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Materials Science in Medicine: Not Just for NASA Engineers

Vitalism is the idea that living beings differ from inanimate objects by possessing a transcendent force or spark which is unexplainable by natural processes.  At its peak, it was a movement in intellectual history embodied by the French philosopher Henri Bergson who coined the term elan vital to describe an idea of vitalism.  It was discredited by the early 20th century through a growing awareness of the scientific fact that physiological processes obey physical laws.   

Prior to that, the discovery of the chemical synthesis of urea in 1828, a molecule which previously had been only found in vivo, is felt by some historians of science to have begun turning the tide against vitalism.  Observations of digestion made by the renown U.S. surgeon William Beaumont in the living stomach of his patient Alexis St. Martin, as published in the 1830’s, surely played a role in demystifying this area of physiology.  

In this commentary, I attempt to examine possible reasons for the persistence of vitalistic thinking in medical education.  Sadly and alarmingly, I see vestiges of vitalism in our U.S. medical community’s approach today in the underutilization of well-established principles of engineering, physics, and materials science in explaining disease.   

In their classic textbook McDonald’s Blood Flow in Arteries, Nichols and O’Rourke noted this failure while discussing the mechanical fatigue of aortic elastin molecules.  With each pulse, these molecules are reversibly stretched.  Like any other molecule subject to cyclic deformation, elastin molecules eventually fatigue and fracture, with the result that the aorta and elastic arteries become progressively stiffer with age.

Why is aortic compliance so important?   Aortic compliance causes blood to flow backwards in the aorta and its proximal branches during late systole and early diastole.   This increases flow to the heart, which is perfused only during diastole.  The retrograde flow also prevents formation of thrombi and development of atherosclerosis.  In one study, retrograde aortic blood flow began to disappear by age 23 and was absent in all subjects by age 36.  

These data remind me that humans evolved to maximize reproductive capacity not for maximum longevity.  Optimizing blood viscosity, heart rate, and blood pressure will preserve yours and your patient’s aortic compliances for as long as possible.   

What Is Healing?

As a pathologist, I see healing tissue several times a day.  I take healing for granted to the extent that when I once dented my car, for the first fraction of a second I expected the car would heal, too!  Human activities such as healing, reproducing, and creating all seemingly violate the second law of thermodynamics, which states that in a closed system, disorder increases.  Faith in the body’s ability to heal may be why material failure is under recognized in biomedicine.  

Another reason may be the assumption that elastin molecules are constantly replaced.  In the 1950’s it was shown using radioactive isotopes that 98% of atoms in the human body are replaced every year.  Indeed, it is reported in the lay press that there is 100% turnover of every atom in the body at least every five years.  Unfortunately, elastin molecules are not replaced throughout life.  You can see the effect of material fatigue on elastin in the decreased elasticity of aged skin.  All elastin molecules in the aorta are present when growth ceases, and loss of compliance begins soon after.   

Another possible explanation for the persistence of vitalistic thought is defective learning—incorrect teaching of medical fallacies.  Do scientists ever fail to incorporate new knowledge and overcome fallacious thinking?  In the early 20th century, William Thomson Kelvin, one of the most prominent physicists of his era, was said to have urged his students not to go into physics because all the great discoveries had already been made.  Of course, this was before the discovery of relativity and quantum mechanics.  

Shakespeare had it right:  “There are more things in heaven and earth… than are dreamt of in your philosophy.”   Alas, even scientists can fail to incorporate lessons as thoroughly as they might or ought, and this would not surprise Thomas Kuhn, an acclaimed historian of science, who coined the term paradigm shift and felt that science is an “irrational process that does not converge with the truth.”  

An Engineer’s Lens on Recent Clinical Findings

In a systematic review and meta-analysis, a Brown University team of clinical researchers reported that transfusing blood into patients who have just suffered a heart attack increases their risk of dying two to threefold.  This finding highlights the potential role of blood viscosity as a mechanism of action which intermediates transfusion therapy and higher incidence of myocardial infarction.  

We have known for years that patients with heart disease are more likely to have pathologically elevated blood viscosity, particularly at low shear rates.  Transfusing these patients will increase their blood viscosity even more.   While this might increase their oxygen carrying capacity, the beneficial effect would not be immediate because it takes one to three days to restore normal deformability to transfused erythrocytes.  Thus, oxygen delivery by newly transfused erythrocytes can be impaired for an acute period.   

The clinical trial CYTO-PV demonstrated that lowering hematocrit with therapeutic phlebotomy and other measures in polycythemia vera patients reduced cardiovascular morbidity and mortality.  This important clinical research produced an insight on the role of hematocrit, a proven Framingham risk factor, but it also highlights a critical gap in the researchers’ approach.  

Polycythemia vera is a blood disease in which red cells are overproduced and hematocrit is elevated.  Naturally, this increases blood viscosity exponentially as a function of hematocrit, and patients are at risk for cardiovascular death and thrombosis.   Hematocrit typically comprises over one-half of the variability of human blood viscosity levels; plasma content, and red blood cell deformability and aggregation constitute nearly all of the rest.  

Monitoring blood viscosity is a unique opportunity for applying materials science to medicine.  Viscosity is a fundamental property of any fluid and directly modulates friction and flow resistance, yet the impact of blood viscosity in health and disease has yet to be felt in mainstream medicine.  When it is, it could qualify as a medical revolution or paradigm shift.  

The blood viscosity profile would enhance and may one day overtake the lipid profile. Therapeutic phlebotomy would be far more commonplace—more commonplace than bariatric surgeries performed in the U.S., and new medicines will be developed.  

Cardiovascular drug therapy is and will continue to be necessary because of limited venous access for therapeutic phlebotomy and the need for longer term viscosity control.  Perhaps a new class of therapeutics will include an antagonist to erythropoietin.  Antagonists of erythrocyte aggregation will be persistent targets for drug development.  HDL is a naturally occurring antagonist of erythrocyte aggregation, which is part of the reason that it has been of interest to drug developers.  

The impact of optimizing blood viscosity will be such that the average lifespan in the U.S. will increase, and the quality of those increased life-years will also increase.  Thick and sticky blood, or elevated blood viscosity, will be recognized as the most important adverse health consequence of the sedentary, industrialized lifestyle, more important than obesity or hypercholesterolemia.  

My question is:  Will the revolution take 100 years to happen, as did the Copernican revolution, 35 years, like the Mendelian revolution, or just 10 years, like the Helicobacter pylori revolution?       


For Further Reading:

Atomic Tune-up:  How the Body Rejuvenates Itself.  National Public Radio, 2007.

Sloop, GD, et al.  A Description of Two Morphologic Patterns of Aortic Fatty Streaks, and a Hypothesis of Their Pathogenesis.

Nichols WW, and O’Rourke MF.  McDonalds’s Blood Flow in Arteries:  Theoretical, Experimental, and Clinical Principles,  Fourth Edition.  London: Arnold, 1998

Last Updated:  2014-12-30

 

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