July 25, 2007

From John S. Torday:

Re: Claim of reversed human evolution provokes skepticism, interest (Feb. 27): we have also suggested that evolution can be reversed during injury to the lung [see reference], as a way of understanding why the lungs of emphysema patients look and even behave like frogs’ lungs.

The rationale is based on the idea that the molecular signaling mechanisms that have ‘driven’ the lung phenotype [form] from fish to reptile to man and bird have been amplified through natural selection. When these signaling genes are injured, the structure can revert back to a simpler/evolutionarily earlier structure/function relationship which is the equivalent of a phylogenetic [evolutionary] predecessor, man to frog.

In this way the organism can survive until it can reproduce, using the same physiologic principle, but in a somewhat less efficient form. Physicians actually take advantage of this relationship by generating positive pressure on the lung when they apply mechanical ventilation to the patient (called CPAP)- that’s how frogs breathe! They actually force air into their lungs actively, because they don’t have a diaphragm. By understanding the interrelationships between physiologic structure and function between phyletic [evolutionary] groups we can better understand human disease from first principles of physiology. And by dissecting out the molecular signaling mechanisms that have determined structure and function, we will be able to diagnose and treat disease based on the biologic principles by which they were formed through evolution, rather than on the way they appear to function.

Perhaps the genetic defect that’s associated with reverting to quadrupedal locomotion in the Unter Tan study will provide insight into why man is bipedal.

John S. Torday, MSc,PhD
Department of Pediatrics and
Obstetrics and Gynecology
Director, The Henry L. Guenther Laboratory
for Cell/Molecular Research
Harbor-UCLA Medical Center
Los Angeles, Calif.

Reference: J.S. Torday, V.K. Rehan, 2007. The evolutionary continuum from lung development to homeostasis and repair. Am. J. Physiol. Lung Cell Mol. Physiol. 292, L608-L611.


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