Using Epidemiology to Explain Disease Causation to Judges and Juries

2020 ◽  
pp. 173-183
Author(s):  
Linda S. Erdreich
Keyword(s):  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Vincent Bessonneau ◽  
Roy R. Gerona ◽  
Jessica Trowbridge ◽  
Rachel Grashow ◽  
Thomas Lin ◽  
...  

AbstractGiven the complex exposures from both exogenous and endogenous sources that an individual experiences during life, exposome-wide association studies that interrogate levels of small molecules in biospecimens have been proposed for discovering causes of chronic diseases. We conducted a study to explore associations between environmental chemicals and endogenous molecules using Gaussian graphical models (GGMs) of non-targeted metabolomics data measured in a cohort of California women firefighters and office workers. GGMs revealed many exposure-metabolite associations, including that exposures to mono-hydroxyisononyl phthalate, ethyl paraben and 4-ethylbenzoic acid were associated with metabolites involved in steroid hormone biosynthesis, and perfluoroalkyl substances were linked to bile acids—hormones that regulate cholesterol and glucose metabolism—and inflammatory signaling molecules. Some hypotheses generated from these findings were confirmed by analysis of data from the National Health and Nutrition Examination Survey. Taken together, our findings demonstrate a novel approach to discovering associations between chemical exposures and biological processes of potential relevance for disease causation.


Author(s):  
Bijaya Naik ◽  
Chandramani Singh ◽  
Bijit Biswas ◽  
Sanjay Pandey ◽  
Santosh Nirala ◽  
...  

2021 ◽  
pp. e1-e19
Author(s):  
Ruff Joseph Macale Cajanding

COVID-19 has emerged as one of the most devastating and clinically significant infectious diseases of the last decade. It has reached global pandemic status at an unprecedented pace and has placed significant demands on health care systems worldwide. Although COVID-19 primarily affects the lungs, epidemiologic reports have shown that the disease affects other vital organs of the body, including the heart, vasculature, kidneys, brain, and the hematopoietic system. Of importance is the emerging awareness of the effects of COVID-19 on the cardiovascular system. The current state of knowledge regarding cardiac involvement in COVID-19 is presented in this article, with particular focus on the cardiovascular manifestations and complications of COVID-19 infection. The mechanistic insights of disease causation and the relevant pathophysiology involved in COVID-19 as they affect the heart are explored and described. Relevant practice essentials and clinical management implications for patients with COVID-19 with a cardiac pathology are presented in light of recent evidence.


1998 ◽  
Vol 28 (1) ◽  
pp. 153-164 ◽  
Author(s):  
Sheldon W. Samuels

The caste in which workers and occupational health practitioners find themselves is plagued by intertwined but separable conflicts. A Cartesian model of causation, useful in the demonologies of regulation and toxic torts, is not heuristic in the revisions of health care, worker's compensation, and disability systems, nor in the prevention of violence in the workplace. Outside the caste, science progresses beyond mind-body bifurcations, the adverse effects of which are magnified within the caste. An argument is made for an ecological concept of causation, drawn from Darwin's community approach to the web of causal factors in both cultural and biological evolution, subsequently stimulated and developed by G. H. Mead and by biologically oriented and sociologically oriented human ecologists for application in the workplace. The ecological model is found in occupational biomedicine as practiced by leaders as diverse as Tichauer and Selikoff. The model integrates environmental, lifestyle, and genetic vectors in a community system bonded by communication and embracing a view of work unbifurcated from other activities.


2014 ◽  
Vol 281 (1788) ◽  
pp. 20140094 ◽  
Author(s):  
M. J. Sweet ◽  
A. Croquer ◽  
J. C. Bythell

Coral diseases have been increasingly reported over the past few decades and are a major contributor to coral decline worldwide. The Caribbean, in particular, has been noted as a hotspot for coral disease, and the aptly named white syndromes have caused the decline of the dominant reef building corals throughout their range. White band disease (WBD) has been implicated in the dramatic loss of Acropora cervicornis and Acropora palmata since the 1970s, resulting in both species being listed as critically endangered on the International Union for Conservation of Nature Red list. The causal agent of WBD remains unknown, although recent studies based on challenge experiments with filtrate from infected hosts concluded that the disease is probably caused by bacteria. Here, we report an experiment using four different antibiotic treatments, targeting different members of the disease-associated microbial community. Two antibiotics, ampicillin and paromomycin, arrested the disease completely, and by comparing with community shifts brought about by treatments that did not arrest the disease, we have identified the likely candidate causal agent or agents of WBD. Our interpretation of the experimental treatments is that one or a combination of up to three specific bacterial types, detected consistently in diseased corals but not detectable in healthy corals, are likely causal agents of WBD. In addition, a histophagous ciliate ( Philaster lucinda ) identical to that found consistently in association with white syndrome in Indo-Pacific acroporas was also consistently detected in all WBD samples and absent in healthy coral. Treatment with metronidazole reduced it to below detection limits, but did not arrest the disease. However, the microscopic disease signs changed, suggesting a secondary role in disease causation for this ciliate. In future studies to identify a causal agent of WBD via tests of Henle–Koch's postulates, it will be vital to experimentally control for populations of the other potential pathogens identified in this study.


Author(s):  
Joseph E. Davis

The Introduction sets out the major themes of the book. These include medicine’s role in the moral and cultural agendas of contemporary society, challenges to the biomedical model represented by new regimes of disease and disorder, and the limitations of principlist bioethics for moving in a more holistic direction. In the working definition of the book, “reductionism” suggests a mechanistic and narrowly somatic understanding of disease, monocausal theories of disease, and an exclusive preoccupation with cure to the neglect of prevention. Meanwhile, “holism” refers to a contextual understanding of disease causation, intervention, or practice. A systemic concern with the whole organism, a focus on the interconnected effects of the larger environment, and ethical concerns with the clinical encounter, can all be characterized as holistic. The Introduction situates the struggle between these perspectives in historical context, and calls for a renewed focus on the social determinants of health and a more holistic ethical perspective.


2007 ◽  
Vol 12 (2) ◽  
pp. 419-428 ◽  
Author(s):  
Michael Kundi

There is an ongoing debate regarding how and when an agent's or determinant's impact can be interpreted as causation with respect to some target disease. The criteria of causation, originating from the seminal work of Sir Austin Bradford Hill and Mervyn Susser, are often schematically applied and, furthermore, there is a tendency to misinterpret the lack of evidence for causation as evidence for lack of a causal relation. There are no criteria for the assessment of evidence concerning an agent's or determinant's propensity to cause a disease, nor are there criteria to dismiss the notion of causation. In this commentary, I propose a dialogue approach for the assessment of an agent or determinant. Starting from epidemiologic evidence, four issues need to be addressed: temporal relation, association, environmental equivalence, and population equivalence. If there are no valid counterarguments, a factor is attributed the potential of disease causation. More often, there will be insufficient evidence from epidemiologic studies. In these cases, other evidence can be used that increases or decreases confidence in a factor being causally related to a disease. Even though every verdict of causation is provisional, action must not be postponed if our present knowledge appears to demand immediate measures for health protection.


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