Explore chapters and articles related to this topic
The authority of advance directives 1
Published in Govert den Hartogh, What Kind of Death, 2023
My explanation of why death is an evil could be objected to by saying that it seems to imply a form of backward causation that is usually held to be impossible. The key to a clear understanding here lies in the theory of action. Actions have a teleological structure, an action is designed to bring about a situation which only obtains as a result of the action. Therefore, the success of that action can only be judged afterwards. No reverse causation is involved: the facts themselves are not determined retroactively, only the meaning and the value of those facts. An action may of course be valuable as such, even if it is not successful. But it is also possible that only needless expenses have been incurred when it fails to achieve its object.
Exposure Assessment
Published in Ted W. Simon, Environmental Risk Assessment, 2019
Around 2000, the term “reverse causation” sprouted in studies of body weight and mortality. Generally, reverse causation is the situation in which the outcome is actually causal to the effect. For example, some claim that an active lifestyle protects cognitive function in old age; those older adults with high cognitive function may, however, choose a more active lifestyle. Which one is the cause, and which is the effect?
Extreme Exercise and High Intensity Interval Training in Cardiac Rehabilitation
Published in James M. Rippe, Lifestyle Medicine, 2019
A similar reverse J-shaped association was reported in a German cohort study of 1,038 subjects with stable CAD in which the frequency of strenuous leisure-time PA was assessed over a 10-year period after discharge from an inpatient rehabilitation clinic following an acute cardiovascular event or coronary revascularization procedure.39 Most subjects were ≥60 years of age (57%), male (85%), overweight or obese (76%), and had a history of AMI and hypertension. To reduce the likelihood of reverse causation bias, leading to an overestimation of the hazards in the inactive patient subset and an underestimation in the most physically active cohort, the investigators adjusted for potential confounders, including a baseline history of co-morbid conditions and for self-reported poor health. The highest hazards for cardiovascular and all-cause mortality were found in the least active patient group, as compared with the reference group of patients who were active two to four times per week. However, significantly increased hazards were also observed in the most physically active groups (i.e. daily vigorous exercise), indicating a reverse J-curve pattern of physical activity level with cardiovascular and all-cause mortality (Table 67.3).39 In fact, these hazard ratios were approximately twice those of the reference group.
Establishing target systolic and diastolic blood pressure in diabetic patients with hypertension: what do we need to consider?
Published in Expert Review of Cardiovascular Therapy, 2021
There are limitations to this evidence, firstly it is important to bear in mind that retrospective analysis and observational data is lower-level evidence. Secondly, is the possibility of reverse causation as the contributor to the J point phenomenon. Reverse causation refers to a direction of cause-and-effect contrary to a common presumption. Indeed, because EPHESUS was a trial of adults with systolic dysfunction after recent myocardial infarction and because the decision to revascularize or not was non-randomized, it is possible that the J curve was only seen in the non-revascularized group in this study because these persons were too sick or frail to undergo revascularization (noting that standard of care after MI with systolic dysfunction would be to pursue revascularization).
Post-traumatic stress disorder in a population of 2008 Wenchuan earthquake survivors with disabilities: the role of environmental barriers
Published in Disability and Rehabilitation, 2021
J. D. Reinhardt, X. Zhang, C. Van Dyke, C. Ehrmann, L. Li, Z. Zhao, M. Zhou, H. Li
Our study has several limitations. Since participation required earthquake survivors to come to the study sites at the county or township hospitals, selection bias may have occurred. Those with more severe PTSD symptoms and disabilities, people living in remote areas, and survivors with lack of support and transportation may have been less likely to participate. In addition, people who had recovered from their injury may also have had a reduced probability of participating in the study. These factors could lead to an under- or overestimation of prevalence for the outcome variables. More efforts need to be taken to reach both of those populations in future research and services evaluation. One possibility would be to offer home visits or telephone interviews. As with every cross-sectional study causal inference is not possible, and reverse causation is conceivable. Enhanced encounter with environmental barriers may have influenced PTSD mediated via physical and mental function or increased PTSD symptoms may have amplified the perception of environmental barriers. However, reversing arrows in our model as indicated above produced inferior model fit (RMSEA = 0.135 for unadjusted model, RMSEA = 0.13 for adjusted model).
Vitamin D as disease-modifying therapy for multiple sclerosis?
Published in Expert Review of Clinical Immunology, 2021
Matthew R Lincoln, Raphael Schneider, Jiwon Oh
Observational studies are prone to confounding by unmeasured causal factors and to reverse causation. For example, people with MS may avoid sun exposure because heat exacerbates their symptoms. Thus, low serum vitamin D in MS patients may be a consequence of MS, rather than a cause. We lack large-scale randomized controlled trials (RCTs) of vitamin D in preventing MS. As vitamin D may act in concert with other genetic and environmental factors years before symptom onset, long-term studies of large cohorts would be required. A therapeutic dose or serum level has not been determined for vitamin D, and it is possible that exposure above a sufficient level has a smaller influence on risk, further decreasing power. Vitamin D is commonly used by MS patients, making recruitment and adherence major challenges. Given these challenges to RCT design, recent studies have used Mendelian randomization to demonstrate that insufficient vitamin D is a cause of MS [9,10]. These studies use genetic variants that influence serum vitamin D as instruments to assess vitamin D’s effect on MS risk. Because genetic variants are ‘randomized’ at meiosis, Mendelian randomization permits establishment of causality in a fashion analogous to RCTs. Genetically lowered vitamin D is thus shown to cause MS in both adult [9] and pediatric [10] populations.