|
|

|
FACTOIDS
(past
factoids) |
- "People who take antidepressants of any kind
have only a modestly increased risk of suicidal behavior and a decreased
risk of completed suicide. Despite the media attention regarding selective
serotonin reuptake inhibitors [SSRIs] and suicide, little is known about the
real risk. Among people who have been hospitalized for attempted suicide,
the most important variable is the number of prior suicide attempts before
the index hospitalization. All classes of antidepressants were associated
with an increased risk of suicide: tricyclics, SSRIs, and serotonin
norepinephrine receptor inhibitors. However, when the investigators adjusted
medication use as a time-dependent variable, the association was not
statistically significant. Treated patients were less likely to complete
suicide. In addition, some preliminary evidence showed that untreated
patients were more likely to use violent means, such as shooting or hanging.
Those receiving SSRIs were less likely to die of cardiovascular or
cerebrovascular causes. However, among patients aged 10 to 19 years,
those who were taking paroxetine were significantly more likely to attempt
suicide. These findings suggest that all patients who have just started
treatment be monitored closely, especially young patients. This validates
earlier findings that the greatest risk for suicide and SSRI use is at the
beginning of treatment. More data are needed regarding the reduced risk of
cardiovascular and cerebrovascular death associated with SSRIs, and whether
there is an antithrombotic effect associated with the drug class."
- "Cognitive complaints in older adults may
indicate underlying neurodegenerative changes, even in the presence of
normal neuropsychological test results. Individuals who complain of
significant memory problems but who had normal memory testing scores had a
3% reduction in gray-matter (GM) density compared with a 4% reduction among
patients diagnosed with mild cognitive impairment (MCI). Individuals,
who were previously dismissed by many clinicians as the 'worried well,' are
actually detecting changes within themselves and that what we thought were
quite sensitive tests are not able to detect these subtle changes.
Compared with the healthy control (HC) group, the cognitive-complaint and
MCI groups showed similar patterns of decreased GM on whole-brain analysis,
with differences evident in the bilateral medial temporal, frontal, and
other neocortical regions. In addition, higher levels of cognitive
complaints were associated with decreased GM density in the left and right
hippocampi. The pattern of GM density change observed in the study indicates
structural brain changes, similar to those seen in MCI, are present even in
cognitively intact, nondepressed older adults with significant memory
complaints — a finding that may signify a very early stage of the dementia
process and constitute a pre-MCI stage. It is clear that clinicians who
encounter patients with cognitive complaints should take them very seriously
— particularly when other potential causes of memory loss, such as
depression, have been eliminated. Otherwise-healthy, nondepressed elderly
people with significant self-perceived and informant-perceived cognitive
complaints should undergo a careful assessment that includes clinical
evaluation and cognitive testing." Neurology. 2006;67:834-842.
- "Young adults who were exposed to alcohol in
utero are at increased risk for developing an alcohol disorder. These
results suggest that it is not just environmental factors, such as exposure
to maternal drinking and smoking during childhood and adolescence, that
determine a person's risk of alcohol disorders in adulthood, the authors
note. The findings suggest there is also a biologic origin for such
disorders. In utero alcohol exposure to 3 or more glasses per occasion
raised the risk of an alcohol disorder in adulthood, the report indicates.
Alcohol exposure in early pregnancy almost tripled the risk of onset of an
alcohol disorder between 13 and 17 years of age. The effect was even more
pronounced for onset of an alcohol disorder between 18 and 21 years...fetal
exposure to alcohol consumption of three or more glasses per occasion, in
addition to and beyond genetic heritability and environmental factors, may
play an important role in the causal pathway that leads to alcohol disorders
in adulthood." Arch Gen Psychiatry 2006;63:1009-1016.
- "Patients admitted with acute coronary
syndrome (ACS) who have severe chest pain and who are depressed, angry,
hostile or express other negative emotions, are more likely to experience
symptoms of post-traumatic stress disorder (PTSD) afterward. Acute stress
symptoms, depression, negative affect, hostility and high pain scores at
admission were independent predictors of PTSD. Of no predictive value were
severity of disease or demographic factors such as age, income and level of
education. The presence of PTSD after myocardial infarction is a matter of
concern because "coexisting PTSD and coronary heart disease are a
potentially malignant problem with a clear threat to well-being and future
risk of death." Heart 2006;92:1225-1229.
- Mood disorders are a frequent and important
consequence of stroke, but predicting which stroke patients will experience
mood disturbances is difficult. Key baseline predictors of abnormal mood
were disability and history of depression. Pre-stroke patient factors and
clinical stroke factors measured in the acute phase were not helpful in
predicting mood disturbances, according to the team. Also, contrary to
research in the general population, sex and age were poor predictors of
altered mood following stroke. This study emphasizes the complex nature of
mood disturbance after stroke and that multiple factors are likely to
contribute to mood disorders. At present, we only have relatively crude
indicators that disability and a history of depression may predict abnormal
mood. A simple, clinically useful predictive model for use in stroke care
appears difficult to develop. A sizable proportion of patients who
experience abnormal mood after stroke are not being treated, This represents
a significant problem, and may reflect uncertainty among clinicians
concerning the most appropriate treatment, inadequate follow up of patients,
insufficient access to healthcare services, and unwillingness to receive a
diagnosis or medication. Stroke 2006;37:2123-2128.
- Personality traits in childhood are
associated with the potential for heart disease in adulthood, as measured by
carotid artery intima media thickness (IMT). Atherosclerosis is believed to
originate in childhood Previous research has documented that the three
personality traits they assessed -- hyperactivity, negative emotionality,
and low sociability -- predict social and mental problems and high stress
vulnerability in adulthood. Childhood temperament predicted some of the risk
factors associated with cardiovascular disease, including smoking. The early
traits were also related to BMI, systolic blood pressure, and educational
level in adult women.
After adjusting for childhood and adulthood risk factors, childhood
temperament was still significantly associated with IMT in women. This
suggests that temperament may contribute to the development of IMT in two
ways, by influencing risk factors, such as smoking and BMI or by directing
effecting IMT. When evaluated individually, temperament factors still
correlated with risk factors, but only hyperactivity correlated with IMT.
Researchers project that "the difference of 0.03 mm between high and low
hyperactivity groups would imply about a 15% to 20% difference in subsequent
cardiovascular risk. Psychosom Med 2006;68:509-516.
- "Post-traumatic stress disorder (PTSD) is
associated with increased levels of two coagulation factors -- clotting
factor VIII activity and fibrinogen -- and may thereby promote
atherosclerosis and increase the risk of cardiovascular disease. Several
studies have demonstrated the increased cardiovascular risk associated with
PTSD, even years after the trauma. Suggested mediators of this relationship
include unhealthy lifestyle, chronic low-grade inflammation, and coagulation
activation. The levels of specific PTSD symptoms (re-experiencing,
avoidance, and hyperarousal) as well as depression and anxiety were assessed
by interview. From blood samples, the investigators measured resting plasma
levels of clotting factor VII activity (FVII:C), clotting factor VIII
activity (FVIII:C) and clotting factor XII (FXII:C), as well as fibrinogen
and D-dimer. Hyperarousal severity and PTSD symptom severity were associated
with FVIII:C, regardless of covariates. Also, in the PTSD group alone,
hyperarousal and PTSD symptom scores were associated with fibrinogen level,
although the association was attenuated after controlling for depression and
anxiety. FVIII is crucially involved in the formation of thrombin, which in
turn converts fibrinogen to fibrin. Fibrin is the major component of an
intravascular clot and is also found in the atherosclerotic vessel
wall....even subthreshold PTSD with minor levels of stress symptoms after a
trauma could elicit FVIII:C, and diagnosed PTSD could increase fibrinogen
levels. Thus, symptoms associated with PTSD could lead to a hypercoagulable
state, which "could be of particular clinical importance in terms of an
elevated cardiovascular risk and overall mortality several years down the
line." Psychosom Med 2006:68:598-604
- Changes in EEG patterns predict response to
antidepressant therapy in patients with major depressive disorder. Previous
studies have shown that changes in prefrontal EEG cordance after the start
of antidepressant therapy are associated with clinical outcomes in patients
with major depressive disorder. Changes in prefrontal EEG cordance during
the placebo lead-in phase were significantly associated with final Hamilton
depression scale scores for patients randomized to one of the antidepressant
medications. Decreases in prefrontal cordance were associated with lower
final depression scores, the results indicate, and medication responders
differed significantly from medication nonresponders. Some
neurophysiological changes that are associated with endpoint antidepressant
outcome may reflect nonpharmacodynamic factors. Am J Psychiatry
2006;163:1-7.
- Cognitive behavioral therapy (CBT) can
improve somatization disorder (SD). Patients diagnosed having SD present
with a lifetime history of multiple, medically unexplained physical
symptoms. No psychotherapeutic or pharmacologic intervention has been
found to produce clinically meaningful improvement in symptoms or
functioning of patients with SD, but somatization symptoms were less severe
when treated with CBT. These patients also were significantly more likely to
be rated as either "very much improved" or "much improved" than patients
treated only with augmented standard medical care. The CBT group also fared
better than the standard care group in terms of greater improvements in
self-reported functioning and somatic symptoms and a greater decrease in
healthcare costs. For patients diagnosed as having SD, CBT may produce
clinical benefits beyond those that result from the current state-of-the-art
treatment. CBT may contribute to producing enduring, clinically meaningful
benefits in patients with SD. Arch Intern Med. 2006;166:1512-1518.
- Capsulotomy can be an effective treatment
for the most severe forms of obsessive-compulsive disorder (OCD) and
anxiety, but patients often experience a major personality change, including
persistent apathy and sexual disinhibition.The patients themselves, however,
seemed glad to trade their OCD symptoms for the apathy and other side
effects experienced. While the operation often led to resolution of the most
severe OCD symptoms, over a third of patients developed apathy and had
problems planning and executing activities. Other serious side effects
included epilepsy, sexual disinhibition, and urinary incontinence. In light
of these findings, initial "enthusiasm for capsulotomy as a treatment for
severe OCD has faded. The good news is that in recent years some effective
psychological methods of treating severe OCD and anxiety have appeared,
including intensive cognitive behavioral therapy.
- The first gene known to control the internal
clock of humans and other mammals works exactly in reverse of what was
previously believed. The finding could mean a dramatic reversal in the way
circadian rhythm disorders such as depression, insomnia, and chronic fatigue
are treated. Previously, it was believed the tau mutation caused a decrease
in activity of the casein kinase 1 epsilon (CK1) gene, which in turn caused
the body's circadian rhythm to speed up. But, in fact, researchers have now
discovered the opposite is true, and it is an increase in activity of the
CK1 gene that causes affected animals to have a shorter day. Several
pharmaceutical companies have been developing inhibitors of CK1 activity
based on the hypothesis that CK1 loss of function speeds up the clock. But
this new insight means drug studies are going to have to be redesigned.
Computer simulations of how the tau mutation influenced the mammalian body
clock using the prevailing theory that the mutation decreased CK1 gene
activity showed the day became longer instead of shorter. This highlights
the importance of developing detailed quantitative models and putting them
to the test. This mathematical model turned out to be an extremely powerful
tool and was the first to suggest the conventional wisdom that the tau
mutation causes a loss of function was incorrect. CK1 is one of the best
drug targets in the circadian rhythm system, and this finding could have
major implications for patients suffering from familial advanced sleep phase
syndrome, as well as more common circadian rhythm disorders such as seasonal
affective disorder and depression. Proc Natl Acad Sci. 2006;103:10618-10623
- A low serum docosahexaenoic acid level and
elevated omega-6/omega-3 ratio predict suicidal behavior among patients with
major depression. Depressive disorders are associated with low levels of
omega-3 plasma polyunsaturated fatty acids and elevated omega-6/omega-3
ratios, while augmentation with omega-3 plasma polyunsaturated fatty acids
is reportedly therapeutic. Researchers examined whether an association
exists between plasma polyunsaturated fatty acid status and suicide attempt.
They measured plasma polyunsaturated fatty acid levels and percentages of
total phospholipid fatty acids for docosahexaenoic acid, eicosapentaenoic
acid, arachidonic acid, and omega-6/omega-3 ratio in depressed patients
monitored for suicide attempt over 2 years. Depression and suicidal thoughts
were measured using the 24-item Hamilton Depression Rating Scale and the
Beck Scale for Suicidal Ideation. Lower docosahexaenoic acid percentage of
total phospholipid fatty acids and higher omega-6/omega-3 ratios were
predictive of suicide attempts. Of the clinical and demographic variables,
only age and suicidal ideation had significant correlations with
docosahexaenoic acid percentages of total phospholipid fatty acids. If
confirmed, this finding would have implications for the neurobiology of
suicide and reduction of suicide risk. Am J Psychiatry 2006;163:1100-1102.
-
"Age-associated loss of executive function appears to inhibit the ability to
control negative, ruminative thoughts, which then leads to depression that
manifests only after age 60. Normal deficits in executive function in older
age include losses of attentional control, inhibitory ability, flexible
thinking, memory, and problem-solving ability. Executive dysfunction may
lead to ruminative thinking, manifested as decreased ability to inhibit
persistent negative thoughts in the face of negative life events, which in
turn increases the risk of late-onset depression. Late-onset depressive
symptoms were associated with poorer performance on tests of executive
function. And only in the late-onset group was executive dysfunction
positively correlated with rumination. Interventions to improve executive
function or reduce ruminative thought patterns -- such as physical exercise,
cognitive-behavioral or problem-solving therapies -- may prevent or improve
symptoms of depression in later life." Cogn Ther Res 2006.
|
|
Clinical
Services | Educational
Services | OnLine
Referral |
Contact Us |
|
©2006 David B. Adams,
Ph.D. |
|