Depression and Endocrine Disorders: Focus on the Thyroid and Adrenal System

Of the various hypothalamic–pituitary–end organ axes, the thyroid and adrenal systems have been implicated most often in affective disorders. Patients with primary thyroid disease have high rates of depression, and patients with Addison's disease or Cushing's syndrome have relatively high rates of affective and anxiety symptoms. However, the major support for these endocrine axes in the pathophysiology of mood disorders comes from studies in which alterations in components of the hypothalamic–pituitary–thyroid (HPT) and the hypothalamic–pituitary–adrenal (HPA) axes have been documented in patients with primary depression. Concerning the HPT axis, depressed patients have been reported to have: (a) alterations in thyroid-stimulating hormone response to thyrotropin-releasing hormone (TRH); (b) an abnormally high rate of antithyroid antibodies; and (c) elevated cerebrospinal fluid (CSF) TRH concentrations. Moreover, tri-iodothyronine has been shown conclusively to augment the efficacy of various antidepressants. Concerning the HPA axis, depressed patients have been reported to exhibit: (a) adrenocorticoid hypersecretion; (b) enlarged pituitary and adrenal gland size; and (c) elevated CSF corticotropin-releasing factor concentrations. All of the HPA axis alterations in depression studied thus far are state-dependent, whereas the HPT axis alterations may be partially trait and partially state markers

Depression, alterations in platelet function, and ischemic heart disease

Platelets, the smallest corpuscular component of human blood, are central to various crucial biologic pathways in the human body. Diminished platelet function is thought to contribute to the increased risk of ischemic heart disease in patients with major depressive disorder, and to the increased morbidity and diminished survival of depressed patients after an index myocardial infarction. We reviewed both recent studies that evaluated platelet function in various patient groups and recent information regarding the potential beneficial effects of selective serotonin reuptake inhibitors on platelet reactivity

Chapter 5 Depression really does hurt your heart: stress, depression, and cardiovascular disease

The interplay of stress, personality traits, and psychiatric symptoms syndromes with the cardiovascular system, has long intrigued investigators in their search for psychosocial and psychiatric contributions for the development and progression of atherosclerotic heart disease. Surveillance of the established risk factors for atherosclerotic heart disease (IHD), e.g. smoking, hypertension, hypercholesterolemia, and age, leave a substantial portion of the differences in rates of IHD unexplained. Indeed, the Type A personality pattern has been extensively studied as a risk factor for coronary artery disease, (CAD). However, increasing evidence is accumulating suggesting that an affective disorder, major depression, is a major contributing factor, not only to elevated morbidity and mortality after an index myocardial infarction (MI), but as an independent risk factor in the development of atherosclerotic heart disease. Major depression and depressive symptoms are considerably more common in patients with a variety of medical illnesses than in individuals in the general population. Indeed, receiving a diagnosis of a serious, life-threatening illness often results in a cascade of emotional responses, including feelings of sadness, shock, disbelief, anxiety, or a myriad of other emotional responses

Prevalence and Improvement in Psychopathology in Opioid Dependent Patients Participating in Methadone Maintenance

Questions continue in the literature concerning potential cause and effect relationships between opiate dependency and several organically-based psychiatric disorders. For example, does opiate dependency produce secondary anxiety and dysthymic syndroms in otherwise healthy persons? or is narcotics a misuse by a patient an attempt to self-medicate pre-existing psychopathology? Does the severity of psychopathologic symptoms decrease with time in treatment? To resolve such questions, we routinely conduct psychiatric treatment evaluations on all opioid dependent patients enrolled into methadone maintenance. In this study, we report upon treatment outcomes for a cohort of 71 patients evaluated for psychopathology upon intake and followed up after being in treatment for a mean time of 24.5 (SD 8.0) months. Based upon objective psychometric testing with confirmatory clinical interview, significant, longitudinal improvements were seen in the symptom severity of anxiety and dysthemia present upon intake evaluation. Personality profiles also improved with treatment. In general, patients presenting with more severe psychopathology required more visits with professional staff in order to stabilize their life situations and personal relationships. No correlation was noted between drug use and severity of psychopathology. Data support the thesis that many opioid dependent patients are self-medicating themselves for preexisting organic psychopathology, most commonly, a combined anxiety-dysthemia syndrome. Improvement seems to occur secondary to the mood stabilizing properties of methadone in disorders thought to be mediated or moderated by endogenous endorphins rather than because of psychotherapeutic interventions

Are platelets the link between depression and ischemic heart disease?

The role of platelets as the link between ischemic heart disease and depression is reviewed. Platelet function abnormalities, including increased platelet reactivity, may predispose depressed patients to clotting diatheses and may explain their vulnerability to cardiovascular disease. Platelet physiologic characteristics, influences on platelet response, and indicators of platelet reactivity are discussed. Measurements of platelet activation, secretion, and aggregation have enabled the study of platelet responses in patients with major depression. The findings of clinical trials evaluating platelet responses to antidepressant treatment are described, and recommendations for future studies are proposed. (Am Heart J 2000;140:S57-62.

The Relationship of Depression to Cardiovascular Disease: Epidemiology, Biology, and Treatment

This article reviews the burgeoning literature on the relationship of mood disorders and heart disease. Major depression and depressive symptoms, although commonly encountered in medical populations, are frequently underdiagnosed and undertreated in patients with cardiovascular disease (CVD). This is of particular importance because several studies have shown depression and its associated symptoms to be a major risk factor for both the development of CVD and death after an index myocardial infarction. This review of the extant literature is derived from MEDLINE searches (1966-1997) using the search terms "major depression," "psychiatry," "cardiovascular disease," and "pathophysiology." Studies investigating pathophysiological alterations related to CVD in depressed patients are reviewed. The few studies on treatment of depression in patients with CVD are also described. Treatment of depression in patients with CVD improves their dysphoria and other signs and symptoms of depression, improves quality of life, and perhaps even increases longevity. Recommendations for future research are proposed.Arch Gen Psychiatry. 1998;55:580-592--

Stress, depression, and coronary artery disease: Modeling comorbidity in female primates

Depression and coronary heart disease (CHD) are leading contributors to disease burden in women. CHD and depression are comorbid; whether they have common etiology or depression causes CHD is unclear. The underlying pathology of CHD, coronary artery atherosclerosis (CAA), is present decades before CHD, and the temporal relationship between depression and CAA is unclear. The evidence of involvement of depression in early CAA in cynomolgus monkeys, an established model of CAA and depression, is summarized. Like people, monkeys may respond to the stress of low social status with depressive behavior accompanied by perturbations in hypothalamic–pituitary–adrenal (HPA), autonomic nervous system, lipid metabolism, ovarian, and neural serotonergic system function, all of which are associated with exacerbated CAA. The primate data are consistent with the hypothesis that depression may cause CAA, and also with the hypothesis that CAA and depression may be the result of social stress. More study is needed to discriminate between these two possibilities. The primate data paint a compelling picture of depression as a whole-body disease

Depression and cardiac disease

The relationship of mood disorders to cardiovascular disease is receiving considerable attention. The literature on diagnosing depression in patients with cardiovascular disease (CVD), is briefly summarized. There is overwhelming evidence that major depression and other mood disorders, though common, are underdiagnosed and undertreated in patients with coronary artery disease (CAD). This is of paramount importance because depression appears to be a major risk factor in both the development of CAD and in death after myocardial infarction. The pathophysiological alterations in depression that may underlie vulnerability to cardiovascular disease are reviewed with a focus on alterations in heart rate variability and platelet aggregation. The studies on treatment of depression in patients with CAD are also summarized. Treatment of depression in CAD patients appears to be effective, improves quality of life, and might increase longevity. Depression and Anxiety, Volume 8, Supplement 1:71–79, 1998. © 1998 Wiley‐Liss, Inc