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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.

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©2006 David B. Adams, Ph.D.