Measuring Health: A Guide to Rating Scales and Questionnaires

The dopamine hypothesis of schizophrenia has been one of the most enduring ideas in psychiatry. Initially, the emphasis was on a role of hyperdopaminergia in the etiology of schizophrenia (version I), but it was subsequently reconceptualized to specify subcortical hyperdopaminergia with prefrontal hypodopaminergia (version II). However, these hypotheses focused too narrowly on dopamine itself, conflated psychosis and schizophrenia, and predated advances in the genetics, molecular biology, and imaging research in schizophrenia. Since version II, there have been over 6700 articles about dopamine and schizophrenia. We selectively review these data to provide an overview of the 5 critical streams of new evidence: neurochemical imaging studies, genetic evidence, findings on environmental risk factors, research into the extended phenotype, and animal studies. We synthesize this evidence into a new dopamine hypothesis of schizophrenia-version III: the final common pathway. This hypothesis seeks to be comprehensive in providing a framework that links risk factors, including pregnancy and obstetric complications, stress and trauma, drug use, and genes, to increased presynaptic striatal dopaminergic function. It explains how a complex array of pathological, positron emission tomography, magnetic resonance imaging, and other findings, such as frontotemporal structural and functional abnormalities and cognitive impairments, may converge neurochemically to cause psychosis through aberrant salience and lead to a diagnosis of schizophrenia. The hypothesis has one major implication for treatment approaches. Current treatments are acting downstream of the critical neurotransmitter abnormality. Future drug development and research into etiopathogenesis should focus on identifying and manipulating the upstream factors that converge on the dopaminergic funnel point.

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The Dopamine Hypothesis of Schizophrenia: Version III—The Final Common Pathway

We now know that depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity, as well as activation of the compensatory anti-inflammatory reflex system. It is similarly accompanied by increased oxidative and nitrosative stress (ON these include psychosocial stressors, poor diet, physical inactivity, obesity, smoking, altered gut permeability, atopy, dental cares, sleep and vitamin D deficiency. The identification of known sources of inflammation provides support for inflammation as a mediating pathway to both risk and neuroprogression in depression. Critically, most of these factors are plastic, and potentially amenable to therapeutic and preventative interventions. Most, but not all, of the above mentioned sources of inflammation may play a role in other psychiatric disorders, such as bipolar disorder, schizophrenia, autism and post-traumatic stress disorder.

/pdf/so-depression-is-an-inflammatory-disease-but-where-does-the-2843tu0lea.pdf

So depression is an inflammatory disease, but where does the inflammation come from?

Cardiovascular disease is the leading cause of mortality in American women. Since 1984, the annual cardiovascular disease mortality rate has remained greater for women than men; however, over the last decade, there have been marked reductions in cardiovascular disease mortality in women. The dramatic decline in mortality rates for women is attributed partly to an increase in awareness, a greater focus on women and cardiovascular disease risk, and the increased application of evidence-based treatments for established coronary heart disease. This is the first scientific statement from the American Heart Association on acute myocardial infarction in women. Sex-specific differences exist in the presentation, pathophysiological mechanisms, and outcomes in patients with acute myocardial infarction. This statement provides a comprehensive review of the current evidence of the clinical presentation, pathophysiology, treatment, and outcomes of women with acute myocardial infarction.

Acute Myocardial Infarction in Women: A Scientific Statement from the American Heart Association

The following article presents the theoretical model of strength and vulnerability integration (SAVI) to explain factors that influence emotion regulation and emotional well-being across adulthood. The model posits that trajectories of adult development are marked by age-related enhancement in the use of strategies that serve to avoid or limit exposure to negative stimuli but by age-related vulnerabilities in situations that elicit high levels of sustained emotional arousal. When older adults avoid or reduce exposure to emotional distress, they often respond better than younger adults; when they experience high levels of sustained emotional arousal, however, age-related advantages in emotional well-being are attenuated, and older adults are hypothesized to have greater difficulties returning to homeostasis. SAVI provides a testable model to understand the literature on emotion and aging and to predict trajectories of emotional experience across the adult life span.

/pdf/strength-and-vulnerability-integration-a-model-of-emotional-fawcwwzvyf.pdf

Strength and vulnerability integration: a model of emotional well-being across adulthood.

Attached to the web — harmful use of the Internet and its correlates

Context Prenatal smoking exposure modulates brain development, which may deviate mental development of the offspring. Objective To study the effects of prenatal smoking exposure on psychiatric morbidity and mortality among Finnish young adults by means of population-based longitudinal register data. Design Information on maternal smoking as reported by the mothers (0, 10 cigarettes a day) and other background factors (maternal age and parity and child's sex, gestational age, birth weight, and 5-minute Apgar score) was derived from the Finnish Medical Birth Register. Information on children's psychiatric diagnoses related to outpatient visits (1998-2007), children's inpatient care (1987-2007), and mothers' psychiatric inpatient care (1969-1989) was derived from the Finnish Hospital Discharge Register. Information on deaths and their causes for the children (1987-2007) was received from the Cause-of-Death Register. Setting Population-based study of all singletons born in Finland from 1987 to 1989 with information on prenatal smoking exposure. Patients The source population included all singleton births in Finland from January 1, 1987, through December 31, 1989 (n = 175 869), excluding children with major congenital anomalies (3.1%) and children who died during the first week of life (0.3%). Main Outcome Measures Psychiatric morbidity and mortality. Results The prevalence of maternal smoking was 15.3%. The risk of psychiatric morbidity was significantly higher in the exposed children than in the unexposed children. Among the offspring of mothers who smoked fewer than 10 cigarettes a day, 21.0% had any psychiatric diagnoses (adjusted odds ratio [OR], 1.53 [95% confidence interval (CI), 1.47-1.60]) compared with 24.7% among those of mothers who smoked more than 10 cigarettes a day (1.85 [1.74-1.96]) and 13.7% in the unexposed children (the reference group). The risk was significantly increased for most of the psychiatric diagnoses. The strongest effects were in psychiatric disorders due to psychoactive substance use and in behavioral and emotional disorders. The risk of mortality was significantly higher in children exposed to more than 10 cigarettes a day (OR, 1.69 [95% CI, 1.31-2.19]) compared with unexposed children. Conclusion Prenatal smoking exposure is associated with an increased risk of psychiatric morbidity, whereas prenatal exposure to more than 10 cigarettes a day increases the risk of mortality in childhood, adolescence, and young adulthood.

https://jamanetwork.com/journals/jamapsychiatry/articlepdf/210861/yoa90119_841_849.pdf

Prenatal smoking exposure and the risk of psychiatric morbidity into young adulthood.

Background Studies suggest that childhood adversities are important determinants of various types of later illnesses as well as poor health behaviour. However, few large-scale prospective studies have examined the associations between childhood adversities and cardiovascular disease. Objective To investigate whether childhood adversities are associated with increased risk of incident cardiovascular disease Design and setting Participants were 23 916 men and women in four age groups (20–24, 30–34, 40–44, and 50–54 years) from the Health and Social Support study, a longitudinal study on a random sample representative of the Finnish population. Data from national health registers on coronary heart disease and cerebrovascular disease during a mean follow-up of 6.9 years were linked to survey responses on childhood adversities. Cox proportional hazard models were adjusted for age group and potential mediators (education, health risk behaviours, diabetes and depression). Results There was a significant linear trend between the number of childhood adversities and disease end points in women. The risk of incident cardiovascular disease was threefold among women exposed concurrently to three types of childhood adversities (financial difficulties, interpersonal conflicts and longstanding illness of a family member). Among men, increased risk was observed only among those with longstanding illness of a family member (HR=1.44; 95% CI 1.06 to 1.96). Conclusions In this prospective population-based sample, childhood adversities were associated with a significantly increased risk of objectively verified cardiovascular disease, especially among women but to a lesser extent among men. More studies with prospective settings are needed to confirm the association and possible mechanisms.

Childhood adversities as predictors of incident coronary heart disease and cerebrovascular disease

Environmental factors such as maternal smoking can significantly modulate genetically programmed brain development during foetal life. This review looks at how prenatal smoking exposure modulates brain development, including new evidence on the effects of smoking on foetal brain development and function.

Conclusion
Smoking during pregnancy exposes the foetus to thousands of health-threatening chemicals, restricting foetal body and head growth. Alterations in brain structure and function have been seen in children exposed to prenatal smoking.

Jyrki Korkeila

Papers

Attached to the web — harmful use of the Internet and its correlates

Prenatal smoking exposure and the risk of psychiatric morbidity into young adulthood.

Childhood adversities as predictors of incident coronary heart disease and cerebrovascular disease

Smoking during pregnancy affects foetal brain development

Striatal dopamine synthesis in first-degree relatives of patients with schizophrenia.