I am fascinated with data. The stories we can tell are meaningful and informative although the absence of accurate interpretation of data often misleads.
Here is one example of how journalism switches an observational study into a causative effect by utilizing a misleading title. I follow Alzheimers Disease research closely and it is definitely the low hanging fruit if you want to look at the break down of science and factual reporting.
Here is one example of how journalism switches an observational study into a causative effect by utilizing a misleading title. I follow Alzheimers Disease research closely and it is definitely the low hanging fruit if you want to look at the break down of science and factual reporting.
Effect of intellectual enrichment on AD biomarker trajectories, a longitudinal imaging study is the title of the original research article. The Washington Post decided to make a causal claim without the science or statistics to make such a claim Keeping mentally active doesn’t stave off Alzheimer’s disease — only its symptoms. We can't make claims of causality in the absence of a randomized clinical trial...although as you can see, even the best researchers fall prey.
“There’s a misconception that if you’re mentally or physically active, you can ward off Alzheimer’s disease.”--study author Prashanthi Vemuri, PhD
| After stratifying by educational levels the data becomes more interesting. Brain fluorodeoxyglucose (FDG) retention is a surrogate for changes in brain metabolism. FDG is nonspecific and may demonstrate derangement in response to inflammation or for a variety of clinical reasons. Structural MRI as described in this study is a surrogate for hippocampal volume downstream from the actual molecular pathology. This measure is a nonspecific result of neuronal damage. |  Similarly, amyloid imaging tends to be a binary diagnostic. Although highly specific for AD pathology, a negative scan provides limited if any information about the potential etiology. |
Journalists need to lead with the context of reported findings.
The limitations of this study are as follows.
(1) We took a simplistic approach of investigating the influence of lifestyle enrichment on the 3 AD biomarkers independently and did not consider the possible interactions between the different biomarker variables, which may be influenced by enrichment variables.
(2) The AD biomarkers used in this study may not be capturing the brain compensatory mechanisms invoked by pathology due to lifestyle enrichment, e.g., recruitment of additional neuronal changes not measured here.
(3) The activity questionnaires are self-reported.
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