Who, me?? Why did I clog my 'widow maker'? [on medical cause and effect...and how we know, if we know]

So, having just returned from and now recuperating from coronary bypass surgery, I have to ask the ‘complexity’ question–a very personal one in this case: Why me? I’ve lived a physically and physiologically vigorous life.  My diet may not have always been the very best for cardio health (though, for reasons we’ve discussed here many times over the years, it’s not completely clear what that diet should actually be), but it wasn’t particularly bad, given what’s thought these days to be a “healthy” diet.  

The surgeon who remodeled me at Penn State’s fine medical complex in Hershey, said he knows the risk factors in a population but couldn’t know why any given individual developed clogged coronary arteries, nor which artery would be affected.  His job was to replace, not explain them, one might say.  So, he didn’t even attempt to tell me why I was now in need of bypass surgery.  

As he said, there are five known major risk factors: obesity, unhealthy diet, high cholesterol, genetic predisposition, and smoking. Yes, having diabetes and high blood pressure are risk factors as well, but correlated enough with obesity that perhaps he considers these two conditions to be side effects of obesity.  In any case, these risk factors have been determined by looking at associations between possible causal variables and heart disease in populations.  Resulting statistics describe the population, not identifying specific high-risk individuals within it.  Indeed, some people with heart disease have all the risk factors, some have a combination of a few, and some have none.  And even then, it’s not possible to say which was the cause of the disease in most individual cases.   

I have none of these risk factors — though, I could make up a story.  I smoked when I was young, my father had a pacemaker when he was old, but he lived to 99.  Still, I have done vigorous exercise my whole life, thinking that was my “get cancer program” since it meant, I thought, that I would go out with a coronary.  What caused my artery to clog?  Indeed, why in my case was the clog in an unstentable artery location, and hence required major surgery? 

This brings up, again, the question of whether one’s individual risk can even be known with any sort of ‘precision’. Or is that an illusion? Is it a culpably false promise made by the calculating Dr Collins at NIH, to get NIH funding, rather than to give the public a realistic understanding of what we know and what we can hope to know based on research investment of the type he favors?

How, based on current methods of science, can it really be individual? What kind of information would that require, just considering actual, i.e., past effects, assuming they could really be ascertained to any reasonable measurement standard?  What would you need to consider?  Diet, exercise, personality (temperament, for example).  Climate?  Profession? The effects of war, drought, epidemic?  Genes, even?

Of course, the gross and inexcusable BS of promising ‘precision genomic medicine’ based on very costly, open-ended genomic (and other ‘omic) data collection enterprises is culpable.  It is an often openly acknowledged way of getting, and keeping, mega-funding without having any real ideas (and understandable since medical schools culpably don’t pay faculty salaries or basic research costs as part of their jobs).  Focused science has chances of finding things out; blind data enumeration, far less so–and what we’ve done of that so far shows this quite clearly.

We often say ‘family history’, and clinically this may be the most useful piece of predictive information, but what does that actually explain?  Did Dad or Uncle Jane have the same trait because of genes, or because of their shared family habits and lifestyles?  How could you really tell?  A surgeon need not care, as their job is to fix the clogged pipes, and if heart disease runs in a family the physician will treat his or her patient as high risk.  Still, to prevent this sort of thing, we need to know what causes it. 

This is a central biomedical question!  It is hard enough to know, much less accurately measure, all factors in life that might in this or that way be a ‘risk’ factor for a given disease, like clogged coronary plumbing.  Is it a delusion to think we could identify, much less measure all the factors?  If, as seems obvious, there isn’t just a single factor, and probably everyone’s exposure set is different (and their effects need not be ‘additive’), how on earth can we even know how well we are measuring, or ascertaining, such factors?

And, if we can do this, it only applies directly to current cases and their past lifestyle exposures.  But what we would like to do, for individuals and for public health, is to predict the future to lower risks.  However, there is no way, not even in principle, no reasonable chance of knowing what future exposures will be, not even for populations.  Diets and lifestyles change in ways we cannot predict, nor can we predict major future events–climate, war, pestilence, food types and availability, etc., that would be highly relevant.

So what should we do with our understanding of these unpredictable factors?  Perhaps just level with patients and the public, and stop using the public to endow a particular, and particularly costly, part of the university research empire.  Maybe a return to focused, hypothesis–based research–actual science–in my view.