I was one of those medical students who was more impressed by what was wrong with what we were being taught than with what the professors extolled as truth.
This did not apply to static things, like anatomy, but to understanding how disease processes proceeded; it was a relevant mode of learning.
One of the most basic things we were taught was that heart attacks occurred when cholesterol plaque accumulated like rust in the pipes, concentrically layering until the stream of blood which could surge through the cylindrical arteries was so narrowed it simply couldn't keep up with demand downstream from the heart muscle which depended on that vital irrigation.
There were problems even then, with this theory. Occlusions seen in arteries occurred a few months after a coronary catherization had shown that same artery to be mostly open.
Clots were found in arteries with not much internal plaquing. It wasn't clear if those clots were simply the result of post mortem changes--pooled blood simply clotting after death.
And always there were those perplexing marathon runners who dropped dead of heart attacks despite their low body weights, low cholesterols and high level of exercise.
Recently, the New York Times ran a piece about CHIP, clonal hematopoiesis of indeterminate potential, which is about stem cells in the bone marrow which carry mutations in the DNA of one or more of three genes (DNMT3A, TET, ASXL1--such memorable names) and what exactly these mutations do to the cells which harbor them is not exactly clear, but these mutated cells accumulate in the bone marrow, living in parts of the marrow "less hospitable" sort of like sickle cells live in a blood stream afflicted with malaria parasites. They survive, although the may cause trouble.
People with these mutations die of heart attacks and strokes at high rates, even if they have normal LDL cholesterol, blood pressure, body weight and even if they exercise.
These mutations accumulate through life, but they don't seem to happen much before the age of 40, as if these stem cells just fray or pill like an old wool sweater. Lots of 70 year old people carry these CHIP cells in their marrow; few 40 year olds do.
So now we have a new idea of how heart attacks happen, at least in some people.
Which means all those answers I marked on my medical school exams which were counted as correct and moved me toward my MD degree were wrong. The total cholesterol in the blood was not put there by eating too many eggs; the trouble in the coronary arteries was not caused by high levels of total cholesterol--it was the LDL portion of the total that wound up in the plaques; the plaques were not gradually strangling off blood flow but were gelatinous and would occasionally rupture, attracting clot which occluded blood flow and the plaques themselves may have formed and been vulnerable because of the accumulation of cells with CHIP mutations inside them.
You may say, what I was taught was not really wrong, just incomplete. I beg to differ. Those professors were very certain of their knowledge.
I was the doubter. There were too many cases which didn't fit their theory.
That's the way science is: constantly changing, a work in progress.
So it is with climate science, climate change. I would not be so sure human activity is warming the planet, but living with uncertainty is the human condition. In the case of climate change you have to ask: If we are wrong and burning fossil fuels has not harmed the planet, what have we lost by shifting to sun and wind?
This did not apply to static things, like anatomy, but to understanding how disease processes proceeded; it was a relevant mode of learning.
One of the most basic things we were taught was that heart attacks occurred when cholesterol plaque accumulated like rust in the pipes, concentrically layering until the stream of blood which could surge through the cylindrical arteries was so narrowed it simply couldn't keep up with demand downstream from the heart muscle which depended on that vital irrigation.
New York Hospital-Cornell Medical Center |
There were problems even then, with this theory. Occlusions seen in arteries occurred a few months after a coronary catherization had shown that same artery to be mostly open.
Clots were found in arteries with not much internal plaquing. It wasn't clear if those clots were simply the result of post mortem changes--pooled blood simply clotting after death.
And always there were those perplexing marathon runners who dropped dead of heart attacks despite their low body weights, low cholesterols and high level of exercise.
Recently, the New York Times ran a piece about CHIP, clonal hematopoiesis of indeterminate potential, which is about stem cells in the bone marrow which carry mutations in the DNA of one or more of three genes (DNMT3A, TET, ASXL1--such memorable names) and what exactly these mutations do to the cells which harbor them is not exactly clear, but these mutated cells accumulate in the bone marrow, living in parts of the marrow "less hospitable" sort of like sickle cells live in a blood stream afflicted with malaria parasites. They survive, although the may cause trouble.
People with these mutations die of heart attacks and strokes at high rates, even if they have normal LDL cholesterol, blood pressure, body weight and even if they exercise.
Van Gogh |
These mutations accumulate through life, but they don't seem to happen much before the age of 40, as if these stem cells just fray or pill like an old wool sweater. Lots of 70 year old people carry these CHIP cells in their marrow; few 40 year olds do.
So now we have a new idea of how heart attacks happen, at least in some people.
Which means all those answers I marked on my medical school exams which were counted as correct and moved me toward my MD degree were wrong. The total cholesterol in the blood was not put there by eating too many eggs; the trouble in the coronary arteries was not caused by high levels of total cholesterol--it was the LDL portion of the total that wound up in the plaques; the plaques were not gradually strangling off blood flow but were gelatinous and would occasionally rupture, attracting clot which occluded blood flow and the plaques themselves may have formed and been vulnerable because of the accumulation of cells with CHIP mutations inside them.
Add caption |
You may say, what I was taught was not really wrong, just incomplete. I beg to differ. Those professors were very certain of their knowledge.
I was the doubter. There were too many cases which didn't fit their theory.
That's the way science is: constantly changing, a work in progress.
So it is with climate science, climate change. I would not be so sure human activity is warming the planet, but living with uncertainty is the human condition. In the case of climate change you have to ask: If we are wrong and burning fossil fuels has not harmed the planet, what have we lost by shifting to sun and wind?