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Heiner Fangerau

Publications and source records attributed to Heiner Fangerau.

10 recordsLinked to original sources
PubMed2006

Why should we bother? Ethical and social issues in individualized medicine.

Individualized medicine, methodologically rooted in pharmacogenetics and pharmacogenomics, is now venturing into clinical application. Prescribing the right drug in the right dose to the right patient according to specific health needs and individual characteristics is a core mission of individualized medicine. The intrinsic values of this mission are so self-evident that--at first glance--the ethical and social issues raised by individualized medicine seem to be negligible. However, the translation of pharmacogenetics and pharmacogenomics into clinical routine not only requires the collection and evaluation of large amounts of individual genetic data, but also heralds the need for further clinical studies on the applicability of genotype-related pharmacotherapy. Both requirements raise a set of specific normative issues. We argue that ethical and social questions of the desirability and applicability of individualized medicine should be integrated in a reconstructive approach to biomedical ethics, which is guided by criteria of social accountability. As a first step, we analyse the ethical and social issues of individualized medicine in the transition to clinical practice, using social accountability heuristically and as an evolutionary approach. Since the pharmacogenetics and pharmacogenomics of neuropsychiatric disorders are among the most advanced fields of individualized medicine, as a second step we use depressive disorders to elucidate the specific, crucial ethical and social questions involved in assessing patients' situations, disease entities and phenotypes to relate them to genetic variations for the purpose of individualized drug regimens.

Ethics, Medical↗
PubMed2006

["Smoked meat, full of rind, hardly edible"--patient's complaints and doctor's rebuttal in the first German state-run mental sanatory "Rasemühle" between 1903 and 1932].

Around 1900 a psychiatric reform movement propagated the foundation of sanatoriums for the lower middle class in Germany. These sanatoriums were supposed to cure patients suffering from neurasthenia and associated disorders. Many private sanatoriums existed for curing neurasthenia. Visiting them was a luxury beyond most of the patients' means. Therefore, the so called "Volksnervenheilstätten"-movement aimed at providing sanatorium care for free or at very low costs. One of the first sanatoriums that arose from this movement was the "Rasemühle" close to Goettingen. It was founded in 1903. As a governmentally funded institution for the less wealthy the "Rasemühle" constantly moved between legitimation and critique. Areas of conflict included on the one hand the need to operate economically (as requested by the sponsor) and on the other hand the demands of neurasthenic patients for optimal care and cure. Patients' complaints about the sanatorium addressed to the financiers or governmental institutions and the reactions of the sanatorium's director serve as a valuable tool for reconstructing these areas of conflict. An analysis of the complaint files of the "Rasemühle" between 1903 and 1932 reveals that complaints usually included food, accommodation and the doctors' behaviour. Before the First World War the sanatorium's reaction usually aimed at pathologising patients who put forward complaints. Complaining was described as a symptom of the treated disorder. After financiers and insurance companies had reduced their engagement for neurasthenics during the late 1920s financing the sanatorium became more difficult. With the vanishing neurasthenia discourse the "Rasemühle" had to enter the market of private patients to survive. Now the reaction to complaints shifted to understanding. The responsible government agency was asked to invest into the sanatorium to make it competitive on the market. Patients were not seen anymore as unwilling petitioners but as customers whose needs and demands should be fullfilled.

Germany↗
PubMed2005

Suicide attempts in schizophrenia and affective disorders with relation to some specific demographical and clinical characteristics.

Demographical and clinical characteristics have been reported to modulate the risk for suicide. This study analysed demographical and clinical characteristics with respect to lifetime suicide attempts in 500 individuals affected with schizophrenic or affective disorders. Suicide attempts were associated with poor premorbid social adjustment, low age at onset, low scores on the "Global Assessment Scale" and childlessness in females.

Adult↗
PubMed2004

From degeneration to genetic susceptibility, from eugenics to genethics, from Bezugsziffer to LOD score: the history of psychiatric genetics.

Reviewing the history of psychiatric genetics is a difficult task, since--in contrast to genetic research into most other disorders--it cannot simply be done by chronologically listing methodological achievements and major findings. Instead, it necessitates a comprehensive assessment of how the aetiological concept of mental disorders has developed since as early as the world of ancient Greece. Furthermore, it has to touch upon the sensitive issue of the eugenic movement that was closely linked to the study of heredity in mental disorders in the first half of the 20th century and, in Nazi Germany, led to the systematic mass murder of psychiatric patients. Finally, reviewing the scientific dimensions, history of psychiatric genetics is at the same time a walk through the history of complex genetics in general. In our review, we try to pay tribute to this complexity. We argue that psychiatric genetics has not only propelled our understanding of mental disorders but has significantly benefited genetic research into other complex disorders through the development of methodologically robust approaches (e.g., systematic phenotype characterisation, methods to control for ascertainment biases, age-correction). Given the recent reasons for new optimism, i.e., the identification of susceptibility genes for psychiatric phenotypes, a continued methodologically sound approach is needed more than ever to guarantee robust results. Finally, psychiatric genetic research should never again be performed in an environment void of ethical standards.

Ethics, Medical↗
PubMed2004

Computer-assisted phenotype characterization for genetic research in psychiatry.

Psychiatric disorders differ from other complex phenotypes in their lack of objectively assessable biological markers that contribute to the establishment of a research diagnosis for genetic studies. To nevertheless allow for the delineation of genetically meaningful diagnostic entities for psychiatric genetic research, comprehensive phenotype characterization procedures are required. It is widely agreed that these should include the standardized assessment of life-time clinical symptomatology, sociodemographic, and environmental factors. Data should be based on several sources, i.e. diagnostic interviews with probands and their relatives as well as a thorough review of medical records, and final assignment of diagnosis should follow robust algorithms (i.e. best-estimate procedures, consensus diagnosis). Here, we outline a practical implementation of such a phenotype characterization strategy, including patient recruitment, study enrolment procedures, comprehensive diagnostic assessment, and data management. We argue that successful psychiatric phenotype characterization requires flexible tools. For this purpose, we have developed a computer-assisted phenotype characterization inventory, built around the backbone of a relational database. It allows for the straightforward assessment of symptoms, automated error checks and diagnostic assignment, easily manageable data storage and handling, and flexible data transfer between various research centers even across language barriers, while at the same time keeping up with the highest standards for the protection of sensitive patient data.

Algorithms↗
PubMed2003

Improving information systems in Europe: EURETHNET.

The efforts of the European Commission to create a "European Research Area" in the field of biotechnology are accompanied by a growing demand for an ethical discourse. Cultural differences between the European Union's member states create a vital need to improve bioethical information structures in Europe so as to foster European bioethics discourses and to cope with ethical pluralism. Responding to the need for an increased European contribution to the international discussion on ethics in medicine and biotechnology, some of Europe's leading bioethics institutions have joined forces to establish the international network "EURETHNET". 18 partners from nine European countries agreed to develop an information network and knowledge base in the field of ethics in medicine and biotechnology. This short communication displays the aims, scope and realisation of the network.

Bioethics↗
PubMed2003

["Baur-Fischer-Lenz" in 1921-1940 critical book reviews: a quantitative study of contemporary reception of racial eugenics theories].

In 1921 the distinguished scientists Erwin Baur, Eugen Fischer and Fritz Lenz published the book "Menschliche Erblichkeitslehre und Rassenhygiene" in two volumes. Until 1941 their work went through 5 editions and became the standard textbook on human heredity and racial hygiene (eugenics) in Germany. Between 1921 and 1941 Baur's, Fischer's and Lenz's book was reviewed in many German and foreign scientific and popular journals. 325 of these reviews have been systematically analysed. They paint a representative picture of the book's contemporary reception. The analysis of the reviews helps to quantify the acceptance of the book among the German scientific community and shows how the reviewers created the image of the book as a standard work. Furthermore, the analysis elucidates the style of thinking that was prevalent among the reviewers.

Ethnicity↗
PubMed2002

Association study between two variants in the DOPA decarboxylase gene in bipolar and unipolar affective disorder.

Irregularities of dopaminergic and serotonergic neurotransmission have been implicated in a variety of neuropsychiatric disorders. DOPA decarboxylase (DDC), also known as aromatic L-amino acid decarboxylase, is an enzyme involved directly in the synthesis of dopamine and serotonin and indirectly in the synthesis of noradrenaline. Therefore, the DDC gene can be considered as a candidate gene for affective disorders. Recently, two novel variants were reported in the DDC gene: a 1-bp deletion in the promoter and a 4-bp deletion in the untranslated exon 1. Subsequently, an association case-control study including 112 English patients and 80 Danish patients with bipolar affective disorder (BPAD) revealed a significant association with the 1-bp deletion. This finding prompted us to analyze whether this effect was also present in a larger and ethnically homogeneous sample of 228 unrelated German patients with BPAD (208 patients with BP I disorder, 20 patients with BP II disorder), 183 unrelated patients with unipolar affective disorder (UPAD), and 234 healthy control subjects. For both BPAD and UPAD we could not detect a genetic association with either variant. Thus, our results do not support an involvement of the 1-bp or 4-bp deletion within the DDC gene in the etiology of affective disorders.

Adult↗
PubMed2002

Pharmacogenetics of tardive dyskinesia: combined analysis of 780 patients supports association with dopamine D3 receptor gene Ser9Gly polymorphism.

Variability among individuals in their therapeutic response to psychotropic drugs and in susceptibility to adverse effects is considerable. Pharmacogenetics addresses the contribution of genetic factors to this variability. An important focus of interest in pharmacogenetics has been on candidate genes that play a role in susceptibility to the antipsychotic drug-induced adverse effect, tardive dyskinesia (TD). Four published studies have reported an association between a serine (ser) to glycine (gly) polymorphism in exon 1 of the dopamine D3 receptor gene (DRD3) and TD; three failed to replicate this finding and one found an insignificant trend. We examined the association in a pooled sample of 780 patients (317 with TD and 463 without TD) drawn from 6 research centers, who were divided into 8 groups based on their population origin. The analysis employed stepwise logistic regression so as to allow confounding effects of group, age, and gender to be taken into account. TD was significantly associated with DRD3 gly allele carrier status (x(2)=4.46, df 1, p =.04) and with DRD3 genotype (x(2)=6.62, df 2, p =.04) over and above the effect of group. Similar positive effects were observed when controlling for age and gender (x(2)=5.02, df 1, p =.02 for gly allele carrier status; x(2) = 7.51, df 2, p =.002 for genotype). Examining abnormal involuntary movement scores as a continuous variable, we found that patients homozygous for the gly allele had significantly higher scores than ser-gly heterozygotes (p =.006) or ser-ser homozygotes (p <.0001). We also performed a meta-analysis that included, besides the groups in the combined analysis, three other published studies on DRD3 and TD. The Mantel-Haenszel pooled odds ratio for DRD3 gly allele carrier status increasing susceptibility to TD was 1.33 (95% CI 1.04-1.70, p =.02); the cumulative pooled estimate showed an odds ratio of 1.52 (95% CI 1.08-1.68, p <.0001). These findings support a small but significant contribution of the DRD3 ser9gly polymorphism to TD susceptibility that is demonstrable over and above population effects and the effect of age and gender on the phenotype.

Adult↗