Health as Complete Well-Being: The WHO Definition and Beyond

Abstract The paper defends the World Health Organisation (WHO) definition of health against widespread criticism. The common objections are due to a possible misinterpretation of the word complete in the descriptor of health as ‘complete physical, mental and social well-being’. Complete here does not necessarily refer to perfect well-being but can alternatively mean exhaustive well-being, that is, containing all its constitutive features. In line with the alternative reading, I argue that the WHO definition puts forward a holistic account, not a notion of perfect health. I use historical and analytical evidence to defend this interpretation. In the second part of the paper, I further investigate the two different notions of health (holistic health and perfect health). I argue that both ideas are relevant but that the holistic interpretation is more adept for political aims.</jats:p

The Quantitative Problem for Theories of Dysfunction and Disease

Many biological functions allow for grades. For example, secretion of a specific hormone in an organism can be on a higher or lower level, compared to the same organism at another occasion or compared to other organisms. What levels of functioning constitute instances of dysfunction; where should we draw the line? This is the quantitative problem for theories of dysfunction and disease. I aim to defend a version of biological theories of dysfunction to tackle this problem. However, I will also allow evaluative considerations to enter into a theory of disease. My argument is based on a distinction between a biological and a clinical perspective. Disease, according to my reasoning, is restricted to instances that fall within the boundaries of biological dysfunctions. Responding to the quantitative problem does not require arbitrary decisions or social value-judgements. Hence, I argue for a non-arbitrary, fact-based method to address the quantitative problem. Still, not all biological dysfunctions are instances of disease. Adding a clinical perspective allows us to prevent the potential over-inclusiveness of the biological perspective, because it restricts the boundaries of disease even further.</jats:p

Zeitschrift für Praktische Philosophie / Die politische Quacksalberei des libertären Paternalismus

Der libertäre Paternalismus befürwortet Eingriffe in die Entscheidungsfindung von Bürgern, ohne ihnen Optionen völlig nehmen zu wollen. Vielmehr soll die Lenkung des Willens durch Schubser (nudges) geschehen. Im folgenden Beitrag möchte ich zeigen, dass der libertäre Paternalismus auf tönernen Füßen steht. Ich bediene mich dabei des polemischen Bilds von Quacksalbern. Dieses Bild passt zu meinem argumentativen Vorgehen, da ich erstens zeigen will, dass der libertäre Paternalismus falsche Diagnosen über vermeintliche Krankheiten der Willensbildung stellt, und zweitens, dass er die falsche Therapie empfiehlt. Im ersten Teil des Artikels kritisiere ich die Diagnose des libertären Paternalismus, wonach Menschen in ihrer Entscheidungsfindung systematisch fehlschlagen. Die Auswirkungen der zugrundeliegenden psychologischen Forschung werden missinterpretiert und damit vielen menschlichen Entscheidungen eine Art Defekt zugeschrieben. Der zweite Teil des Beitrags hinterfragt die Therapie des libertären Paternalismus. Für entsprechende Interventionen in die Wahlarchitektonik muss Wissen erlangt werden über die Richtung, in welche die Menschen jeweils geschubst werden sollten. Die hier genannte epistemische Aufgabe kann mit den theoretischen Mitteln des libertären Paternalismus nicht gelöst werden.The Libertarian Paternalism is in favour of interfering in the decision making process of citizens, without wanting to take all their options away. Instead, the guiding of citizens will should rather happen in form of so called nudges. In the following article I want to show that the Libertarian Paternalism stands on feet of clay. Thereby I employ the polemic picture of charlatans. This picture fits my argumentative method, as I firstly want to show that Libertarian Paternalism misdiagnoses alleged problems of decision making; and secondly, that it recommends the wrong sort of therapy. In the first part of this article I criticise the Libertarian Paternalism diagnosis that people systematically fail in decision making processes. The consequences of the underlying psychological research findings were misinterpreted, which led to mislabelling many human decisions as sort of defective. The second part questions the therapy form of Libertarian Paternalism. It is necessary to first gain knowledge about the direction in which humans respectively want to be nudged, to be able to intervene appropriately in the decision making process. This epistemic problem cannot be solved by the theoretical means of Libertarian Paternalism

Who cares what the people think? Revisiting David Miller’s approach to theorising about justice

David Miller’s methodological approach to theorising about justice, articulated most explicitly in Principles of Social Justice (1999) but informing his work up to and including the recent Strangers in Our Midst (2016), takes people’s existing beliefs and sentiments – ‘what the people think’ – to play a fundamental constitutive role in the development of normative principles of justice. In this critical exchange, Alice Baderin, Andreas Busen, Thomas Schramme and Luke Ulas¸ subject differing aspects of this methodology to critique, before Miller responds

ADAM10 is expressed in human podocytes and found in urinary vesicles of patients with glomerular kidney diseases

<p>Abstract</p> <p>Background</p> <p>The importance of the Notch signaling in the development of glomerular diseases has been recently described. Therefore we analyzed in podocytes the expression and activity of ADAM10, one important component of the Notch signaling complex.</p> <p>Methods</p> <p>By Western blot, immunofluorescence and immunohistochemistry analysis we characterized the expression of ADAM10 in human podocytes, human urine and human renal tissue.</p> <p>Results</p> <p>We present evidence, that differentiated human podocytes possessed increased amounts of mature ADAM10 and released elevated levels of L1 adhesion molecule, one well known substrate of ADAM10. By using specific siRNA and metalloproteinase inhibitors we demonstrate that ADAM10 is involved in the cleavage of L1 in human podocytes. Injury of podocytes enhanced the ADAM10 mediated cleavage of L1. In addition, we detected ADAM10 in urinary podocytes from patients with kidney diseases and in tissue sections of normal human kidney. Finally, we found elevated levels of ADAM10 in urinary vesicles of patients with glomerular kidney diseases.</p> <p>Conclusions</p> <p>The activity of ADAM10 in human podocytes may play an important role in the development of glomerular kidney diseases.</p

現代語の終助詞「さ」の機能に関する考察

本稿では,長崎(1998)の追調査として,昭和初期から現代に至る終助詞「さ」の機能的変遷を観察した。長崎(1998)では,江戸語における終助詞「さ」の機能を調査し,その主たる機能は断定の働きであったこと,またこの働きが,明治から大正にかけて,現在のように情意表現を主体とした終助詞の機能に移行していく経過を報告した。本調査では,終助詞「さ」を,昭和前期(第二次大戦前),昭和後期(第二次大戦後),平成期に分けて,その機能的変遷を観察した。昭和前期には,終助詞「さ」の用法として,江戸語に見られた丁寧な会話にも使用される用例が見られた。特に江戸語の名残のある女性の言葉遣いの中心その用法が見られた。戦後は,終助詞「さ」の女性の用例は減少し,用言に接続する用例加増加し,「さ」は主に男性が使用する終助詞として定着した。平成に入ると,「さ」は終助詞としての使用より,間投助詞としての使用が目立つようになる。特に若い世代では終助詞「さ」は,男性にもあまり使用されなくなっている。この結果から,今後「さ」の終助詞としての機能は,衰退していくことが予想される

Molecular medicine and concepts of disease: the ethical value of a conceptual analysis of emerging biomedical technologies

Although it is now generally acknowledged that new biomedical technologies often produce new definitions and sometimes even new concepts of disease, this observation is rarely used in research that anticipates potential ethical issues in emerging technologies. This article argues that it is useful to start with an analysis of implied concepts of disease when anticipating ethical issues of biomedical technologies. It shows, moreover, that it is possible to do so at an early stage, i.e. when a technology is only just emerging. The specific case analysed here is that of ‘molecular medicine’. This group of emerging technologies combines a ‘cascade model’ of disease processes with a ‘personal pattern’ model of bodily functioning. Whereas the ethical implications of the first are partly familiar from earlier—albeit controversial—forms of preventive and predictive medicine, those of the second are quite novel and potentially far-reaching