Evolving Backwards

 by Imran Rahman

Adaptive evolution is rarely free from genetic, functional, development and selective constraints - Arnold 1992

One thing commendable about the human body is its ability to withstand immense environmental pressure and keep up with the times. From simple prokaryotic cells to complex multicellular beings, the process of evolution has helped us become the exemplification of a dominant species; bipedalism, brain expansion, and culture all being examples of what deviates us from other organisms.

Nevertheless, the human body isn't perfect. A vast array of symptoms occur because of the mechanical faults in our body, such as appendicitis or imminent back pain due to an unsound spine but arguably most importantly, how we evolved. How can one of our excelling factors be our demise? 

When we were bipedal creatures, we were limited in our effective movements. Over time we evolved to walk upright as it posed significant advantages such as looking over tall grasses to watch out for predators, or terrestrially hunt and sneak up on prey. But there were limitations to this stature. As we started to walk upright, pressure started building pressure on various structures which lead to common diseases associated with humans such as hernias, varicose veins. Pressure built up on systems such as the back, knee and hips which lead to spasms, aches and stunted development. But most significantly bipedal locomotion posed a threat on fetal development and complicated labour and delivery. As we stood up, our hips shrank. Unaware of this deformity, human heads started to increase in size to accommodate brain growth during this time. A larger head having to fit through a smaller pelvis ultimately made humans one of the worst organism at reproducing and the risk of birth-related diseases became more prevalent between humans. More efficient means of transport resulted in disease and disorder. This idea of a trade-off becomes more common later on in history. 

In 1910 a new “strange” disease plagued the medical scene. As physicians observed the blood of these patients, an inherent “sickled” appearance was observed on the red blood cells. This disease; sickle cell anaemia. The malformed shape of the red blood cell prohibited oxygen attachment to the haemoglobin groups coupled with mass clumping characteristic of the cells to the epithelium of capillaries caused mass anaemia in the body by prohibiting tissue the essential oxygen it needs for respiration. People with SCA have a single gene mutation (GAG→GTG and CTC→CAC) which results in defective haemoglobin produced by protein synthesis. These defective haemoglobins can polymerise when deoxygenated resulting in “rod-like structures” forming in the depression inside an RBC. These structures give a noticeable sickle shape. It's no coincidence that the frequency of sickle cell anaemia geographically is associated with malaria-endemic areas. In the past, this genetic disorder was a desired trait in West Africa to give resistance to malaria. since humans/animals with the sickle-cell trait have to break down and detoxify sickled red blood cells their entire lives, their immune system is already in place when the malarial parasite attacks their system. The body sends sickled red blood cells to the spleen for elimination, consequently destroying the parasites hitchhiking on the RBCs. The parasite also needs nutrients from the red blood cells during this period. The cell membranes of the sickled red blood cells are stretched by their unusual shape and become porous thereby leaking nutrients, like potassium, that the parasite needs to survive, so the parasite dies. People with this disease are effectively immune from malaria and natural selection takes its course as the rate of death from malaria during that time was incrementally higher than that of anaemic related symptoms resulting in SCA being a wanted gene for the genome. 

Genome types that promote adaptation in one scenario are expected to promote maladaptation in alternative environments. In any field of science, everything is selective and nothing is constant. In retrospect the future is promising; homoeopathic stem cell research, CAS9 proteins and lentiviral gene deliverance systems pose significant development which can effectively replace deleterious mutations that cause harm and replace them with the correct nitrogenous bases that fix all problems.

References

The emergence of performance trade-offs during local adaptation: insights from experimental evolution Lisa M Bono 1, Leno B Smith Jr 1, David W Pfennig 1, Christina L Burch 1

Disease consequences of human adaptation Justin C. Fay

Resistance to Plasmodium falciparum in sickle cell trait erythrocytes is driven by oxygen-dependent growth inhibition Natasha M. Archer, Nicole Petersen, Martha A. Clark, Caroline O. Buckee, Lauren M. Childs, and Manoj T. Duraisingh