Imagine that you've got a case involving a drug or chemical and there exist multiple well done studies including randomized controlled trials that show consistently strong and statistically significant associations between the drug or chemical and the plaintiff's disease. There's also a very plausible biologic mechanism whereby the substance causes the disease which has been proposed in the scientific literature. Furthermore, the medical records demonstrate via biomarkers that the plaintiff was indeed extensively exposed to the drug or chemical. Causation's a snap, right?

Probably, but it shouldn't be. Consider the case of periodontal disease (PD) and atherosclerotic vascular disease (ASVD). As we've noted previously there are some very intriguing studies published in the literature suggesting a link between the two; a link that has been theorized for many decades. Now, using an evidence-based approach to deriving recommendations from available research (Level of evidence A: recommendation based on evidence from multiple randomized trials or meta-analyses; Level of evidence B: recommendation based on evidence from a single randomized trial or nonrandomized studies; Level of evidence C: recommendation based on expert opinion, case studies, or standards of care) the American Heart Association has put the theory to the test and found it wanting.

You can download (free) a copy of the paper, "Periodontal Disease and Atherosclerotic Vascular Disease: Does the Evidence Support an Independant Association? A Scientific Statement From the American Heart Association" and see how sound causal inferences are made.

Even though "[a]n association between PD and ASVD is supported by evidence that meets standards for Level of Evidence A" and "[a] benefit of periodontal intervention in decreasing local periodontal inflammation is also supported by level A evidence. Causation of ASVD by PD is not supported by either level A or level B evidence." How could this be?

"[P]eriodontal and cardiovascular diseases share multiple risk factors that are prevalent and powerful promoters of disease, including tobacco use, diabetes mellitus, and age." Accordingly, "statements that imply a causative association between PD and specific ASVD events or claim that therapeutic interventions may be useful on the basis of that assumption are unwarranted."

So again, correlation, even strong and consistent, and even coupled to biologic plausibility, ain't causation.