proinflammatory cytokines correlate with the severity of depressive symptoms in studies. In addition, administration of cytokine antagonists can effectively reverse depressive symptoms in patients, Dr. Andrew H. Miller said.

“We really stand at a point that is very exciting in terms of novel therapies and translation of research,” Dr. Miller said. “The notion quite simply is that stress or depression affects the HPA [hypothalamic-pituitary-adrenal] axis, [affects] the endocrine system, alters the immune system, and leaves patients open to diseases.”

Physicians from many specialties already recognize that inflammation plays a key role in cardiovascular disease, diabetes, metabolic syndrome, and cancer, said Dr. Miller, professor in the department of psychiatry and behavioral sciences at Emory University, Atlanta.

“We did not want to be left out in terms of psychiatry,” said Dr. Miller, who also is director of the psychiatric oncology program at the Winship Cancer Institute at Emory.

There are multiple possible mechanisms whereby inflammation could cause depression. Inflammatory cytokines released peripherally might reach the brain through active transport, passage through leaky regions in the blood-brain barrier, or transmission through afferent nerve fibers (vagus nerve), Dr. Miller said. There is a cytokine network in the central nervous system, and glia and microglia are the richest source of cytokines in the brain. Neurons also produce and express cytokines.

“We've learned these cytokines have access to the brain and … ultimately can change behavior,” Dr. Miller said. Inflammatory cytokines cause anhedonia, fatigue, cognitive dysfunction, and other flu-like symptoms in sick patients. In addition, researchers induced behavioral changes that resemble major depression in human and animal studies with administration of proinflammatory cytokines.

Some therapeutic cytokines cause depression. For example, interferon-α (IFN-α) is used to treat viral infections and cancer because it is a potent inducer of the inflammatory cytokine network, especially interleukin-6, Dr. Miller said. “Oncologists told us early on this drug causes a lot of depression.”

A total of 60% of patients treated with IFN-α reported depressed mood in one study (Neuropsychopharmacology 2002;26:643–52). Dr. Miller and his associates also found a 45% incidence of major depression among patients with malignant melanoma treated with IFN-α (N. Engl. J. Med. 2001;344:961–6).

The good news is that paroxetine (Paxil) aggressively blocked development of depression. “Just 11% developed depression, so there was a fourfold reduction with this pretreatment.

“There is a caveat. If you give a drug that causes release of dopamine–for example, paroxetine–that dopamine becomes oxidized and in the long term can damage basal ganglia,” Dr. Miller said in response to a question from a person attending the meeting. “So we're using dopamine antagonists to block this until we get more information about what we are doing to patients.”

Physician reaction to his study varied, Dr. Miller said. “The people who got on us the most for that study with paroxetine were the ones who were treating hepatitis C. They said we'd expose a lot of people to antidepressants who don't really need them.” However, “with melanoma, many patients will not go back on interferon therapy, and giving antidepressant prophylaxis might help.”

In another study, patients with psoriasis treated with the cytokine antagonist etanercept experienced reversal of their depressive symptoms (Lancet 2006;367:29–35). Improvement in depression was independent of the drug's effect on disease progress.

The wider picture may be a link between stress, depression, and illness, Dr. Miller said. In one study in review, patients with major depressive disorder exhibited an exaggerated inflammatory response to stress.

“There is an interesting possible link between depression and a wide variety of medical disorders where inflammation plays a role,” Dr. Miller said. It “may explain high comorbidity of some medical conditions with depression.

“Psychiatry is now catching up to other medical specialties in recognizing the adverse effects of inflammation,” Dr. Miller added. “Psychiatrists need to keep an eye on this. The idea that the immune system might affect the brain and vice versa presents a lot of novel targets for treating psychiatric disorders.”

SAN JUAN, P.R. – Growing evidence points to an association between inflammation and depression, according to a presentation at the annual meeting of the American College of Psychiatrists.

For example, depressed patients have elevated inflammatory markers–such as interleukin-6 and C-reactive protein. In fact, the levels of proinflammatory cytokines correlate with the severity of depressive symptoms in studies. In addition, administration of cytokine antagonists can effectively reverse depressive symptoms in patients, Dr. Andrew H. Miller said.

“We really stand at a point that is very exciting in terms of novel therapies and translation of research,” Dr. Miller said. “The notion quite simply is that stress or depression affects the HPA [hypothalamic-pituitary-adrenal] axis, [affects] the endocrine system, alters the immune system, and leaves patients open to diseases.”

Physicians from many specialties already recognize that inflammation plays a key role in cardiovascular disease, diabetes, metabolic syndrome, and cancer, said Dr. Miller, professor in the department of psychiatry and behavioral sciences at Emory University, Atlanta.

“We did not want to be left out in terms of psychiatry,” said Dr. Miller, who also is director of the psychiatric oncology program at the Winship Cancer Institute at Emory.

There are multiple possible mechanisms whereby inflammation could cause depression. Inflammatory cytokines released peripherally might reach the brain through active transport, passage through leaky regions in the blood-brain barrier, or transmission through afferent nerve fibers (vagus nerve), Dr. Miller said. There is a cytokine network in the central nervous system, and glia and microglia are the richest source of cytokines in the brain. Neurons also produce and express cytokines.

“We've learned these cytokines have access to the brain and … ultimately can change behavior,” Dr. Miller said. Inflammatory cytokines cause anhedonia, fatigue, cognitive dysfunction, and other flu-like symptoms in sick patients. In addition, researchers induced behavioral changes that resemble major depression in human and animal studies with administration of proinflammatory cytokines.

Some therapeutic cytokines cause depression. For example, interferon-α (IFN-α) is used to treat viral infections and cancer because it is a potent inducer of the inflammatory cytokine network, especially interleukin-6, Dr. Miller said. “Oncologists told us early on this drug causes a lot of depression.”

A total of 60% of patients treated with IFN-α reported depressed mood in one study (Neuropsychopharmacology 2002;26:643–52). Dr. Miller and his associates also found a 45% incidence of major depression among patients with malignant melanoma treated with IFN-α (N. Engl. J. Med. 2001;344:961–6).

The good news is that paroxetine (Paxil) aggressively blocked development of depression. “Just 11% developed depression, so there was a fourfold reduction with this pretreatment.

“There is a caveat. If you give a drug that causes release of dopamine–for example, paroxetine–that dopamine becomes oxidized and in the long term can damage basal ganglia,” Dr. Miller said in response to a question from a person attending the meeting. “So we're using dopamine antagonists to block this until we get more information about what we are doing to patients.”

Physician reaction to his study varied, Dr. Miller said. “The people who got on us the most for that study with paroxetine were the ones who were treating hepatitis C. They said we'd expose a lot of people to antidepressants who don't really need them.” However, “with melanoma, many patients will not go back on interferon therapy, and giving antidepressant prophylaxis might help.”

In another study, patients with psoriasis treated with the cytokine antagonist etanercept experienced reversal of their depressive symptoms (Lancet 2006;367:29–35). Improvement in depression was independent of the drug's effect on disease progress.

The wider picture may be a link between stress, depression, and illness, Dr. Miller said. In one study in review, patients with major depressive disorder exhibited an exaggerated inflammatory response to stress.

“There is an interesting possible link between depression and a wide variety of medical disorders where inflammation plays a role,” Dr. Miller said. It “may explain high comorbidity of some medical conditions with depression.

“Psychiatry is now catching up to other medical specialties in recognizing the adverse effects of inflammation,” Dr. Miller added. “Psychiatrists need to keep an eye on this. The idea that the immune system might affect the brain and vice versa presents a lot of novel targets for treating psychiatric disorders.”

SAN JUAN, P.R. – Growing evidence points to an association between inflammation and depression, according to a presentation at the annual meeting of the American College of Psychiatrists.

For example, depressed patients have elevated inflammatory markers–such as interleukin-6 and C-reactive protein. In fact, the levels of proinflammatory cytokines correlate with the severity of depressive symptoms in studies. In addition, administration of cytokine antagonists can effectively reverse depressive symptoms in patients, Dr. Andrew H. Miller said.

“We really stand at a point that is very exciting in terms of novel therapies and translation of research,” Dr. Miller said. “The notion quite simply is that stress or depression affects the HPA [hypothalamic-pituitary-adrenal] axis, [affects] the endocrine system, alters the immune system, and leaves patients open to diseases.”

Physicians from many specialties already recognize that inflammation plays a key role in cardiovascular disease, diabetes, metabolic syndrome, and cancer, said Dr. Miller, professor in the department of psychiatry and behavioral sciences at Emory University, Atlanta.

“We did not want to be left out in terms of psychiatry,” said Dr. Miller, who also is director of the psychiatric oncology program at the Winship Cancer Institute at Emory.

There are multiple possible mechanisms whereby inflammation could cause depression. Inflammatory cytokines released peripherally might reach the brain through active transport, passage through leaky regions in the blood-brain barrier, or transmission through afferent nerve fibers (vagus nerve), Dr. Miller said. There is a cytokine network in the central nervous system, and glia and microglia are the richest source of cytokines in the brain. Neurons also produce and express cytokines.

“We've learned these cytokines have access to the brain and … ultimately can change behavior,” Dr. Miller said. Inflammatory cytokines cause anhedonia, fatigue, cognitive dysfunction, and other flu-like symptoms in sick patients. In addition, researchers induced behavioral changes that resemble major depression in human and animal studies with administration of proinflammatory cytokines.

Some therapeutic cytokines cause depression. For example, interferon-α (IFN-α) is used to treat viral infections and cancer because it is a potent inducer of the inflammatory cytokine network, especially interleukin-6, Dr. Miller said. “Oncologists told us early on this drug causes a lot of depression.”

A total of 60% of patients treated with IFN-α reported depressed mood in one study (Neuropsychopharmacology 2002;26:643–52). Dr. Miller and his associates also found a 45% incidence of major depression among patients with malignant melanoma treated with IFN-α (N. Engl. J. Med. 2001;344:961–6).

The good news is that paroxetine (Paxil) aggressively blocked development of depression. “Just 11% developed depression, so there was a fourfold reduction with this pretreatment.

“There is a caveat. If you give a drug that causes release of dopamine–for example, paroxetine–that dopamine becomes oxidized and in the long term can damage basal ganglia,” Dr. Miller said in response to a question from a person attending the meeting. “So we're using dopamine antagonists to block this until we get more information about what we are doing to patients.”

Physician reaction to his study varied, Dr. Miller said. “The people who got on us the most for that study with paroxetine were the ones who were treating hepatitis C. They said we'd expose a lot of people to antidepressants who don't really need them.” However, “with melanoma, many patients will not go back on interferon therapy, and giving antidepressant prophylaxis might help.”

In another study, patients with psoriasis treated with the cytokine antagonist etanercept experienced reversal of their depressive symptoms (Lancet 2006;367:29–35). Improvement in depression was independent of the drug's effect on disease progress.

The wider picture may be a link between stress, depression, and illness, Dr. Miller said. In one study in review, patients with major depressive disorder exhibited an exaggerated inflammatory response to stress.

“There is an interesting possible link between depression and a wide variety of medical disorders where inflammation plays a role,” Dr. Miller said. It “may explain high comorbidity of some medical conditions with depression.

“Psychiatry is now catching up to other medical specialties in recognizing the adverse effects of inflammation,” Dr. Miller added. “Psychiatrists need to keep an eye on this. The idea that the immune system might affect the brain and vice versa presents a lot of novel targets for treating psychiatric disorders.”

DENVER – Increased risk of coronary heart disease is significantly associated with stronger symptoms of depression in diabetic adults, Susan M. Barry-Bianchi, Ph.D., reported in a poster presented at the annual meeting of the American Psychosomatic Society.

Dr. Barry-Bianchi of the Behavioural Cardiology Research Unit at the University Health Network in Toronto, and her colleagues recruited 353 patients for the study from an ongoing investigation, the Community Outreach and Health Risk Reduction Trial. The average patient age was 56 years.

The average score on the Beck Depression Inventory (BDI) was 11.1 among the 184 patients at high risk for coronary heart disease (CHD), compared with 8.8 among the 169 patients at low risk for CHD, Dr. Barry-Bianchi wrote. The 10-year absolute risk for CHD was nearly 22% for high-risk patients and 9% for the low-risk patients. CHD risk for each patient was determined using the Framingham index.

Given the significant difference in the depression levels based on the risk for developing heart disease, depression and CHD risk should be evaluated jointly, when investigating morbidity and mortality in diabetic patients, the investigators suggested. They also suggested that treatment of CHD risk factors in diabetic patients may correspond with a reduction in depressive symptoms and improved overall health.

In addition, the results supported previous findings of increased depression among women and patients with low levels of emotional support. Women demonstrated a significantly higher average BDI score, compared with men (11.4 vs. 8.4). Patients with low reported levels of emotional support demonstrated a significantly higher average BDI score, compared with those who reported more support (12 vs. 8).

DENVER – Increased risk of coronary heart disease is significantly associated with stronger symptoms of depression in diabetic adults, Susan M. Barry-Bianchi, Ph.D., reported in a poster presented at the annual meeting of the American Psychosomatic Society.

Dr. Barry-Bianchi of the Behavioural Cardiology Research Unit at the University Health Network in Toronto, and her colleagues recruited 353 patients for the study from an ongoing investigation, the Community Outreach and Health Risk Reduction Trial. The average patient age was 56 years.

The average score on the Beck Depression Inventory (BDI) was 11.1 among the 184 patients at high risk for coronary heart disease (CHD), compared with 8.8 among the 169 patients at low risk for CHD, Dr. Barry-Bianchi wrote. The 10-year absolute risk for CHD was nearly 22% for high-risk patients and 9% for the low-risk patients. CHD risk for each patient was determined using the Framingham index.

Given the significant difference in the depression levels based on the risk for developing heart disease, depression and CHD risk should be evaluated jointly, when investigating morbidity and mortality in diabetic patients, the investigators suggested. They also suggested that treatment of CHD risk factors in diabetic patients may correspond with a reduction in depressive symptoms and improved overall health.

In addition, the results supported previous findings of increased depression among women and patients with low levels of emotional support. Women demonstrated a significantly higher average BDI score, compared with men (11.4 vs. 8.4). Patients with low reported levels of emotional support demonstrated a significantly higher average BDI score, compared with those who reported more support (12 vs. 8).

DENVER – Increased risk of coronary heart disease is significantly associated with stronger symptoms of depression in diabetic adults, Susan M. Barry-Bianchi, Ph.D., reported in a poster presented at the annual meeting of the American Psychosomatic Society.

Dr. Barry-Bianchi of the Behavioural Cardiology Research Unit at the University Health Network in Toronto, and her colleagues recruited 353 patients for the study from an ongoing investigation, the Community Outreach and Health Risk Reduction Trial. The average patient age was 56 years.

The average score on the Beck Depression Inventory (BDI) was 11.1 among the 184 patients at high risk for coronary heart disease (CHD), compared with 8.8 among the 169 patients at low risk for CHD, Dr. Barry-Bianchi wrote. The 10-year absolute risk for CHD was nearly 22% for high-risk patients and 9% for the low-risk patients. CHD risk for each patient was determined using the Framingham index.

Given the significant difference in the depression levels based on the risk for developing heart disease, depression and CHD risk should be evaluated jointly, when investigating morbidity and mortality in diabetic patients, the investigators suggested. They also suggested that treatment of CHD risk factors in diabetic patients may correspond with a reduction in depressive symptoms and improved overall health.

In addition, the results supported previous findings of increased depression among women and patients with low levels of emotional support. Women demonstrated a significantly higher average BDI score, compared with men (11.4 vs. 8.4). Patients with low reported levels of emotional support demonstrated a significantly higher average BDI score, compared with those who reported more support (12 vs. 8).

SANTA ANA PUEBLO, N.M. – Different populations may require different screening instruments for depression, according to investigators who compared the accuracy of methods for detecting depression in 209 terminally ill cancer patients in Japan.

The patients' total score on the Hospital Anxiety and Depression Scale (HADS), the most indirect tool in the study, was the most accurate indicator, Dr. Tatsuo Akechi reported in a poster at the annual meeting of the Academy of Psychosomatic Medicine.

Direct questions such as “Are you depressed?” and “Have you lost interest or pleasure?” were the least effective, identifying fewer than half the patients who were diagnosed with depression or an adjustment disorder.

“This is a very interesting and important finding because most Japanese people are not likely to express their emotion,” Dr. Akechi of Nagoya City University, Honshu, Japan, said in an interview at the meeting. “We can obtain much more information if we use [HADS] than just screening positive and negative,” he said.

Dr. Akechi and his colleagues conducted the study because similar ones had shown different results in North America and Britain. The North American study found asking “Are you depressed?” to be the best method for screening the terminally ill (Am. J. Psychiatry 1997;154:674–6), while British investigators found that method to be less effective (Palliat. Med. 2003;17:40–3; Gen. Hosp. Psychiatry 2004;26:384–9).

The HADS questionnaire asks indirect questions, such as whether patients feel tense or wound up, enjoy the things they used to enjoy, or can sit at ease and feel relaxed.

Dr. Akechi reported the total HADS score had a sensitivity of 80% and a specificity of 67% in the Japanese patients. The HADS depression subscale was nearly as accurate, with a sensitivity of 78% and specificity of 58%.

Though highly specific, the direct questions each had a sensitivity of only 47% when considered alone. Asking a Japanese patient both questions and considering both answers raised the sensitivity only to 68%.

“When the screening target includes both an adjustment disorder and major depression, the HADS is a more useful screening method than the single-item interviews,” the investigators concluded.

Two-thirds of the patients were men. Their mean age was 61. Dr. Akechi reported that 22% were diagnosed with depression: 33 patients with an adjustment disorder and 14 with major depression.

SANTA ANA PUEBLO, N.M. – Different populations may require different screening instruments for depression, according to investigators who compared the accuracy of methods for detecting depression in 209 terminally ill cancer patients in Japan.

The patients' total score on the Hospital Anxiety and Depression Scale (HADS), the most indirect tool in the study, was the most accurate indicator, Dr. Tatsuo Akechi reported in a poster at the annual meeting of the Academy of Psychosomatic Medicine.

Direct questions such as “Are you depressed?” and “Have you lost interest or pleasure?” were the least effective, identifying fewer than half the patients who were diagnosed with depression or an adjustment disorder.

“This is a very interesting and important finding because most Japanese people are not likely to express their emotion,” Dr. Akechi of Nagoya City University, Honshu, Japan, said in an interview at the meeting. “We can obtain much more information if we use [HADS] than just screening positive and negative,” he said.

Dr. Akechi and his colleagues conducted the study because similar ones had shown different results in North America and Britain. The North American study found asking “Are you depressed?” to be the best method for screening the terminally ill (Am. J. Psychiatry 1997;154:674–6), while British investigators found that method to be less effective (Palliat. Med. 2003;17:40–3; Gen. Hosp. Psychiatry 2004;26:384–9).

The HADS questionnaire asks indirect questions, such as whether patients feel tense or wound up, enjoy the things they used to enjoy, or can sit at ease and feel relaxed.

Dr. Akechi reported the total HADS score had a sensitivity of 80% and a specificity of 67% in the Japanese patients. The HADS depression subscale was nearly as accurate, with a sensitivity of 78% and specificity of 58%.

Though highly specific, the direct questions each had a sensitivity of only 47% when considered alone. Asking a Japanese patient both questions and considering both answers raised the sensitivity only to 68%.

“When the screening target includes both an adjustment disorder and major depression, the HADS is a more useful screening method than the single-item interviews,” the investigators concluded.

Two-thirds of the patients were men. Their mean age was 61. Dr. Akechi reported that 22% were diagnosed with depression: 33 patients with an adjustment disorder and 14 with major depression.

SANTA ANA PUEBLO, N.M. – Different populations may require different screening instruments for depression, according to investigators who compared the accuracy of methods for detecting depression in 209 terminally ill cancer patients in Japan.

The patients' total score on the Hospital Anxiety and Depression Scale (HADS), the most indirect tool in the study, was the most accurate indicator, Dr. Tatsuo Akechi reported in a poster at the annual meeting of the Academy of Psychosomatic Medicine.

Direct questions such as “Are you depressed?” and “Have you lost interest or pleasure?” were the least effective, identifying fewer than half the patients who were diagnosed with depression or an adjustment disorder.

“This is a very interesting and important finding because most Japanese people are not likely to express their emotion,” Dr. Akechi of Nagoya City University, Honshu, Japan, said in an interview at the meeting. “We can obtain much more information if we use [HADS] than just screening positive and negative,” he said.

Dr. Akechi and his colleagues conducted the study because similar ones had shown different results in North America and Britain. The North American study found asking “Are you depressed?” to be the best method for screening the terminally ill (Am. J. Psychiatry 1997;154:674–6), while British investigators found that method to be less effective (Palliat. Med. 2003;17:40–3; Gen. Hosp. Psychiatry 2004;26:384–9).

The HADS questionnaire asks indirect questions, such as whether patients feel tense or wound up, enjoy the things they used to enjoy, or can sit at ease and feel relaxed.

Dr. Akechi reported the total HADS score had a sensitivity of 80% and a specificity of 67% in the Japanese patients. The HADS depression subscale was nearly as accurate, with a sensitivity of 78% and specificity of 58%.

Though highly specific, the direct questions each had a sensitivity of only 47% when considered alone. Asking a Japanese patient both questions and considering both answers raised the sensitivity only to 68%.

“When the screening target includes both an adjustment disorder and major depression, the HADS is a more useful screening method than the single-item interviews,” the investigators concluded.

Two-thirds of the patients were men. Their mean age was 61. Dr. Akechi reported that 22% were diagnosed with depression: 33 patients with an adjustment disorder and 14 with major depression.