In biology, effects rarely have one cause.
I have a confession to make. In spite of the fact that I currently earn a good chunk of my living by writing articles explaining medical conditions to lay people, reading medical-type articles in the popular press makes me kind of twitchy – sort of “where did that spider that I just saw crawling along the wall go?” twitchy. There’s an inherent problem with any article, even mine, that attempts to give a simplified and reasonably coherent explanation of a scientific study or of a medical condition.
The problem is the word “simplified.”
Humans like cause and effect. Flip the light switch; turn on the light. Buy flowers or candy; get lucky. Wrestle a pig; get muddy. Cause-and-effect seems simple and straightforward. Do A; get result B. No muss, no fuss, no shifts in the space-time continuum.
The problem is that in biology, effects rarely have one cause. Diseases, disease risk, and health benefits are rarely all-or-nothing events. “A causes B” really means something more like, “A (plus 42, Q, and a genetic propensity for X15) causes B (if M is present in the absence of 729z and under W climate conditions). (Maybe)”
This complexity is hard to explain, and it comes up more often than most of us would like to admit. My husband and I recently conversed about an article he’d read by a cardiologist proclaiming the “real” cause of heart disease in humans. Some of the points in the article seem to be pretty valid, but I was struggling to explain to my husband (who, by the way, majored in physiology in college) why I’m so uncomfortable with any article that claims to have the ONE answer to any medical condition, let alone one as complex as heart disease.
An old maxim is quite disappointingly true: The more we know, the less we understand. (Unless the knowledge pertains to Marvel characters or the Star Trek universe.) In the example of the article my husband and I discussed, the author proposed that the increasing incidence of heart disease in modern society is due to inflammation secondary to an imbalance in Omega fatty acid ratios in processed foods.
Ok, we do know that certain fatty acids seem to protect against inflammation. We also know that the inflammatory cascade does seem to tie directly to heart disease. We also know that modern, first world societies eat Roman-orgy worthy loads of processed foods. But that’s kind of where the knowledge part stops and the understanding part gets foggy and swirly like the combination of a bad hangover and one missing contact lens. Because there are plenty of things that either we don’t know or that this explanation leaves out.
We don’t know about actual trends in the incidence of heart disease (or any other disease). What we know is the incidence of reported disease. The question that should arise with any condition where we see a rise in cases over time is: Are we seeing more of this disease, or are we getting better at diagnosing it/over-diagnosing it? As our medical technologies have advanced, our ability to detect disease (and at earlier stages) has improved. So, with certain diseases, one might expect to see a rise, just like we have seen with heart disease, cancers, and autism. But, there is another factor beyond a true increase in the amount of a disease that may cause an increase in reported cases. If you start to look for elephants, pretty soon everything looks like an elephant. I do not recommend testing this theory while looking at your spouse or children unless you like eating cheap takeout alone in a shabby hotel room.
Possible causes for increased “incidence” of a disease include:
- True increase in cases
- Better diagnostics (the cases were always there; we just didn’t see them before)
- Increased vigilance/over-reporting
- All of the above.
Sticking with the heart disease thing, even if one subscribes to an inflammation-as-sole-cause-of-heart-disease theory, causes of inflammation in the body are myriad. The inflammatory cascade is an elaborate domino-maze, and those little chemicals and cells are just waiting for a finger to knock them over. Stress, infection, trauma, surgery, chemicals, all sorts of things can leap in and trigger an inflammatory event.
This is the problem with trying to over-simplify disease explanations, and part of why it seems like every third news story that reports a scientific study on a given disease contradicts the previous two stories. Bodies are complicated things, and biology is less like a Lego sculpture and more like an M.C. Escher print with fish turning into birds and stairs going the wrong way.
Sometimes the problem is one thing: Arrow enters dog’s leg and suddenly dog is limping. Yep, the arrow probably caused the limp.
But, sometimes, cause and effect may not be so simple to pin down. For instance, mother-in-law moved into house and dog began limping. It may be easy - and often desirable - to blame the mother-in-law, but maybe she isn’t kicking the dog (or shooting it with arrows). Maybe the dog always had bad hips or a propensity to ligament or joint issues because his mother was also his sister, aunt, grandmother, and nephew’s uncle’s cousin’s college buddy. Maybe the family recently switched brands of dog food and is unknowingly feeding the same amount of a higher calorie food. Maybe the kids started feeding the dog their leftovers from grandma’s attempts at baking (her eyesight is bad and she mixed up the vanilla with the mint, but the dog doesn’t seem to care). Maybe the mother-in-law tripped over the dog in the hall at night when she got lost heading for the bathroom but wound up in the kitchen, and both she and the dog are too embarrassed to mention the incident. The dog did accept the blame for the kitchen floor, however. So, the dog’s limp could be the result of:
- Bad hips/ligaments/joints
- Genetic propensities
- Weight gain from:
b. Too many half-baked, weirdly green cookies
- The unspeakable kitchen entanglement
- Any combination of the above.
We learn new details about medicine and physiology daily, and the more we know, the more we realize we have to learn. Sequencing of various species’ genomes alone has produced evidence that genetic influence over disease is far more complicated than anything we could have imagined. We used to think that a mutation in Gene A means that the animal will develop disease X. However, we are now learning that multiple genes can work together, that environmental factors can “switch on” genes that make disease more or less likely, and that mutations in certain genes can turn on or off other genes. Chances are this field will get more confusing and complex from here.
We are barely scratching the surface of complexity as we discover ways in which genetics, nutrition, immunology, and more areas of study work together in the causes and progression of disease. Reaching into the genomes, not just of human and animal patients but also of the pathogens that infect them, is giving new clues to the mysteries of disease – such as why the same disease agent can cause different signs in different dogs and cats and why disease progression and recovery rates can vary so much.
All this progress is great, but it also makes practitioners in the field want to hit the bottle (of Advil, soda, or adult beverage) because our best explanations are no longer the ones most people want to hear. People want “yes,” “no,” definitive answers. They want to know exactly what caused their pet’s condition. They don’t want to hear “well, it could be this, or this might also be influencing it, and maybe we should check for such-and-such.” And who can blame them? Certainty is reassuring.
Here is one certainty – medicine is complex.
There. Feel better?